Psy3241 - User contributions [en]

Autotopagnosia

Daveecee — Sun, 04 May 2008 18:41:21 GMT

Daveecee:

[[Category:Neuropsychological syndromes]]
'''Autotopagnosia''' is a neuropsychological syndrome characterized by the inability to name or locate parts of one's own (or, in some cases, another person's) body. This peripersonal space disorder is usually associated with generalized brain damage or lesions of the left parietal lobe.

The symptoms of autotopagnosia are widely varied. For example, some individuals with the disorder can correctly identify parts of inanimate objects or animals, but are unable to locate the parts of a human body, whether it is their own or someone else’s. Others can effectively identify isolated parts of a human body (for instance, a picture of an arm by itself), but are unable to identify body parts when they are presented as a whole human body. Because of the symptoms are so highly varied across affected individuals, autotopagnosia (along with most other neuropsychological disorders) likely has more than one underlying cause.

There are several main hypotheses describing the underlying cognitive deficits that might cause the disorder:

*It is a language problem. More specifically, it is a category-specific comprehension deficit. Because the disorder is often associated with a lesion in the posterior left hemisphere (the part of the brain responsible for language), difficulty in describing body parts (or describing things in general) is likely to occur in affected individuals.
*It is a visuospatial problem. If the lesion causing the disorder is located in the (visuospatial) parietal lobe, the affected individual would probably have difficulty pointing to parts of an object.
*It is a body image problem. Since body image is mediated by systems in the left parietal lobe, a disruption of this region might lead to the inability to point to human body parts.

Reference:

Ogden, J. A. (2005). Fractured Minds: A Case Study Approach to Neuropsychology. Second Edition. New York: Oxford University Press.

Synesthesia

Daveecee — Sun, 27 Apr 2008 06:42:47 GMT

Daveecee:

[[Category:Neuropsychological syndromes]]

Synesthesia is a neurological syndromein which stimulation of one sensory modality automatically and uncontrollably triggers another sensory modality. The types of synesthesia discussed in class include:

#Color-graphemic synesthesia: written letters induce vivid color experiences
#Colored-hearing: color experiences induced by spoken words
#Numbers are projected into a spatial layout in front of the patient's chest, and are colored
#Periods of time are conceptualized in a colored spatial layout

Synesthesia often begins in early childhood, but it can be brought about as a result of brain injury or sensory dedeafferentation.

Most of the time, synesthesia is unidirectional (for example, most colored-hearing synesthetes do not hear sounds when they see colors). Also, even if patients have the same form of synesthesia, it is unlikely that their concurrents are the same, meaning: letters will not produce the same colors to different synesthetes.

== Color-graphemic ==

[[image:synesthesia.png|250px|thumb|How somebody with color-graphemic synesthesia may read words and numbers]]

In Color-graphemic synesthesia, written words, letters, and numbers induce vivid color experiences. The actual experience of color tends to vary from patient to patient. Patients may report any of the following:

#As seen in the image, perceiving letters and numbers as being colored rather than monochrome (black).
#Seeing certain letters/words/numbers may cause the patient to see a screen of color "projected" onto their "mind's eye."
#As above, but rather than being fully colored, the screen is a blurry and colored version of the letter they are seeing.
#Patients may simply have an association between colors and letters/words/numbers without actually having a visual perception of color.

Sperling et. al (2006) found evidence that color-graphemic synesthesia is caused by an activation in the color areas ([[V4]]/V8) in the visual cortex as well as the inferior temporal lobe, another region known to be a cortical color processing system. A possible explanation for perceiving colors when seeing writing can be derived from activation of the superior temporal lobe and insula, which are hypothesized to mediate pathway convergence during the induction of a synesthetic-colour experience, leading to feedback-activation of visual areas responsible for color perception.

== Colored-hearing ==

In colored-hearing synesthesia, sounds produce an extrasensory experience of color. This is usually in response to tones or other aspects of sound. Usually, the sounds that produce colors in colored-hearing synesthetes are musical sounds, or environmental sounds (such as alarm clocks, or birds chirping). Like in color-graphemic synesthesia, activation in V4/V8 has been associated with the experience of color in response to music or environmental sounds.

== Number → Color & Shape ==

In (number)→(color/shape) synesthesia, the patient will project numbers in front of themselves in, for example, a coloured arc.

== Time → Location ==

In (time)→(location) synesthesia, the patient will arrange periods of time in a colored shape. For example, they may conceptualize the months of the year into a flat, horizontal loop surrounding them, and each month being a different color.

== Causes ==

It is believed that synesthesia may have a genetic link, according to a twin study done by Hancock (2006). Hancock observed monozygotic twins, who both had color-number associations. The boys did not report seeing colors or even perceiving color experiences but, rather, had a simple association between numbers and colors, as if the numbers ''could be'' represented by colors. The genetic link was made possible by the discovery that the boys' mother also has a color-number association.

Synesthesia can also be a learned association. Witthoft and Winawer (2006) describe a case study in which their patient had a learned color-letter association as a byproduct of having colored refrigerator magnets as a child. Interestingly enough, this case also described the possibility that synesthetic color-letter associations can transfer between letters; their patient moved to Russia at the age of three, and her color-graphemic synesthesia transferred to Russian Cyrillik.

== References ==

Grossenbacher, P.G., & Lovelace, C.T. (2001). Mechanisms of synesthesia: Cognitive and physiological constraints. ''TRENDS in Cognitive Sciences, 5''(1), 36-41.

Hancock, P (2006). Monozygotic twins’ colour-number association: A case study. ''Cortex, 42'', 147-150.

Sperling, J. M., Prvulovic, D., Linden, D.E.J., Singer, W., & Stirn, A. (2006). Neuronal correlates of a colour-graphemic synaesthesia: A fMRI study. ''Cortex, 42'', 295-303.

Witthoft, N., & Winawer, J. (2006). Synesthetic colors determined by having colored refrigerator magnets in childhood. ''Cortex, 42'', 175-183.

== External Links ==

[http://youtube.com/watch?v=DvwTSEwVBfc Tasting Colors]

Synesthesia

Daveecee — Sun, 27 Apr 2008 06:42:12 GMT

Daveecee:

[[Category:Neuropsychological syndromes]]

Synesthesia is a neurological syndromein which stimulation of one sensory modality automatically and uncontrollably triggers another sensory modality. The types of synesthesia discussed in class include:

#Color-graphemic synesthesia: written letters induce vivid color experiences
#Colored-hearing: color experiences induced by spoken words
#Numbers are projected into a spatial layout in front of the patient's chest, and are colored
#Periods of time are conceptualized in a colored spatial layout

Synesthesia often begins in early childhood, but it can be brought about as a result of brain injury or sensory dedeafferentation.

Most of the time, synesthesia is unidirectional (for example, most colored-hearing synesthetes do not hear sounds when they see colors). Also, even if patients have the same form of synesthesia, it is unlikely that their concurrents are the same, meaning: letters will not produce the same colors to different synesthetes.

It is believed that synesthesia may have a genetic link, according to a twin study done by Hancock (2006). Hancock observed monozygotic twins, who both had color-number associations. The boys did not report seeing colors or even perceiving color experiences but, rather, had a simple association between numbers and colors, as if the numbers ''could be'' represented by colors. The genetic link was made possible by the discovery that the boys' mother also has a color-number association.

Synesthesia can also be a learned association. Witthoft and Winawer (2006) describe a case study in which their patient had a learned color-letter association as a byproduct of having colored refrigerator magnets as a child. Interestingly enough, this case also described the possibility that synesthetic color-letter associations can transfer between letters; their patient moved to Russia at the age of three, and her color-graphemic synesthesia transferred to Russian Cyrillik.

== Color-graphemic ==

[[image:synesthesia.png|250px|thumb|How somebody with color-graphemic synesthesia may read words and numbers]]

In Color-graphemic synesthesia, written words, letters, and numbers induce vivid color experiences. The actual experience of color tends to vary from patient to patient. Patients may report any of the following:

#As seen in the image, perceiving letters and numbers as being colored rather than monochrome (black).
#Seeing certain letters/words/numbers may cause the patient to see a screen of color "projected" onto their "mind's eye."
#As above, but rather than being fully colored, the screen is a blurry and colored version of the letter they are seeing.
#Patients may simply have an association between colors and letters/words/numbers without actually having a visual perception of color.

Sperling et. al (2006) found evidence that color-graphemic synesthesia is caused by an activation in the color areas ([[V4]]/V8) in the visual cortex as well as the inferior temporal lobe, another region known to be a cortical color processing system. A possible explanation for perceiving colors when seeing writing can be derived from activation of the superior temporal lobe and insula, which are hypothesized to mediate pathway convergence during the induction of a synesthetic-colour experience, leading to feedback-activation of visual areas responsible for color perception.

== Colored-hearing ==

In colored-hearing synesthesia, sounds produce an extrasensory experience of color. This is usually in response to tones or other aspects of sound. Usually, the sounds that produce colors in colored-hearing synesthetes are musical sounds, or environmental sounds (such as alarm clocks, or birds chirping). Like in color-graphemic synesthesia, activation in V4/V8 has been associated with the experience of color in response to music or environmental sounds.

== Number → Color & Shape ==

In (number)→(color/shape) synesthesia, the patient will project numbers in front of themselves in, for example, a coloured arc.

== Time → Location ==

In (time)→(location) synesthesia, the patient will arrange periods of time in a colored shape. For example, they may conceptualize the months of the year into a flat, horizontal loop surrounding them, and each month being a different color.

== References ==

Grossenbacher, P.G., & Lovelace, C.T. (2001). Mechanisms of synesthesia: Cognitive and physiological constraints. ''TRENDS in Cognitive Sciences, 5''(1), 36-41.

Hancock, P (2006). Monozygotic twins’ colour-number association: A case study. ''Cortex, 42'', 147-150.

Sperling, J. M., Prvulovic, D., Linden, D.E.J., Singer, W., & Stirn, A. (2006). Neuronal correlates of a colour-graphemic synaesthesia: A fMRI study. ''Cortex, 42'', 295-303.

Witthoft, N., & Winawer, J. (2006). Synesthetic colors determined by having colored refrigerator magnets in childhood. ''Cortex, 42'', 175-183.

== External Links ==

[http://youtube.com/watch?v=DvwTSEwVBfc Tasting Colors]

Nikolic et al. (2007)

Daveecee — Sun, 27 Apr 2008 06:37:56 GMT

Daveecee:

[[Category:Synesthesia Symposium]]

Color Opponency in Synaesthetic Experiences
by Danko Nikolic, Philipp Lichti, and Wolf Singer

== Synaesthesia? ==

Synaesthesia is a harmless perceptual condition in which there is a blending of the senses. Generally letters and numbers are seen as different colors or where music initiates the perception of color. A synaesthetic individual could be said to have the ability to see sound. Some synaesthetes are categorized as associators which is the perception of a color on an internal screen or in the mind, while others are considered projectors where color is seen on objects in space such as colored letters on a page.

==The Stroop Test ==

A Stroop test which was developed in 1935 by J. R. Stroop, an individual is instructed to name the ink color of a word that refers to a color. The reaction times to identify the ink color for the individual is measured and analyzed. Reaction times are generally longer if the color of the ink and the meaning of the word do not match (incongruent condition), for example if yellow is written in red ink. This test can be applied to study synaesthetic individuals by adjusting the meaning of the words to match the perceptual experience a person has to that word. In summary, a synaesthetic person would look at a word that evokes a red perception that would be colored in red ink and would be able to react faster than a non-synaesthetic individual.

== Color Opponency in Synaesthetic Experiences ==

In the current study researchers are taking advantage of the color opponent receptive fields of the brain. The color opponent receptive fields are cells that are excited by red and inhibited by green and cells that are excited by yellow and inhibited by blue. This fact allows researchers to study which receptive fields are active during real and synaesthetic perceptions.

== Experiment 1 ==

===Subjects===
6 synaesthetic individuals participated in the study, four were women and two were men and five of these people had other forms of Synaesthesia. 12 nonsynaesthetes participated in the study as the control group who matched the synaesthetes in gender and age.

===Procedure===
The subjects were tested on color associations. There were three conditions: the congruent condition in which the color of each grapheme was the same as the synaesthetic color; the incongruent opponent condition in which the color of each grapheme was opposite to the synaesthetic color; the incongruent independent condition in which the color of each grapheme and the synaesthetic color were represented by different opponent-color channels; and the baseline condition in which the experimenters used a grapheme that did not have a synaesthetic color association. The experiment took place in a dimly lit room with a computer running the visual stimulation tool. The subjects were given 200 trials in which they were told to accurately name the real color of each grapheme as fast and as they could. The entire experiment took approximately 25 minutes.

===Results===
The subjects response accuracy was very high (98%) but a Tukey HSD test for a post hoc comparison indicated that subjects named the correct color faster in the congruent condition than in the incongruent condition. The experimenters found significant results between the incongruent independent condition (which was named faster) and the incongruent opponent condition. They found that opponent incongruent colors produced more interference than the independent incongruent colors. They also found that the congruent synaesthetic colors helped the subjects to name the real colors of the graphemes.

==Experiment 2==
The experimenters examined semantic associations between shape and color using the Stroop task. The stimuli that they used were commonly known everyday associations between shape and color. The experimenters hypothesized that semantic associations do not involve the opponent-color system. They used four of the synaesthetes and 8 of the control subjects from experiment 1. They also used the same methods as for the synaesthetic Stroop test except that only three objects were used and each only appeared in three stimulation conditions. The subjects were presented each stimulus 25 times, given a total of 225 trials overall.

===Results===
Once again, the response accuracy was very high, indicating that color opponency does in fact affect the semantic associations between shape and color differently than synaesthetic associations.

==Conclusion==

Overall, the experimenters concluded that opponent synaesthetic and real colors interfere the most with the naming and perception of a real color. Conversely, when synaesthetic and real colors are identical, the color-naming process is assisted and the response times are decreased. These findings show that the color experiences stimulated by this experiment involve color-opponent channels and thus neurons in the V1 to V4/V8 areas. The results of experiments 1 and 2 suggest that the semantic associations between graphemes and colors explain the interference between nonopponent colors.

File:Synesthesia.png

Daveecee — Sun, 27 Apr 2008 06:00:42 GMT

Daveecee:

Primary auditory cortex

Daveecee — Sun, 27 Apr 2008 04:16:36 GMT

Daveecee:

[[image:Brodmann_41_42.png|300px|thumb|Brodmann areas 41 and 42: the primary auditory cortex]]

The primary auditory cortex, denoted as Brodmann areas 41 and 42, is the area in the brain which receives sensory auditory information directly from the ears. Like most sensory modalities, information from the right ear is directed to the left primary auditory cortex, and information from the left ear is sent to the right primary auditory cortex. The primary auditory cortex is located on Heschl's gyrus the lateral sulcus, and the posterior half of the superior temporal gyrus.

== Plasticity ==

The cortex has been observed to be plastic. When an area of the brain is deprived of its usual sensory input, it sometimes "switches" to another sensory modality to, in a way, help out with processing. The primary auditory cortex has shown to be activated by visual stimuli when deprived of auditory input.

== Deaf Hearing ==

Deaf hearing is the auditory analogue to [[blindsight]]. Like in blindsight, patients with deaf hearing have bilateral lesions in temporal areas involved in auditory perception, especially the primary auditory cortex. However, due to subcortical auditory pathways in the midbrain and brainstem remaining active, some level of auditory processing remains despite the fact that the patient experiencing cortical deafness has no awareness of hearing sounds. Although the patient has no awareness of hearing sounds, they display orienting reflexes to auditory stimuli despite insisting they heard nothing.

== References ==

Garde, M. M., & Cowey, A. (2000). "Deaf hearing": Unacknowledged detection of auditory stimuli in a patient with cerebral deafness. ''Cortex, 36'', 71-80.

Newton, J. R., & Sur, M. Rewiring Cortex: functional plasticity of the auditory cortex during development. ''Department of Brain & Cognitive Sciences, Picower Center for Learning & Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts.''

[[Category:Brain areas]]

Primary auditory cortex

Daveecee — Sun, 27 Apr 2008 04:16:02 GMT

Daveecee:

Corpus callosum

Daveecee — Fri, 25 Apr 2008 07:28:04 GMT

Daveecee:

[[Category:Brain areas]]

The '''corpus callosum''' (Latin for “tough body”) is a broad, thick bundle of nerve fibers in the entire nervous system, running from side to side and consisting of millions and millions of nerve fibers. If we cut a brain in half down the middle, we would also cut through the fibers of the corpus callosum.

When looking at the middle side of one half of the brain, in magnetic resonance imaging (MRI), the corpus callosum looks like a section of a mushroom cap located at the center of the brain. [http://www.youtube.com/watch?v=7zOa3LLrHKc Video of Corpus callosum]
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[[Image:Col.gif]]

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== Development ==
In a healthy infant’s brain, the corpus callosum develops between 12 to 16 weeks after conception. The fibers of the corpus callosum continue to become more and more effective into adolescence. By the time a child is around the age of 12 years, the corpus callosum functions will in adulthood, allowing rapid interaction between the two sides of the brain. From this age on the corpus callosum becomes increasingly functional in their typically developing children.
----
== Close-up Sagittal Section of Hemisphere ==
[[Image:Bbb.gif]]

1.)Rostrum of corpus callosum

2.)Genu of corpus callosum

3.)Body of corpus callosum

4.)Splenium of corpus callosum

5.)Septum pellucidum

6.)Anterior commissure

7.)Fornix

8.)[[Hippocampus]]

9.)Cingulate gyrus

10.)Paraterminal gyrus

== Corpus callosotomy ==

Severing the corpus callosum became a method of dealing with and localizing severe epileptic seizures. Sometimes, seizures in the brain will begin in one place and spread throughout the entire brain. The corpus callosum can be severed to prevent seizures from reaching the other hemisphere or, in some cases, to stop the seizures altogether. This procedure is known as a ''corpus callosotomy'' and results in the split-brain condition.

The split-brain condition is where hemispheres of the brain can no longer interact with each other due to the severing of the corpus callosum. For example, when a split-brain patient is shown an object, such as a cup, in their left visual field, they will be unable to name it. This is because the visual stimulus enters the right hemisphere through the left eye, but the information can not travel to the left hemisphere to be recognized by the language center of the brain. Thus it is impossible for the subject to name the object unless they are able to turn their head and move the object into their right visual field. However, if they are asked to identify the object using a pencil in their left hand to draw or write with, they can identify the object.

== References ==
The Anatomy Project, (2000). Close-up Sagittal Section of Hemisphere. Retrieved April 19, 2008, from Medical Gross Anatomy Web site: http://anatomy.med.umich.edu/atlas/n1a5p8.html

Hubel, D. H (2006). THE CORPUS CALLOSUM. Retrieved April 21, 2008, from Eye, Brain, and Vision Web site: http://hubel.med.harvard.edu/b34.htm

NODCC, (2006). What is the Corpus Callosum? . Retrieved April 21, 2008, from National Organization for Disorders in the CorpusCallosum Web site: http://www.nodcc.org/what_is_the_corpus_callosum.php

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Corpus callosum

Daveecee — Fri, 25 Apr 2008 07:20:29 GMT

Daveecee:

Hippocampus

Daveecee — Fri, 25 Apr 2008 07:18:20 GMT

Daveecee: /* '''Importance of the Hippocampus''' */

[[Category:Brain areas]]

The hippocampus is the medial part of the left temporal lobe. The hippocampus, like many other parts of the brain, got its name from its shape which looks like a seahorse. The etiology is Greek from the words hippos (horse) and kampos (a sea monster). [[Image:Amygdala hippocampus lateral large.jpg]]

=='''Importance of the Hippocampus'''==

The hippocampus has many functions. First, the hippocampus is very influential in memory. According to Stirling, the hippocampus is important on the formation of new explicit- declarative long term memories, a process called consolidation(139). Also, in the Bechara article that we read, researchers found that it also aids in the establishment of declarative knowledge. The participant with bilateral damage hippocampus didn’t acquire the declarative facts about which visual or auditory stimuli were paired with the unconditioned stimulus but did acquire conditioned autonomic responses to visual or auditory stimuli. Finally, the hippocampus is also important in navigation. In a study that was mentioned in class, the hippocampus of taxi drivers in London was bigger than bus drivers in London. This suggests that because the taxi drivers’ job utilizes more navigation than a bus driver with a stagnant route, these demands have had an impact on their hippocampus.

The function of the hippocampus was widely unknown until its destruction in the brain of [[H.M. (patient)|H.M.]] in 1953. Following H.M.'s operation, his inability to form new memories prompted further study, greatly enhancing knowledge of human memory systems.

=='''References'''==
Stirling, John. Introducing Neuropsychology.
Hippocampus. http://www.medterms.com/script/main/art.asp?articlekey=3757

Hippocampus

Daveecee — Fri, 25 Apr 2008 07:18:03 GMT

Daveecee: /* '''Importance of the Hippocampus''' */

[[Category:Brain areas]]

The hippocampus is the medial part of the left temporal lobe. The hippocampus, like many other parts of the brain, got its name from its shape which looks like a seahorse. The etiology is Greek from the words hippos (horse) and kampos (a sea monster). [[Image:Amygdala hippocampus lateral large.jpg]]

=='''Importance of the Hippocampus'''==

The hippocampus has many functions. First, the hippocampus is very influential in memory. According to Stirling, the hippocampus is important on the formation of new explicit- declarative long term memories, a process called consolidation(139). Also, in the Bechara article that we read, researchers found that it also aids in the establishment of declarative knowledge. The participant with bilateral damage hippocampus didn’t acquire the declarative facts about which visual or auditory stimuli were paired with the unconditioned stimulus but did acquire conditioned autonomic responses to visual or auditory stimuli. Finally, the hippocampus is also important in navigation. In a study that was mentioned in class, the hippocampus of taxi drivers in London was bigger than bus drivers in London. This suggests that because the taxi drivers’ job utilizes more navigation than a bus driver with a stagnant route, these demands have had an impact on their hippocampus.

The function of the hippocampus was widely unknown until its destruction in the brain of [[H.M.|H.M. (patient)]] in 1953. Following H.M.'s operation, his inability to form new memories prompted further study, greatly enhancing knowledge of human memory systems.

=='''References'''==
Stirling, John. Introducing Neuropsychology.
Hippocampus. http://www.medterms.com/script/main/art.asp?articlekey=3757

Transcranial magnetic stimulation

Daveecee — Fri, 25 Apr 2008 07:13:54 GMT

Daveecee:

[[Image:TMS.jpg|200px|thumb|Transcranial Magnetic Stimulation]]

Transcranial Magnetic Stimulation is a form of controlling brain activity using a magnetic current. An electrical current is passed through a magnetic coil, the shape of which determines the strength and size of the magnetic field. The coil is held above the scalp, not touching the skin. No contact with the head is necessary for TMS. Small magnetic fields emitted from the coil into the brain can make brain areas either more active or less active.

TMS can temporarily influence movement, speech, reaction time, memory, visual perception, and mood. The effect of TMS usually wears off a few minutes after magnetic stimulation has ceased.

TMS is often used to establish causal roles of distinct areas by, for example, showing that performance in a task that draws on a specific brain area is impaired following TMS to that area.

Another form of transcranial magnetic stimulation is repetetive transcranial magnetic stimulation (rTMS). rTMS, in contrast to TMS, produces longer-lasting effects on the target area of the brain. It is often used for treatment of neurological disorders such as depression, Parkinson's disease, and auditory hallucinations, as well as simple headaches and migraines.

[[Category:Neuropsychological methods]]

Transcranial magnetic stimulation

Daveecee — Fri, 25 Apr 2008 07:13:42 GMT

Daveecee:

Transcranial magnetic stimulation

Daveecee — Fri, 25 Apr 2008 07:12:35 GMT

Daveecee:

Transcranial magnetic stimulation

Daveecee — Fri, 25 Apr 2008 06:47:07 GMT

Daveecee:

Transcranial magnetic stimulation

Daveecee — Fri, 25 Apr 2008 06:24:30 GMT

Daveecee:

[[Image:TMS.jpg|200px|thumb|Transcranial Magnetic Stimulation]]

[[Category:Neuropsychological methods]]

File:TMS.jpg

Daveecee — Fri, 25 Apr 2008 06:22:15 GMT

Daveecee:

Ptito et al. (2005)

Daveecee — Fri, 25 Apr 2008 06:15:54 GMT

Daveecee:

[[Category:Plasticity Symposium]]

'''Cross-Modal Plasticity Revealed by Electrotactile Stimulation of the Tongue in the Congenitally Blind (Ptito et al., 2005)'''

The experimenters in this study used PET scanning to study cross-modal plasticity in the congenitally blind, using electrotactile stimulation of the tongue. Before training with the tongue display unit (TDU), neither the blind nor the sighted control subjects showed any change in regional cerebral blood flow (rCBF) in the occipital cortex. After training, however, rCBF in the occipital cortex of the blind subjects increased dramatically, providing evidence of training-induced plasticity

== Participants ==
Participants included 6 blind and 5 sighted blind-folded controls with a mean age of 29 years. MRI scans of the blind subjects were normal. Sighted control subjects also had normal neurological exams and normal vision.

== Training ==
Participants were trained to use their tongue in a Snellen orientation detection task using the TDU. The training lasted for seven days for one-hour sessions. For training, observers projected a T onto the subject's tongue using the TDU. Subjects were allowed to orient the T how they pleased in order to get used to the machine. They were scanned before and after training.

== Results ==
Before training, no significant changes in regional cerebral blood flow (rCBF) were observed in the occipital cortex of either group. After practice for the blind, however, activity in the occipital cortex increased. This increase in activity was not observed in the sighted participants, providing evidence for training-induced plasticity in the congenitally blind.

Interestingly, the rate of learning was actually equal among both groups of blind and sighted subjects.

An inter-regional correlation analysis showed that task-related rCBF changes in the left posterior parietal cortex were positively correlated with rCBF changes in the occipital area of the trained blind participants.

All six blind subjects showed activation in the occipital cortex following training with the TDU.

== Conclusion ==

This data revealed that cross-modal plasticity in the blind develops rapidly and that the occipital cortex is part of a functional neural network for tactile discrimination in conjunction with the posterior parietal cortex. Data further showed that the tongue can act as a portal to convey somatosensory information to visual cortex.

Blind subjects showed activation of the occipital cortex while using the TDU after training while sighted control subjects did not despite an equal learning curve, showing that there is a functional role for the occipital lobe even in the congenitally blind.

In contrast, sighted subjects actually showed a deactivation of the visual cortex. However, this is in line with the observation that focusing on one sensory modality causes decreased activity in areas of the brain focusing on other modalities. Sighted controls showed, instead, activation of the somatosensory cortex.

It has been suggested that the occipital activation can be explained by the fact that it is adjacent to the superior parietal lobe, in which tactile information is processed. Thus the tactile information may be "leaking" into the occipital lobe due to it not being used for anything else.

Talk:Ptito et al. (2005)

Daveecee — Fri, 25 Apr 2008 06:15:43 GMT

Daveecee:

Ptito et al. (2005)

Daveecee — Fri, 25 Apr 2008 06:14:53 GMT

Daveecee:

[[Category:Plasticity Symposium]]

NOTE: PLEASE READ THE DISCUSSION PAGE ABOVE BEFORE EDITING THIS

'''Cross-Modal Plasticity Revealed by Electrotactile Stimulation of the Tongue in the Congenitally Blind (Ptito et al., 2005)'''

The experimenters in this study used PET scanning to study cross-modal plasticity in the congenitally blind, using electrotactile stimulation of the tongue. Before training with the tongue display unit (TDU), neither the blind nor the sighted control subjects showed any change in regional cerebral blood flow (rCBF) in the occipital cortex. After training, however, rCBF in the occipital cortex of the blind subjects increased dramatically, providing evidence of training-induced plasticity

== Participants ==
Participants included 6 blind and 5 sighted blind-folded controls with a mean age of 29 years. MRI scans of the blind subjects were normal. Sighted control subjects also had normal neurological exams and normal vision.

== Training ==
Participants were trained to use their tongue in a Snellen orientation detection task using the TDU. The training lasted for seven days for one-hour sessions. For training, observers projected a T onto the subject's tongue using the TDU. Subjects were allowed to orient the T how they pleased in order to get used to the machine. They were scanned before and after training.

== Results ==
Before training, no significant changes in regional cerebral blood flow (rCBF) were observed in the occipital cortex of either group. After practice for the blind, however, activity in the occipital cortex increased. This increase in activity was not observed in the sighted participants, providing evidence for training-induced plasticity in the congenitally blind.

Interestingly, the rate of learning was actually equal among both groups of blind and sighted subjects.

An inter-regional correlation analysis showed that task-related rCBF changes in the left posterior parietal cortex were positively correlated with rCBF changes in the occipital area of the trained blind participants.

All six blind subjects showed activation in the occipital cortex following training with the TDU.

== Conclusion ==

This data revealed that cross-modal plasticity in the blind develops rapidly and that the occipital cortex is part of a functional neural network for tactile discrimination in conjunction with the posterior parietal cortex. Data further showed that the tongue can act as a portal to convey somatosensory information to visual cortex.

Blind subjects showed activation of the occipital cortex while using the TDU after training while sighted control subjects did not despite an equal learning curve, showing that there is a functional role for the occipital lobe even in the congenitally blind.

In contrast, sighted subjects actually showed a deactivation of the visual cortex. However, this is in line with the observation that focusing on one sensory modality causes decreased activity in areas of the brain focusing on other modalities. Sighted controls showed, instead, activation of the somatosensory cortex.

It has been suggested that the occipital activation can be explained by the fact that it is adjacent to the superior parietal lobe, in which tactile information is processed. Thus the tactile information may be "leaking" into the occipital lobe due to it not being used for anything else.

Ptito et al. (2005)

Daveecee — Fri, 25 Apr 2008 06:02:52 GMT

Daveecee:

[[Category:Plasticity Symposium]]

NOTE: PLEASE READ THE DISCUSSION PAGE ABOVE BEFORE EDITING THIS

'''Cross-Modal Plasticity Revealed by Electrotactile Stimulation of the Tongue in the Congenitally Blind (Ptito et al., 2005)'''

The experimenters in this study used PET scanning to study cross-modal plasticity in the congenitally blind, using electrotactile stimulation of the tongue. Before training with the tongue display unit (TDU), neither the blind nor the sighted control subjects showed any change in regional cerebral blood flow (rCBF) in the occipital cortex. After training, however, rCBF in the occipital cortex of the blind subjects increased dramatically, providing evidence of training-induced plasticity

== Participants ==
Participants included 6 blind and 5 sighted blind-folded controls with a mean age of 29 years. MRI scans of the blind subjects were normal. Sighted control subjects also had normal neurological exams and normal vision.

== Training ==
Participants were trained to use their tongue in a Snellen orientation detection task using the TDU. The training lasted for seven days for one-hour sessions. For training, observers projected a T onto the subject's tongue using the TDU. Subjects were allowed to orient the T how they pleased in order to get used to the machine. They were scanned before and after training.

== Results ==
Before training, no significant changes in regional cerebral blood flow (rCBF) were observed in the occipital cortex of either group. After practice for the blind, however, activity in the occipital cortex increased. This increase in activity was not observed in the sighted participants, providing evidence for training-induced plasticity in the congenitally blind.

Interestingly, the rate of learning was actually equal among both groups of blind and sighted subjects.

An inter-regional correlation analysis showed that task-related rCBF changes in the left posterior parietal cortex were positively correlated with rCBF changes in the occipital area of the trained blind participants.

All six blind subjects showed activation in the occipital cortex following training with the TDU.

== Conclusion ==

This data revealed that cross-modal plasticity in the blind develops rapidly and that the occipital cortex is part of a functional neural network for tactile discrimination in conjunction with the posterior parietal cortex. Data further showed that the tongue can act as a portal to convey somatosensory information to visual cortex.

Blind subjects showed activation of the occipital cortex while using the TDU after training while sighted control subjects did not despite an equal learning curve, showing that there is a functional role for the occipital lobe even in the congenitally blind.

In contrast, sighted subjects actually showed a deactivation of the visual cortex. However, this is in line with the observation that focusing on one sensory modality causes decreased activity in areas of the brain focusing on other modalities.

It has been suggested that the occipital activation can be explained by the fact that it is adjacent to the superior parietal lobe, in which tactile information is processed. Thus the tactile information may be "leaking" into the occipital lobe due to it not being used for anything else.

Talk:Ptito et al. (2005)

Daveecee — Fri, 25 Apr 2008 06:02:26 GMT

Daveecee:

Why are people writing on this article when it isn't theirs? It is kind of vexing me because
this is my assigned article, and when I come to write the wiki, it is already written.

Please leave this to me guys, since the majority of the page is my assignment.

-David

Talk:Ptito et al. (2005)

Daveecee — Fri, 25 Apr 2008 06:02:09 GMT

Daveecee:

Why are people writing on this article when it isn't theirs? It is kind of vexing me because this is my assigned article, and when I come to write the wiki, it is already written.

Please leave this to me guys, since the majority of the page is my assignment.

Ptito et al. (2005)

Daveecee — Fri, 25 Apr 2008 05:58:56 GMT

Daveecee:

[[Category:Plasticity Symposium]]

'''Cross-Modal Plasticity Revealed by Electrotactile Stimulation of the Tongue in the Congenitally Blind (Ptito et al., 2005)'''

The experimenters in this study used PET scanning to study cross-modal plasticity in the congenitally blind, using electrotactile stimulation of the tongue. Before training with the tongue display unit (TDU), neither the blind nor the sighted control subjects showed any change in regional cerebral blood flow (rCBF) in the occipital cortex. After training, however, rCBF in the occipital cortex of the blind subjects increased dramatically, providing evidence of training-induced plasticity

== Participants ==
Participants included 6 blind and 5 sighted blind-folded controls with a mean age of 29 years. MRI scans of the blind subjects were normal. Sighted control subjects also had normal neurological exams and normal vision.

== Training ==
Participants were trained to use their tongue in a Snellen orientation detection task using the TDU. The training lasted for seven days for one-hour sessions. For training, observers projected a T onto the subject's tongue using the TDU. Subjects were allowed to orient the T how they pleased in order to get used to the machine. They were scanned before and after training.

== Results ==
Before training, no significant changes in regional cerebral blood flow (rCBF) were observed in the occipital cortex of either group. After practice for the blind, however, activity in the occipital cortex increased. This increase in activity was not observed in the sighted participants, providing evidence for training-induced plasticity in the congenitally blind.

Interestingly, the rate of learning was actually equal among both groups of blind and sighted subjects.

An inter-regional correlation analysis showed that task-related rCBF changes in the left posterior parietal cortex were positively correlated with rCBF changes in the occipital area of the trained blind participants.

All six blind subjects showed activation in the occipital cortex following training with the TDU.

== Conclusion ==

This data revealed that cross-modal plasticity in the blind develops rapidly and that the occipital cortex is part of a functional neural network for tactile discrimination in conjunction with the posterior parietal cortex. Data further showed that the tongue can act as a portal to convey somatosensory information to visual cortex.

Blind subjects showed activation of the occipital cortex while using the TDU after training while sighted control subjects did not despite an equal learning curve, showing that there is a functional role for the occipital lobe even in the congenitally blind.

In contrast, sighted subjects actually showed a deactivation of the visual cortex. However, this is in line with the observation that focusing on one sensory modality causes decreased activity in areas of the brain focusing on other modalities.

It has been suggested that the occipital activation can be explained by the fact that it is adjacent to the superior parietal lobe, in which tactile information is processed. Thus the tactile information may be "leaking" into the occipital lobe due to it not being used for anything else.

Primary auditory cortex

Daveecee — Fri, 25 Apr 2008 01:37:18 GMT

Daveecee: /* Plasticity */

Primary auditory cortex

Daveecee — Fri, 25 Apr 2008 01:35:49 GMT

Daveecee:

[[image:Brodmann_41_42.png|300px|thumb|Brodmann areas 41 and 42: the primary auditory cortex]]

The primary auditory cortex, denoted as Brodmann areas 41 and 42, is the area in the brain which receives sensory auditory information directly from the ears. Like most sensory modalities, information from the right ear is directed to the left primary auditory cortex, and information from the left ear is sent to the right primary auditory cortex. The primary auditory cortex is located on Heschl's gyrus the lateral sulcus, and the posterior half of the superior temporal gyrus.

== Plasticity ==

The cortex has been observed to be [[plasticity|plastic]]. When an area of the brain is deprived of its usual sensory input, it sometimes "switches" to another sensory modality to, in a way, help out with processing. The primary auditory cortex has shown to be activated by visual stimuli when deprived of auditory input.

== Deaf Hearing ==

Deaf hearing is the auditory analogue to [[blindsight]]. Like in blindsight, patients with deaf hearing have bilateral lesions in temporal areas involved in auditory perception, especially the primary auditory cortex. However, due to subcortical auditory pathways in the midbrain and brainstem remaining active, some level of auditory processing remains despite the fact that the patient experiencing cortical deafness has no awareness of hearing sounds. Although the patient has no awareness of hearing sounds, they display orienting reflexes to auditory stimuli despite insisting they heard nothing.

== References ==

Garde, M. M., & Cowey, A. (2000). "Deaf hearing": Unacknowledged detection of auditory stimuli in a patient with cerebral deafness. ''Cortex, 36'', 71-80.

Newton, J. R., & Sur, M. Rewiring Cortex: functional plasticity of the auditory cortex during development. ''Department of Brain & Cognitive Sciences, Picower Center for Learning & Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts.''

Primary auditory cortex

Daveecee — Fri, 25 Apr 2008 00:41:35 GMT

Daveecee:

[[image:Brodmann_41_42.png|300px|thumb|Brodmann areas 41 and 42: the primary auditory cortex]]

Primary auditory cortex

Daveecee — Fri, 25 Apr 2008 00:41:02 GMT

Daveecee:

[[image:Brodmann_41_42.png|250px|thumb|Brodmann areas 41 and 42: the primary auditory cortex]]

File:Brodmann 41 42.png

Daveecee — Fri, 25 Apr 2008 00:39:25 GMT

Daveecee:

Carl Wernicke

Daveecee — Fri, 25 Apr 2008 00:32:26 GMT

Daveecee:

[[image:Wernicke.jpg|200px|thumb|Carl Wernicke]]

Carl Wernicke was a German psychologist and neuropathologist born on May 15, 1848 in Upper Silesia. He is most known for his work with neurological disorders associated with language. He is often associated with his discovery of [[Wernicke's area]], an area bordering the posterior temporal lobe which is known to be involved in speech comprehension. While examining a stroke patient of his postmortem, he noticed a lesion in the area now known as Wernicke's area. While alive, the patient was able to speak, but could not understand speech himself or written words. Wernicke thus concluded that this area was involved in speech comprehension and the disorder held by the patient came to be known as [[Wernicke's aphasia|fluent aphasia]]. The most common characteristics of Wernicke's aphasia include the capability of speech at a normal rate but with the insertion of nonsensical words, and word substitutions (paraphasias).

Wernicke is also attributed to the discovery of one other form of aphasia, conduction aphasia. In conduction aphasia, the patient is capable of understanding speech but is incapable of repeating anything spoken to them. Conduction aphasics also tend to perform paraphasias, and sometimes even rearrange the phonemes of a word.

== References ==

Margaret Alic "Wernicke, Carl (1848-1905)". Encyclopedia of Psychology.

Stirling, J. (2002). ''Introducing neuropsychology''. Hove: Psychology Press.

[[Category:Neuropsychological profiles]]

Carl Wernicke

Daveecee — Fri, 25 Apr 2008 00:32:13 GMT

Daveecee: /* References */

Carl Wernicke

Daveecee — Fri, 25 Apr 2008 00:30:36 GMT

Daveecee:

[[image:Wernicke.jpg|200px|thumb|Carl Wernicke]]

Carl Wernicke was a German psychologist and neuropathologist born on May 15, 1848 in Upper Silesia. He is most known for his work with neurological disorders associated with language. He is often associated with his discovery of [[Wernicke's area]], an area bordering the posterior temporal lobe which is known to be involved in speech comprehension. While examining a stroke patient of his postmortem, he noticed a lesion in the area now known as Wernicke's area. While alive, the patient was able to speak, but could not understand speech himself or written words. Wernicke thus concluded that this area was involved in speech comprehension and the disorder held by the patient came to be known as [[Wernicke's aphasia|fluent aphasia]]. The most common characteristics of Wernicke's aphasia include the capability of speech at a normal rate but with the insertion of nonsensical words, and word substitutions (paraphasias).

Wernicke is also attributed to the discovery of one other form of aphasia, conduction aphasia. In conduction aphasia, the patient is capable of understanding speech but is incapable of repeating anything spoken to them. Conduction aphasics also tend to perform paraphasias, and sometimes even rearrange the phonemes of a word.

== References ==

Margaret Alic "Wernicke, Carl (1848-1905)". Encyclopedia of Psychology.
Stirling, J. (2002). ''Introducing neuropsychology''. Hove: Psychology Press.

[[Category:Neuropsychological profiles]]

Wernicke's aphasia

Daveecee — Fri, 25 Apr 2008 00:22:26 GMT

Daveecee:

[[Category:Neuropsychological syndromes]]
Wernicke's aphasia (also known as fluent aphasia) is a type of aphasia in which significant damage has been done to [[Wernicke's area]] in the posterior superior temporal gyrus of a person's dominant hemisphere. It was first discovered by [[Carl Wernicke]] and knowledge was significantly advanced by [[Norman Geschwind]].
== External Link ==
[http://www.youtube.com/watch?v=aVhYN7NTIKU Video of patient with Wernicke's aphasia]

Carl Wernicke

Daveecee — Fri, 25 Apr 2008 00:01:10 GMT

Daveecee:

[[image:Wernicke.jpg|200px|thumb|Carl Wernicke]]

[[Category:Neuropsychological profiles]]

Carl Wernicke

Daveecee — Thu, 24 Apr 2008 23:54:50 GMT

Daveecee:

{{ Infobox Scientist
|name = Carl Wernicke
|image =Wernicke.jpg
|image_width =200px
|caption = Carl Wernicke
|field = Psychiatrist, Neuropathologist
|known_for = Discovery of [[Wernicke's Area]], [[Wernicke's aphasia]]
}}

[[Category:Neuropsychological profiles]]

Carl Wernicke

Daveecee — Thu, 24 Apr 2008 23:54:30 GMT

Daveecee:

{{Infobox Scientist
|name = Carl Wernicke
|image =Wernicke.jpg
|image_width =200px
|caption = Carl Wernicke
|field = Psychiatrist, Neuropathologist
|known_for = Discovery of [[Wernicke's Area]], [[Wernicke's aphasia]]
}}

[[Category:Neuropsychological profiles]]

Carl Wernicke

Daveecee — Thu, 24 Apr 2008 23:52:39 GMT

Daveecee:

{Infobox Scientist
|name = Carl Wernicke
|image =Wernicke.jpg
|image_width =200px
|caption = Carl Wernicke
|field = Psychiatrist, Neuropathologist
|known_for = Discovery of [[Wernicke's Area]], [[Wernicke's aphasia]]
}}

[[Category:Neuropsychological profiles]]

File:Wernicke.jpg

Daveecee — Thu, 24 Apr 2008 23:48:19 GMT

Daveecee:

User:Daveecee

Daveecee — Thu, 24 Apr 2008 23:39:38 GMT

Daveecee:

Confused? No more!

Daveecee --> Davee Cee --> Dave C. --> David Celis

Wernicke's area

Daveecee — Thu, 24 Apr 2008 23:35:17 GMT

Daveecee:

[[Category:Brain areas]]
[[Image:wernickesarea.gif]]

Wernicke's area was discovered by [[Carl Wernicke]] in 1874. Located on the left superior temporal gyrus, this area controls the function of connects speech sounds to stored representations of words. Wernicke's area is anatomically linked to Broca's area. A lesion to this area will likely result in difficulties in language comprehension. In an article published by Carl Wernicke in 1874, he reported 10 aphasic patients with difficulties in language comprehension. An autopsy on four of the patients provided results that they had lesions damaging the left temporal lobe. This specfic type of aphasia is now known as ''Wernicke's aphasia''. Recent research by Dronkers et. al. (1998) revealed that 'pure' damage to Wernicke's area most likely results in impairment in repetition rather than comprehension deficits. Damage to the part of the brain linking Broca's area and Wernicke's area, the arcuate fasciculus, can lead to conduction aphasia, in which the patient loses the ability to repeat words.

Other brain areas associated with language function include: [[Broca's area]], the supramarginal gyrus, [[angular gyrus]], and the arcuate fasciculus (a pathway thought to connect Wernicke's area with Broca's area).

== References ==

Stirling, J. (2002). Introducing neuropsychology. New York: Psychology Press.

Ogden, J. A. (2005). Fractured minds. New York: Oxford University Press.

Image taken from:
http://users.fmrib.ox.ac.uk/~stuart/thesis/chapter_3/section3_2.html

Wernicke's area

Daveecee — Thu, 24 Apr 2008 23:27:01 GMT

Daveecee:

[[Category:Brain areas]]
[[Image:wernickesarea.gif]]

Wernicke's area was discovered by [[Carl Wernicke]] in 1874. Located on the left superior temporal gyrus, this area controls the function of connects speech sounds to stored representations of words. Wernicke's area is anatomically linked to Broca's area. A lesion to this area will likely result in difficulties in language comprehension. In an article published by Carl Wernicke in 1874, he reported 10 aphasic patients with difficulties in language comprehension. An autopsy on four of the patients provided results that they had lesions damaging the left temporal lobe. This specfic type of aphasia is now known as ''Wernicke's aphasia''. Recent research by Dronkers et. al. (1998) revealed that 'pure' damage to Wernicke's area most likely results in impairment in repetition rather than comprehension deficits. Damage to the part of the brain linking Broca's area and Wernicke's area, the arcuate fasciculus, can lead to conduction aphasia, in which the patient loses the ability to repeat words.

Other brain areas associated with language function include: [[Broca's area]], supramarginal gyrus, angular gyrus, and arcuate fasciculus.

== References ==

Stirling, J. (2002). Introducing neuropsychology. New York: Psychology Press.

Ogden, J. A. (2005). Fractured minds. New York: Oxford University Press.

Image taken from:
http://users.fmrib.ox.ac.uk/~stuart/thesis/chapter_3/section3_2.html

User:Daveecee

Daveecee — Thu, 24 Jan 2008 16:03:19 GMT

Daveecee: /* External Links */

'''Real Name:''' David Celis

User:Daveecee

Daveecee — Thu, 24 Jan 2008 16:03:06 GMT

Daveecee:

'''Real Name:''' David Celis

== External Links ==

User:Daveecee

Daveecee — Thu, 24 Jan 2008 16:02:39 GMT

Daveecee:

'''Real Name:''' David Celis

=== Test ===

== Test ==

User:Daveecee

Daveecee — Thu, 24 Jan 2008 15:39:40 GMT

Daveecee:

Real Name: David Celis