Psy3241 - User contributions [en]

Norman Geschwind

HDevlin — Tue, 29 Apr 2008 01:50:19 GMT

HDevlin:

[[Category:Neuropsychological profiles]]

[[Image:Norman_geschwind.jpg]]
== Biography ==

Norman Geschwind (1926-1984)was born in New York City and later attended Harvard University to study Mathematics. His education was interrupted when he was matriculated into the Army. Upon returning to Harvard, Geschwind changed his major to Social Relations and later attended medical school. For the majority of Geschwind's medical career he focused on neuroanatomy specifically focusing on the neurological basis of language and higher cognitive functions at the Neurology Department of the Boston Veterans Administration Hospital. Geschwind's inspiring personality is said to have sparked interest among colleagues in the field of Behavioral Neurology, which has grown remarkably in the past three decades.

== Contributions to Neuroscience ==
Norman Geschwind is perhaps most famous for coining the term Behavioral Neurology which encompasses the areas of Neuropsychology and Higher Cortical Functions. Norman Geschwind has also been called the father of American behavioral neurology. Along with cofounding the Boston University Aphasia Research Center, Geschwin was also a respected professor at Harvard Medical School. He specialized in teaching about anatomical hemispheric differences, writing about biological foundations of cerebral dominance, and lecturing about aphasia, epilepsy and dyslexia. In honor of Dr. Geschwind, the Norman Geschwind Award in Behavioral Neurology is awarded annually through the American Academy of Neurology and the Society of Behavioral and Cognitive Neurology. In addition there is a Norman Geschwind-Rodin prize for research in dyslexia presented in Sweden.

== References ==

Duane, D. (2002). ''Norman Geshwind lecture: Geschwind's lesson''. Annals of Dyslexia: 52(25).

Landis, T. (1998), ''Behavioral neurology and the legacy of Norman Geschwind''. European Neurology: 40(2)

http://en.wikipedia.org/wiki/Norman_Geschwind

Norman Geschwind

HDevlin — Tue, 29 Apr 2008 01:49:29 GMT

HDevlin:

[[Category:Neuropsychological profiles]]

[[Image:Norman_geschwind.jpg]]
== Biography ==

Norman Geschwind (1926-1984)was born in New York City and later attended Harvard University to study Mathematics. His education was interrupted when he was matriculated into the Army. Upon returning to Harvard, Geschwind changed his major to Social Relations and later attended medical school. For the majority of Geschwind's medical career he focused on neuroanatomy specifically focusing on the neurological basis of language and higher cognitive functions at the Neurology Department of the Boston Veterans Administration Hospital. Geschwind's inspiring personality is said to have sparked interest among colleagues in the field of Behavioral Neurology, which has grown remarkably in the past three decades.

== Contributions to Neuroscience ==
Norman Geschwind is perhaps most famous for coining the term Behavioral Neurology which encompasses the areas of Neuropsychology and Higher Cortical Functions. Norman Geschwind has also been called the father of American behavioral neurology. Along with cofounding the Boston University Aphasia Research Center, Geschwin was also a respected professor at Harvard Medical School. He specialized in teaching about anatomical hemispheric differences, writing about biological foundations of cerebral dominance, and lecturing about aphasia, epilepsy and dyslexia. In honor of Dr. Geschwind, the Norman Geschwind Award in Behavioral Neurology is awarded annually through the American Academy of Neurology and the Society of Behavioral and Cognitive Neurology. In addition there is a Norman Geschwind-Rodin prize for research in dyslexia presented in Sweden.

[http://www.fchampalimaud.org/images/uploads/ADam%C3%A1sio01_thumb.jpg]Picture of Norman Geschwind

== References ==

Duane, D. (2002). ''Norman Geshwind lecture: Geschwind's lesson''. Annals of Dyslexia: 52(25).

Landis, T. (1998), ''Behavioral neurology and the legacy of Norman Geschwind''. European Neurology: 40(2)

http://en.wikipedia.org/wiki/Norman_Geschwind

File:Norman geschwind.jpg

HDevlin — Tue, 29 Apr 2008 01:47:19 GMT

HDevlin:

Wada test

HDevlin — Tue, 29 Apr 2008 01:44:03 GMT

HDevlin:

[[Category:Neuropsychological methods]]

[[Image:022002stpa1.jpg]]
The Wada test involves administering a fast acting barbiturate to one hemisphere at a time. The barbiturate is adminstered through the left or right carotid artery. For individuals undergoing neuropsychological testing, especially concerning memory and language, it is crucial to determine which hemisphere is primarily dominant. In epileptic patients a person may have verbal and visual impairments on both temporal lobes, meaning that if one hemisphere is removed, the patient will be left with an impaired hemisphere. A patient may undergo a Wada procedure in order to determine the capabilities of each hemisphere including speech, naming, and memory.

== Procedure ==
A baseline procedure is performed to determine the capabilities of the patient while both hemispheres are active. Next, sodium amytal is used as an anesthetic and is injected into the carotid artery of a hemisphere of the brain. This paralyzes the opposite side of the patient's body and the neuropsychological tests are performed.
[http://www.youtube.com/watch?v=TY2FBG39V_w]

File:022002stpa1.jpg

HDevlin — Tue, 29 Apr 2008 01:40:36 GMT

HDevlin:

Iowa gambling task

HDevlin — Tue, 29 Apr 2008 01:32:02 GMT

HDevlin:

[[Category:Neuropsychological methods]]

The Iowa Gambling Task was developed by Bechara, Damasio, A., Domasio, R., and Anderson, S. It was published in their 1994 research, “Insensitivity to future consequences following damage to the human prefrontal cortex”. The IGT is measures a participant’s decision-making ability and ability to learn from previous outcomes. It mimics real life situations because it requires the player to act on schedules of reward and punishment, with an added factor of uncertainty.

The participants are given four decks of cards (A, B, C and D) two of which (A and B) are disadvantageous and two (C and D) are advantageous in the long term. The examiner or computer program asks the participant to pick one card at a time (100 cards total) from any deck. The goal of the task is to accumulate as much money as you can, while picking reward (gain) and punishment cards (loss). The cards are prearranged by the examiner so that every time a card from deck A or B is chosen, the participant gets $100, whereas cards from deck C and D only reward $50. Random punishment cards are in each deck and add up to high losses in the higher paying decks (A and B) and lower losses in the lower paying decks (C and D). The losses in decks A and B add up to a loss of $1250 every ten cards, where decks C and D only add up to be a loss of $250 every ten cards. Therefore, although A and B pay more, they are disadvantageous in the long term because they result in a $250 loss every ten turns where as decks C and D are advantageous because the result in a $250 gain every ten cards.

Many computer versions of the task have been modified. Some include a green or red status bar at the top of the screen to show the participant how much they have “won” or “loss”. Measures to make the task more realistic, such as sound effects and red or black colors on the card faces are also often used.

Typical normal, healthy participants initially sample all decks and usually begin picking more cards from decks C and D after around 40 trials and less cards from decks A and B. Those with decision-making impairment (damage to their [[ventromedial prefrontal cortex (VMF)]] or [[amygdala]]) also initially sample all of the decks, but then continue to pick from the disadvantageous decks and do not increase their choices from the advantageous decks.

Participant’s [[galvanic skin response]] may also be recorded during the Iowa Gambling Task. These responses indicate the presence of somatic markers. The somatic marker hypothesis suggests that emotions or “gut feelings’ have an effect on decision making.
Activity is recorded for five seconds before the participant picks a card and five seconds after they look at the card. This method identifies the participant’s anticipatory response, as well as their response to reward or punishment. Participants with damage to the ventromedial prefrontal cortex or amygdala have less anticipatory galvanic skin responses than normal controls. However, when measuring reward and punishment skin responses, those with VMF damage have similar responses to normal controls. Amygdala patients have significantly lower galvanic skin responses than both groups. These results indicate that somatic states do not influence either group’s judgment, leading them to make poor decisions.

[http://www.biopac.com/ApplicationImages/vr05graph.jpg]

Korsakoff's syndrome

HDevlin — Tue, 29 Apr 2008 01:28:39 GMT

HDevlin:

[[Category:Neuropsychological syndromes]]
[http://images.google.com/imgres?imgurl=http://www.neuropathologyweb.org/chapter8/images8/8-2l.jpg&imgrefurl=http://www.neuropathologyweb.org/chapter8/chapter8Nutritional.html&h=399&w=400&sz=148&hl=en&start=10&um=1&tbnid=OhJrGWAQUh9iBM:&tbnh=124&tbnw=124&prev=/images%3Fq%3DKorsakoff%2527s%2Bsyndrome%26um%3D1%26hl%3Den%26sa%3DN Pictures of a Patient's Brian with Korsakoff's Syndrome]

[http://www.youtube.com/watch?v=wDcyBXJAZNM Video Clip]
== Definition ==
Korsakoff's syndrome is a memory disorder caused by a deficiency of vitamin B1, also called thiamine

Named after Sergei Korsakoff, the neuropsychiatris who popularized the theory

== Description ==
First mentioned in 1822 by James Jackson, a physician at Massachusetts General Hospital and professor at Boston Medical School, in a review of the peripheral neuritis of alcoholism

1868 Sir Samuel Wilks, a physician at Guy's Hopital, London, gave an account of the characteristic mental symptoms in an article on alcoholic paraplegia

In his doctoral thesis, Korsakoff called the condition "cerebropathia psychica toxaemica"

The term Korsakoff's psychosis was introduced by Friedrich Jolly

Korsakoff emphasized the association of alcoholic polyneuropathy with a specific pattern of mental disturbances by stating: "This mental disorder appears at times in the form of sharply delineated irritable weakness of the mental sphere, at times in the form of confusion with characteristic mistakes in orientation for place, time, and situation, and at times as an almost pure form of acute amnesia, where the recent memory is most severely involved, while the remote memory is well preservedÂ¦ Some have suffered so widespread memory loss that they literally forget everything immediately."

Korsakoff's psychosis was used originally to describe the combination of alcoholic polyneuropathy and characteristic mental disturbance and Korsakoff's syndrome was the non-alcoholic form with or without polyneuritis, which resulted from acquired conditions such as head injury, brain tumors, and encephalitis

Blass and Gibson in 1977 identified a genetically determined disturbance of transketolase, which is a thiamine pyrophosphate-binding factor in fibroblasts

Individuals who are homozygous for this defect are at an increased risk for developing thiamine deficiency in circumstances of dietary inadequacy

== Causes and Symptoms ==
The high calorie nature of alcohol is one of the main reasons that alcoholism leads to thiamine deficiency

A large intake of alcohol substitutes alcohol for other calorie sources that contain more nutrition

Food intake drops and multiple vitamin deficiencies develop as alcoholism grows

It is believed that alcohol increases the body's requirement for B vitamins, while also interfering with the absorption of vitamin B1 from the intestine and impairing the body's ability to store and use B1

Thiamine provides energy to the neurons of the brain in a variety of reactions

As thiamine becomes unavailable, these reactions cannot be carried

Because the end products of these reactions cannot be formed, substrates begin to accumulate and cause damage to the neurons

The mamillary bodies and the thalamus of the diencephalon is responsible for the symptoms of this syndrome

Those with Korsakoff's syndrome have difficulty with their memory

Anterograde amnesia- the ability to learn new information is greatly affected, while intelligence and memory of past events is relatively unaffected

Confabulation- a person with Korsakoff's syndrome fills in the gaps of their memory with fabricated or imagined information

Complete unawareness of the memory defect and complete lack of worry or concern when it is pointed out

Involves neuronal loss (damage to neurons), gliosis (result of damage to supporting cells of the central nervous system), and hemorrhage (bleeding in mammillary bodies)

Other symptoms may include delirium, anxiety, fear, depression, confusion, delusions and insomnia; painful extremities, sometimes bilateral wrist drop, more frequent bilateral foot drop with pain or pressure over the long nerves. Additional symptoms are paralasys of muscles controlling the eye, tremors, and confabulation.

== Diagnosis ==
An individual diagnosed with alcoholism and a sudden onset of memory difficulties should be tested for Korsakoff's syndrome

No specific test to diagnose this syndrome

A careful examination of a patient's mental state could reveal the syndrome

Check the patient's retention of factual information and the ability to learn new information

A patient recovering from [[Wernicke's aphasia]] who begins to display memory difficulties is likely to have developed Korsakoff's syndrome

== Treatment ==
Immediate administration of thiamine

Any individual, regardless of the diagnosis of Korsakoff's syndrome, should receive thiamine

== Prognosis ==
15-20% of all patients hospitalized for Wenicke's syndrome will die of Korsakoff's syndrome

Half of those who survive the syndrome will have permanent ataxia (difficulty walking)

The paralysis of the eye muscles almost always have complete recovery with thiamine treatment

Improvement in symptoms can take months of thiamine replacement

Memory-impaired for the rest of their lives

Usually requires a supervised living situation

== Prevention ==
Maintaining a diet with sufficient intake of thiamine

Supplement an inadequate diet with vitamin preparations

Treat the underlying alcohol addiction

== Works Cited==
[http://www.healthatoz.com/healthatoz/Atoz/common/standard/transform.jsp?requestURI=/healthatoz/Atoz/ency/korsakoffs_syndrome.jsp Health A to Z]

[http://en.wikipedia.org/wiki/Korsakoff's_syndrome Korsakoff's Syndrome]

[http://www.ninds.nih.gov/disorders/wernicke_korsakoff/wernicke-korsakoff.htm Wernicke-Korsakoff Syndrome Information Page]

Orbitofrontal cortex

HDevlin — Sun, 27 Apr 2008 23:18:54 GMT

HDevlin:

[[Category:Brain areas]]

== The Orbitofrontal Cortex ==

[http://www.neuro-economics.org/media/images/brain-regions.gif]Picture of the Orbitofrontal Cortex

The Orbitofrontal cortex is located in the region of the prefrontal cortex within the frontal lobes and slightly above the occipital orbits. It is considered one of the most mysterious and understudied regions of the brain thus far. This is a result of the difficulty researchers have had in capturing fMRI images of this area of the brain. This area of the brain is said to have impact on human personality as well as higher emotional and social traits such as responsibility, control of mood, and motivation. In recent years, functional studies have yielded results linking the Orbitofrontal cortex to reward and decision making mechanisms in the brain.

== Imaging ==

Imaging and neuropathological studies have indicated that that there is an involvement with the orbitofrontal cortex and mood disorders. This linkage has been studied in Alzheimer's patients whose neurofibrillary tangles have been studied in addition to observed behavioral abnormalities. Medial parts of the Orbitofrontal cortex are correlated with learning, self monitoring, and memory in response to reinforcement. The lateral Orbitofrontal cortex is correlated with punishers, and the post-anterior section is found to be correlated with complex and abstract reinforcers.

== Damage to the Orbitofrontal Cortex ==

Patients who have experienced damage to the Orbitofrontal Cortex have been known to experience emotional instability as well as problems with substance abuse, drug expectancy, craving and decision making. In addition, patients who have experienced damage to the Orbitofrontal cortex have been known to have problems managing their finances and overusing substances such as nicotine.

== References ==

Cavada, C., Schultz, W. (2000). The Mysterious Orbitofrontal Cortex. Oxford University Press 10(3).

Kringelbach, M. (2005)The human orbitofrontal cortex: linking reward to hedonic experience. Neuroscience 6(9).

http://en.wikipedia.org/wiki/Orbitofrontal_cortex

Norman Geschwind

HDevlin — Sun, 27 Apr 2008 22:38:15 GMT

HDevlin:

[[Category:Neuropsychological profiles]]

== Biography ==

Norman Geschwind (1926-1984)was born in New York City and later attended Harvard University to study Mathematics. His education was interrupted when he was matriculated into the Army. Upon returning to Harvard, Geschwind changed his major to Social Relations and later attended medical school. For the majority of Geschwind's medical career he focused on neuroanatomy specifically focusing on the neurological basis of language and higher cognitive functions at the Neurology Department of the Boston Veterans Administration Hospital. Geschwind's inspiring personality is said to have sparked interest among colleagues in the field of Behavioral Neurology, which has grown remarkably in the past three decades.

== Contributions to Neuroscience ==
Norman Geschwind is perhaps most famous for coining the term Behavioral Neurology which encompasses the areas of Neuropsychology and Higher Cortical Functions. Norman Geschwind has also been called the father of American behavioral neurology. Along with cofounding the Boston University Aphasia Research Center, Geschwin was also a respected professor at Harvard Medical School. He specialized in teaching about anatomical hemispheric differences, writing about biological foundations of cerebral dominance, and lecturing about aphasia, epilepsy and dyslexia. In honor of Dr. Geschwind, the Norman Geschwind Award in Behavioral Neurology is awarded annually through the American Academy of Neurology and the Society of Behavioral and Cognitive Neurology. In addition there is a Norman Geschwind-Rodin prize for research in dyslexia presented in Sweden.

[http://www.fchampalimaud.org/images/uploads/ADam%C3%A1sio01_thumb.jpg]Picture of Norman Geschwind

== References ==

Duane, D. (2002). ''Norman Geshwind lecture: Geschwind's lesson''. Annals of Dyslexia: 52(25).

Landis, T. (1998), ''Behavioral neurology and the legacy of Norman Geschwind''. European Neurology: 40(2)

http://en.wikipedia.org/wiki/Norman_Geschwind

Norman Geschwind

HDevlin — Sun, 27 Apr 2008 22:33:03 GMT

HDevlin:

[[Category:Neuropsychological profiles]]

== Biography ==

Norman Geschwind (1926-1984)was born in New York City and later attended Harvard University to study Mathematics. His education was interrupted when he was matriculated into the Army. Upon returning to Harvard, Geschwind changed his major to Social Relations and later attended medical school. For the majority of Geschwind's medical career he focused on neuroanatomy specifically focusing on the neurological basis of language and higher cognitive functions at the Neurology Department of the Boston Veterans Administration Hospital. Geschwin's inspiring personality is said to have sparked interest among colleagues in the field of Behavioral Neurology, which has grown remarkably in the past three decades.

== Contributions to Neuroscience ==
Norman Geschwin is perhaps most famous for coining the term Behavioral Neurology which encompasses the areas of Neuropsychology and Higher Cortical Functions. Norman Geschwin has also been called the father of American behavioral neurology. Along with cofounding the Boston University Aphasia Research Center, Geschwin was also a respected professor at Harvard Medical School. He specialized in teaching about anatomical hemispheric differences, writing about biological foundations of cerebral dominance, and lecturing about aphasia, epilepsy and dyslexia. In honor of Dr. Geschwind, the Norman Geschwind Award in Behavioral Neurology is awarded annually through the American Academy of Neurology and the Society of Behavioral and Cognitive Neurology. In addition there is a Norman Geschwind-Rodin prize for research in dyslexia presented in Sweden.

Wada test

HDevlin — Sun, 27 Apr 2008 21:56:09 GMT

HDevlin:

[[Category:Neuropsychological methods]]

The Wada test involves administering a fast acting barbiturate to one hemisphere at a time. The barbiturate is adminstered through the left or right carotid artery. For individuals undergoing neuropsychological testing, especially concerning memory and language, it is crucial to determine which hemisphere is primarily dominant. In epileptic patients a person may have verbal and visual impairments on both temporal lobes, meaning that if one hemisphere is removed, the patient will be left with an impaired hemisphere. A patient may undergo a Wada procedure in order to determine the capabilities of each hemisphere including speech, naming, and memory.

== Procedure ==
A baseline procedure is performed to determine the capabilities of the patient while both hemispheres are active. Next, sodium amytal is used as an anesthetic and is injected into the carotid artery of a hemisphere of the brain. This paralyzes the opposite side of the patient's body and the neuropsychological tests are performed.
[http://www.youtube.com/watch?v=TY2FBG39V_w]

Wada test

HDevlin — Sun, 27 Apr 2008 21:44:34 GMT

HDevlin:

Alzheimer's Disease

HDevlin — Sun, 27 Apr 2008 21:26:11 GMT

HDevlin:

Alzheimer's Disease is a form of dementia involving the progressive deterioration of psychological functions as a result of abundant loss of cortical and subcortical neurons. Alzheimer's Disease is the most common form of dementia which rises with increasing age and exceeds one new case per 100 in the 70-80 age group. The time of diagnosis is usually after age 65, as symptoms may not be acknowledged until this time. The time from diagnosis until death is usually about 7 years, and is equally distributed amongst men and women. There is evidence that Alzheimer's may effect the brain gradually for 5 decades before symptoms arise.

== Diagnosis ==
The neurobehavioral and clinical criteria for all types of dementia include inabilities whilst learning new material or inability to recall past material accurately as well as impairment of at least one higher cognitive function. The patient may also develop aphasia, apraxia, or agnosia. These impairments must be significant enough to effect the patients daily life. A physical exam, medical history report, and laboratory tests are carried out to determine etiological relationships concerning dementia. The Demential of the Alzheimer's type (DAT, until recently, was the most common label for Alzheimer's diagnostics. Now, specialist dementia or memory units are more accurate diangnotics in the living patent for determining the presence of Alzheimer's Disease along with MRI brain scans.

== Symptoms and Risk Factors==

Patients with Alzheimer's disease often experience memory loss including aphasia, apraxia, or agnosia. Although the exact cause of Alzheimer's Disease is not yet known there are several causes that have been suggested. Some of these causes include: A slow virus, neurotoxins, oxidative stress with the formation of free radicals, brain trauma or injury, and a genetic predisposition to the disease. Alzheimer's disease is known to occur less in individuals who are highly educated and mentally and physically active.

== Neuropathology ==
The neuropathology of Alzheimer's Disease includes the occurrence of neurofibrillary tangles and amyloid or senile plaques. Although neurofibrillary tangles are present in the majority of the elderly, they occur more abundantly in Alzheimer patients, especially in the hippocampi. The higher the abundance of tangles correlates with the increased intensity of symptoms in Alzheimer's patients.

Alzheimer's Disease

HDevlin — Sun, 27 Apr 2008 19:03:58 GMT

HDevlin:

Alzheimer's Disease

HDevlin — Sun, 27 Apr 2008 18:33:24 GMT

HDevlin:

'''Bold text'''Alzheimer's disease'''Bold text''' is a form of dementia involving the progressive deterioration of psychological functions as a result of abundant loss of cortical and subcortical neurons.