Jared Tanner, PhD – Brain Blogger http://brainblogger.com Health and Science Blog Covering Brain Topics Wed, 23 May 2018 14:00:26 +0000 en-US hourly 1 https://wordpress.org/?v=4.9.6 Uncontrolled Blood Pressure, Genetic Risk, and Alzheimer’s Disease http://brainblogger.com/2013/08/13/uncontrolled-blood-pressure-genetic-risk-and-alzheimers-disease/ http://brainblogger.com/2013/08/13/uncontrolled-blood-pressure-genetic-risk-and-alzheimers-disease/#comments Tue, 13 Aug 2013 11:00:54 +0000 http://brainblogger.com/?p=15135 A new article published in JAMA: Neurology demonstrates a link between genetics, Alzheimer’s disease, and vascular problems.

There continues to be a large focus within dementia research to understand the link between heart health and brain health. This also is a growing area of research not only because most societies are aging (i.e., the average age of the population increases as people live longer and have fewer children) but also because many societies struggle with increasing obesity rates. Obesity and heart disease are strongly linked.

In addition, it has been well-established that people who have higher blood pressure are at greater risk of cognitive decline in old age and at greater risk for developing dementia. Such decline or dementia are believed to be caused, at least in part by, acute or chronic changes to the white matter of the brain. These changes are typically called small or silent strokes by physicians and are visible on magnetic resonance images (MRI) or CT scans. Due to the prevalence of white matter disease in dementia, diagnostic criteria for Alzheimer’s disease have been updated within the past few years to focus more on the role that cerebrovascular disease plays in the Alzheimer’s disease process.

In terms of genetics, the best-verified risk factor for Alzheimer’s disease relates to the apolipoprotein E4 (ApoE) genotype. Individuals who have two copies of the ApoE4 allele have up to a 12-fold increase risk for developing Alzheimer’s disease.

In order to officially diagnose someone as having Alzheimer’s disease, a postmortem pathology examination must be performed on the brain with results demonstrating the presence of groups of proteins called beta-amyloid (plaques) and what are called tau-driven neurofibrillary tangles (basically a twisting and changing of part of the internal structure of neurons – brain cells). While confirming the presence of these plaques and tangles requires pathological dissection, a type of brain scan called positron emission tomography (PET) imaging can be used to look at amount of beta-amyloid plaque build-up in living people.

What the researchers wanted to investigate is whether there is a link between having high blood pressure, the amount of beta-amyloid plaque people without Alzheimer’s disease have, and genetic risk (ApoE4). The researchers found weak and non-significant evidence that people with at least one ApoE4 allele had more plaque build-up in their brains as did people with hypertension. More importantly and significantly, those who had both genetic (ApoE4) and vascular (hypertension) risk had significantly more plaque in their brains. Further analyses showed that people without controlled high blood pressure were the ones who had the most plaque in their brains, on average. Again, the study population included middle-age and older adults without dementia at time of study participation.

What this study demonstrates is that middle- and old-aged people without cognitive difficulties who have genetic risk of developing Alzheimer’s disease (ApoE4 alleles) and who have high blood pressure show much more Alzheimer’s pathology in their brains. Much of this difference is driven by people who do not have well-controlled high blood pressure, meaning that if people have genetic risk of Alzheimer’s disease but do a good job of controlling blood pressure (keeping it under 140/90) do not have much more Alzheimer’s pathology than those without genetic risk and without (or with controlled) high blood pressure.

In summary, middle-age adults who have genetic risk factor for Alzheimer’s disease and who do not control high blood pressure are likely at much higher risk for developing Alzheimer’s disease later in life than those who keep blood pressure under control.

References

Rodrigue KM, Rieck JR, Kennedy KM, Devous MD, Diaz-Arrastia R, & Park DC (2013). Risk Factors for ?-Amyloid Deposition in Healthy Aging: Vascular and Genetic Effects. JAMA neurology, 70 (5), 600-6 PMID: 23553344

Image via Juan Gaertner / Shutterstock.

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Is Breastfeeding Best For Brain Development? http://brainblogger.com/2013/08/10/is-breastfeeding-best-for-brain-development/ http://brainblogger.com/2013/08/10/is-breastfeeding-best-for-brain-development/#comments Sat, 10 Aug 2013 11:00:30 +0000 http://brainblogger.com/?p=15122 Research has demonstrated that children who were exclusively breastfed perform better on tests of cognitive function and intelligence than those who were exclusively formula-fed, even after controlling for potential other explanations (such as socioeconomic status, gestational duration, birth weight, maternal education, and educational opportunities).

There also seems to be a link not just between IQ and whether or not a child was breastfed but also between IQ and the length of breastfeeding, with more breastfeeding correlating with higher IQ (up to a point). Additionally, adolescents who had been exclusively breastfed as infants have thicker cortex in the parietal lobes (involved in many cognitive functions including visuospatial tasks, mathematics, and attention) as well as more white matter (the “wiring” between areas of the brain).

Researchers in a new study from Brown University looked at the white matter of 133 children aged 10 months to 4 years in order to understand if there are early differences in brain development, depending on whether the children had been breastfed.

The study participants were placed in three groups:

  1. Those who had been exclusively breastfed for at least 3 months
  2. Those who were exclusively formula fed, or
  3. Those who received a mixture of breast milk and formula

Children were scanned in MRI machines while they slept, in order to reduce what are called motion artifacts (distortions of images caused by movement). Then the white matter of the children in the three groups was compared to each other. What the researchers found was striking.

Different areas of the brain mature and develop at different rates. White matter in the brain appears white because the neurons in this area of the brain are covered in sheaths of insulating fat (myelin) that work much like insulation around electrical wire, protecting them but also allowing them to send signals more quickly. As the human brain develops, areas of white matter are myelinated at different speeds and different times, continuing into at least a person’s early to mid 20s. Frontal areas of the brain and areas involved in complex cognitive tasks (planning, language, organizing) develop latest with simpler areas of the brain developing earlier.

With this new study, the researchers found that early exclusive breastfeeding was associated with increased development in areas of the white matter that develop and mature last. These regions and connections that had increased development in breastfed children are commonly associated with complex cognitive tasks, including executive functioning, social–emotional functioning, and language. In addition, breastfed infants were found to have improved performance in these cognitive domains. Other areas of the brain in infants exclusively breastfed also showed more development, including areas involved in language performance, visual reception, and motor control.

Based on the findings of this study and other large-scale, exclusively breastfeeding clearly is associated with better brain development early in life and at least into adolescence. Being exclusively breastfed is also associated with higher IQ scores and better performance on cognitive tasks.

Length of breastfeeding is also important, with evidence supporting the benefits for continuing to breastfeed for at least the first two years of a child’s life. What is not known is why breast milk is so much better than formula, or if there is some other as yet undiscovered factor that is the real benefit. Based on these findings, it can be important at the individual, family, community, and societal levels to reduce pressures on mothers to reduce the length of exclusively breastfeeding their children.

References

Deoni SC, Dean DC 3rd, Piryatinsky I, O’Muircheartaigh J, Waskiewicz N, Lehman K, Han M, & Dirks H (2013). Breastfeeding and early white matter development: A cross-sectional study. NeuroImage, 82C, 77-86 PMID: 23721722

Image via Zdenek Fiamoli / Shutterstock.

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Memory – Not as Good as We Think http://brainblogger.com/2011/07/14/memory-not-as-good-as-we-think/ http://brainblogger.com/2011/07/14/memory-not-as-good-as-we-think/#comments Thu, 14 Jul 2011 12:00:41 +0000 http://brainblogger.com/?p=6777 One of the more controversial topics within cognitive psychology is whether or not there are repressed memories and if so, can they accurately be recovered. In order to understand how memories might become repressed, we need to first understand the memory system.

Memory includes both learning and then some sort of recollection. We have to store information first in order to pull it back out of storage later for use. Thus, the process of memory can be affected at either of these two stages — learning or recall. If information is never learned and therefore stored, it can never be remembered. However, if information was learned but something affects the process of retrieving it from storage, then it is possible that with additional help that information could be recalled. This is the basic idea underlying repressed memories. Something was learned and put into storage but a person is not able to retrieve the memories because something is blocking them. Therefore, from what we know of the memory system, repressed memories are technically feasible.

However, there are a number of confounding factors: 1) as best as we know now, memories are not stored in the brain like photographs or audio recordings of events; memories are recreated when they accessed; 2) memory is unreliable; 3) false memories are common.

I’ll briefly address the three possible confounds. What the first implies then is that all the information about a particular memory is stored in the brain and during recall, all this information is assembled to form a memory. Each time something is remembered it is actually recreated. The problem is that each time a memory is recreated it can be changed — dramatically or subtly. This occurs more often than we might think.

This leads into point 2 — memory is unreliable. This is not to say that all memory is unreliable and we should never trust memories but we need to be willing to question the validity of our memory.  Even what we think are strong, solid memories like where we were when we heard JFK was assassinated (if we are old enough to have experienced that) or where and what we were doing when we learned about the events of 9/11. These type of memories are called flashbulb memories. While they can be quite accurate, researchers have shown that they are often affected by news coverage after the fact or discussions with others. Further, how confident people are about these types of memories does not strongly relate to how accurate the memories are. Researchers have shown over and over how easy it is to manipulate memory. Put all this together and we have a relatively unreliable memory system.

This leads into point 3 — false memories are common. Not only can memories be manipulated, they can be created. The great psychologist Jean Piaget was convinced that he had been kidnapped as a child. It was later discovered that this was a story made up by a housekeeper or nanny that he later incorporated as an actual event. False memories have been most controversial in instances of “recovered” childhood sexual abuse. Many instances of childhood sexual abuse are unfortunately real but there have been a number of documented cases where such recovered memories turned out to be false. Just because those memories are false does not mean that someone who has them is lying, although that is the case for some people; however, just because someone believes strongly that a particular even happened, particularly in childhood, does not mean that it actually did. False memories are often strongly emotional. While emotion can help strengthen memories, it also sets them up to potentially be more unreliable because emotions change over time, which changes can affect connected memories.

Are there real repressed memories? Yes, there are. Repressed memories are always linked with traumatic events. Sometimes sufficiently traumatic events can overwhelm a person’s ability to function, such as what happens when someone goes into shock. These strong emotions and associated stress hormones can overwhelm the brain, interfering with the memory system. However, in practical experience, there is little evidence that these types of memories (i.e., those that are repressed) can be reliably recovered years down the road. It has happened, but is extremely rare.

Additional Reading

Loftus, E. F. & Kaufman, L. (1992). Why do traumatic experiences sometimes produce good memory (flashbulbs) and sometimes no memory (repression)? (In E. Winograd & U. Neisser (Eds.), Affect and accuracy in recall: Studies of “flashbulb” memories (pp. 212-223). New York: Cambridge University Press.)

Mendez, M., & Fras, I. (2011). The false memory syndrome: Experimental studies and comparison to confabulations Medical Hypotheses, 76 (4), 492-496 DOI: 10.1016/j.mehy.2010.11.033

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Brain Development and College Football http://brainblogger.com/2010/11/27/brain-development-and-college-football/ http://brainblogger.com/2010/11/27/brain-development-and-college-football/#comments Sat, 27 Nov 2010 15:45:59 +0000 http://brainblogger.com/?p=5696 Most of us have experienced the thrills and agonies of watching our chosen sports teams either perform well or poorly. During college football season in the United States, millions of fans devote their weekends to watching people run up and down fields while trying to avoid getting too injured. Those who follow college football notice that there are not many freshman players who are starting quarterbacks. Why is this? Other than the generally obvious fact that most teams already have quarterbacks who are farther along in their schooling, another reason why there are not many starting freshman quarterbacks is not as obvious.

Quarterbacks are like field officers in the military. They have responsibility for the immediate, tactical plan of the football game. That is one reason that successful quarterbacks are generally intelligent people – they have to keep track of plays and direct the entire offense through the trenches of the field. When it comes down to game time, they need to be able to make decisions under pressure. Some of this ability comes from experience but experience cannot explain everything. So why are freshman quarterbacks not usually starters and when they are, why do many seem to struggle? Further, what does all this have to do with the brain?

It is generally accepted that brain development continues into the third decade of life with some of the most important areas for complex reasoning and decision making developing last. One of these areas is the prefrontal region, which is the most anterior portion of the frontal lobes. While the cortex, or bodies of the brain cells, is changing during this period, it is possible that the greatest changes and development are in the underlying white matter, which is composed of the connections (axons) between brain cell bodies. These white matter changes include increased myelination, which increases the speed brain cells can communicate with each other. Myelination of the white matter (myelin is a fatty substance that looks white) is similar to insulating electrical wires, it helps maintain the integrity of the connections and reduces interference; it also increases the speed at which brain cells communicate.

Because the frontal region of the brain is among the last to develop, cognitive functions that rely on that area of the brain are often the last to mature. Again, the frontal region of the brain, among other things, is involved in decision making, planning, and impulse control. Adolescents who have attention and impulse problems (i.e., ADHD), have been shown to have both functional and white matter structure differences in the frontal portion of the brain. In general, there is a lot of development that occurs in this brain region throughout adolescence. This might partially explain why college freshmen often go a little wild, especially compared to juniors and seniors. There are exceptions, of course, but people generally get better at making decisions as they age and not just because they have more experience — there are changes in the structure of the brain.

Bringing this back to football, we can infer that freshman quarterbacks often struggle in part because the development of the brain is still occurring, especially in areas related to decision making. So some of the improvement in performance over time is due to experience but some of it is because parts of the brain are more fully developed. Knowing this may not help you when your team and young quarterback are struggling but it can give you hope for future seasons once the quarterback gets better connections in his frontal lobes.

Quarterbacks are like field officers in the military. They have responsibility for the immediate, tactical plan of the football game. That is one reason that successful quarterbacks are generally intelligent people — they have to keep track of plays and direct the entire offense through the trenches of the field. When it comes down to game time, they need to be able to make decisions under pressure. Some of this ability comes from experience but experience cannot explain everything. So why are freshman quarterbacks not usually starters and when they are, why do many seem to struggle? Further, what does all this have to do with the brain?It is generally accepted that brain development continues into the third decade of life with some of the most important areas for complex reasoning and decision making developing last. One of these areas is the prefrontal region, which is the most anterior portion of the frontal lobes. While the cortex, or bodies of the brain cells, is changing during this period, it is possible that the greatest changes and development are in the underlying white matter, which is composed of the connections (axons) between brain cell bodies. These white matter changes include increased myelination, which increases the speed brain cells can communicate with each other. Myelination of the white matter (myelin is a fatty substance that looks white) is similar to insulating electrical wires, it helps maintain the integrity of the connections and reduces interference; it also increases the speed at which brain cells communicate.

Because the frontal region of the brain is among the last to develop, cognitive functions that rely on that area of the brain are often the last to mature. Again, the frontal region of the brain, among other things, is involved in decision making, planning, and impulse control. In general, there is a lot of development that occurs in this brain region between the age of 18 and the early 20s. This might partially explain why college freshmen often go a little wild, especially compared to juniors and seniors. There are exceptions, of course, but people generally get better at making decisions as they age and not just because they have more experience — there are changes in the structure of the brain.

Bringing this back to football, we can infer that freshman quarterbacks often struggle in part because the development of the brain is still occurring, especially in areas related to decision making. So some of the improvement in performance over time is due to experience but some of it is because parts of the brain are more fully developed. Knowing this may not help you when your team and young quarterback are struggling but it can give you hope for future seasons once the quarterback gets better connections in his frontal lobes. While there is no research specifically supporting my hypothesis, it is a reasonable extension of well-established brain development research.

References

Silk, T., Vance, A., Rinehart, N., Bradshaw, J., & Cunnington, R. (2009). White-matter abnormalities in attention deficit hyperactivity disorder: A diffusion tensor imaging study Human Brain Mapping, 30 (9), 2757-2765 DOI: 10.1002/hbm.20703

Ashtari M, Cervellione KL, Hasan KM, Wu J, McIlree C, Kester H, Ardekani BA, Roofeh D, Szeszko PR, & Kumra S (2007). White matter development during late adolescence in healthy males: a cross-sectional diffusion tensor imaging study. NeuroImage, 35 (2), 501-10 PMID: 17258911

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Postoperative Cognitive Dysfunction http://brainblogger.com/2009/09/28/postoperative-cognitive-dysfunction/ http://brainblogger.com/2009/09/28/postoperative-cognitive-dysfunction/#comments Mon, 28 Sep 2009 12:00:18 +0000 http://brainblogger.com/?p=3243 In the mid 1950s, Dr. Bedford reported on a number of older adults who exhibited cognitive problems (memory or planning or being able to sustain attention) following surgery where anesthesia was used. This effect is now called postoperative cognitive dysfunction (or decline; POCD). POCD typically lasts for a few months to a year with a small minority of patients exhibiting permanent decline. Studies about it were few at first, with most focusing on cognition following cardiac surgery. Over time and especially more recently, there has been an increase in research of POCD following non-cardiac surgeries (e.g., abdominal or orthopedic) as well as continued interest in POCD following cardiac surgery.

There is considerable evidence that age is the single strongest risk factor for the development of POCD – outside of actually having surgery, of course! This means that the older a surgery patient is, the more likely they are to develop POCD. There is also evidence that prior cognitive impairment, lower education, and pre-surgery depression also place adults at risk for POCD following both cardiac and major non-cardiac surgery. Perioperative events (e.g., strokes and other neurological events) and postoperative pain are additional risk factors for POCD.

As mentioned previously, age is the most consistent predictor of POCD. Those who are older are more susceptible to POCD and for longer periods after surgery. For patients undergoing coronary artery bypass graft (CABG) surgery, the best studies show that 33% of patients have POCD at one week post-surgery. This rate falls to 4% at three months. Other studies show rates as high as 50-60% at one week and 13-20% at three months. However, these have been criticized for less-than-ideal methods. For major non-cardiac surgeries, the trend with POCD in older adults is similar, if with somewhat lower rates. For most studies, about 20% of noncardiac older patients exhibit POCD at one week following surgery with virtually no POCD at three months. However, some studies show higher rates (up to 50% at hospital discharge and 30% at three months post-discharge) of POCD in older adults following noncardiac surgery.

Past research showed widely variable rates in POCD. This inconsistency is due to major variations in the methods. Many researchers focused solely on subjective cognitive complaints or intelligence or general cognition as measured by a screening test such as the Mini Mental Status Examination. The problem is that these measures are insensitive to subtler cognitive changes. Intelligence tests generally have high test-retest reliability even with fairly major cerebral events (in other words, it usually takes major damage to the brain to significantly affect general intelligence). Brief general cognitive tests are usually quite reliable over time but they are insensitive to change because they are so shallow and broad. Minor or specific declines are important to measure because they can cause impairment in everyday functioning.

Even though POCD research has varied in quality, researchers and doctors are confident that POCD is a real effect. Any older adults (POCD researchers typically use age 60 as the threshold for “old adulthood”) who are undergoing major cardiac or non-cardiac surgery should be aware that mild to moderate cognitive deficits can occur following surgery. The cause is generally unknown. The good news is that there is little evidence that these deficits in general last longer than a few months.

References

&NA;, . (2006). The Role of Postoperative Analgesia in Delirium and Cognitive Decline in Elderly Patients Survey of Anesthesiology, 50 (5), 263-264 DOI: 10.1097/01.sa.0000238941.61799.e6

Lewis, M., Maruff, P., Silbert, B., Evered, L., & Scott, D. (2006). Detection of Postoperative Cognitive Decline After Coronary Artery Bypass Graft Surgery is Affected by the Number of Neuropsychological Tests in the Assessment Battery The Annals of Thoracic Surgery, 81 (6), 2097-2104 DOI: 10.1016/j.athoracsur.2006.01.044

&NA;, . (2008). Predictors of Cognitive Dysfunction After Major Noncardiac Surgery Survey of Anesthesiology, 52 (3), 135-136 DOI: 10.1097/01.SA.0000307885.46705.f5

&NA;, . (2007). Postoperative Cognitive Dysfunction After Noncardiac Surgery Survey of Anesthesiology, 51 (6) DOI: 10.1097/sa.0b013e31815c0ff1

Rasmussen, L. S., Larsen, K., Houx, P., Skovgaard, L. T., Hanning, C. D., & Moller, J. T. (2001). The assessment of postoperative cognitive dysfunction. Acta Anaesthesiol Scand, 45, 275-289.

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Mood and Functional Disability – A Positive Feedback Loop http://brainblogger.com/2009/09/01/mood-and-functional-disability-a-positive-feedback-loop/ http://brainblogger.com/2009/09/01/mood-and-functional-disability-a-positive-feedback-loop/#comments Tue, 01 Sep 2009 12:00:44 +0000 http://brainblogger.com/?p=3199 Emotional or mood problems are more frequent in people with disabilities (of any severity or duration) than in the general population. Rates range from about 20% to 50%, depending on the study and the population – from spinal cord injury to multiple sclerosis to stroke. It is important to understand the rates and types of mood disorders because the functional deficits associated with disability (I’m using disability to refer to any sort of loss of function, even if it is only temporary) can manifest similarly to mood disorder symptoms. For example, what might look like anhedonia could simply be inability to do much, or at least the reticence to be active because of pain or functional loss.

While clinicians might accurately understand the difference between physical disability and anhedonia or any number of mood disorder symptoms, patients might not understand that difference, especially as they fill out questionnaires, which are open to the subjectivity of personal interpretation. In other words, a patient might endorse symptoms related to their injury as mood-related, even if the symptoms are not. Clinicians need to take care in order to not over-diagnose mood disorders. On the other hand, depression is common but not inevitable in people with disabilities. This means that while some of the disabling conditions might manifest similarly to symptoms of depression, for example, it is important to not minimize or miss any symptoms of a mood disorder. That’s the catch-22 of mood disorders and disability.

Do Instrumental Activities of Daily Living (IADL) deficits amplify (create or act as part of a positive feedback loop) emotional problems? The evidence presented above of higher rates of depression and other mood disorders in people with disabilities leads to the conclusion that IADL deficits can amplify mood disturbances. John Bowlby was one of the pioneers who demonstrated a link between loss and depression. It is reasonable to assume that functional loss associated with disability can amplify depressive or other mood disorder symptoms.

But do emotional problems amplify IADL deficits? There is good evidence that cognitive dysfunction is related with poorer ADL and IADL performance (Lichtenberg & MacNeill, 2000), although cognitive disturbances usually have to be quite severe to grossly impact ADLs and somewhat less severe to affect IADLs. Those who have greater cognitive problems also tend to have longer or less recovery in rehabilitation. Cognitive deficits can be a significant factor affecting whether or not functional independence is gained through rehabilitation (Lichtenberg & MacNeill, 2000).

So again, is there evidence of a link between mood and IADL impairment? Depression can predict disability onset; it also predicts mortality. This means that those who are depressed are more likely to develop disability and are more likely to die. Further, there is evidence that those who are depressed have more IADL impairments over time than those who are not depressed. Those who are depressed also show fewer functional gains in rehabilitation settings than those who are not depressed (Lichtenberg & MacNeill, 2000).

These results demonstrate a positive feedback loop between both emotional problems and IADL deficits and IADL deficits and emotional problems. It can turn into a vicious cycle unless disrupted by psychological and rehabilitative intervention. Many patients in rehabilitation settings will make functional gains, which will help their mood, but if clinicians recognize mood problems and are able to treat those mood problems, they can help facilitate better functional gains. In this way clinicians can take advantage of this positive feedback loop and utilize it to benefit those who have functional disabilities (e.g., IADL deficits).

Reference

Lichtenberg, P. A., & MacNeill, S. E. (2000). Geriatric Issues. In Handbook of Rehabilitation Psychology (Eds. R. G. Frank & T. R. Elliott). APA, Washington D.C.

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Creating an Artificial Brain http://brainblogger.com/2009/08/20/creating-an-artificial-brain/ http://brainblogger.com/2009/08/20/creating-an-artificial-brain/#comments Thu, 20 Aug 2009 12:00:45 +0000 http://brainblogger.com/?p=3158 Dr. Henry Markram recently announced that he expects to have a computer model of the human brain in ten years. As part of the Blue Brain Project, he is part of a team trying to “reverse-engineer the mammalian brain.”

The human brain is exceedingly complex. There are about 100 billion neurons within the human central nervous system (brain and spinal cord) with an estimated 100 trillion synapses (connections between neurons). However, the brain grows and prunes synapses constantly, so that number is fluid. In addition there are probably 1 trillion glial cells that serve as support among other roles to the neurons. This web of densely-connected cells produces all behavior, thoughts, movements, and emotions. The human brain is the most complex organ on earth and one of the most complex things in the universe, especially gram for gram.

Because it is so complex, the brain does not always function properly. Sometimes various chemicals or substances act as teratogens, which interfere with the normal development of a fetus and often result in serious and permanent neural deficits, such as fetal alcohol syndrome. Other times, genetic abnormalities like trisomy 21 produce Down’s Syndrome. Other abnormal brain developmental pathways can result in anything from mild, even grossly unnoticeable deficits, to death. For the most part and for most people, however, the human brain develops normally and functions as nature intended.

The researchers at the Blue Brain Project are working towards simulating the entire human brain with its billions of neurons and trillions of synapses. How feasible is the project? Currently it takes the equivalent of one computer — one microprocessor — to model a single neuron. The goal of the project is to accurately model individual neocortical columns (a cylindrical volume with a diameter of 0.5 mm and height of 2 mm that contains about 10,000 neurons) in series and then extrapolate that model out to the entire cortex, which should simplify the overall model and reduce needed computing power. Currently to model a single neocortical column the researchers utilize a supercomputer with 10,000 processors. As you can imagine, modeling the entire brain of 100 billion neurons is a mind-boggling task. However, with advances in computer hardware and software, we are moving closer to such models, especially as researchers are able to simplify the overall brain model by modeling it at a more macro level than individual neurons.

One reason the researchers give for wanting to model the entire human brain is so they can hopefully better understand brain diseases and abnormal brain development. Imagine being able to simulate a brain of someone with Down’s Syndrome, or better yet, the development of a brain of someone with Down’s Syndrome! We could then hopefully understand exactly what goes wrong and when and try to correct it genetically or through some other means. Or, researchers could model the brain of an autistic child to try and understand how it functions. There are myriad possibilities.

However, is creating a complete model of the human brain ethical? Would the model develop into a self-aware and potentially sentient entity? If the model has self-awareness would it be ethical or moral to turn off the simulation? Would the model or simulated brain be considered alive? What are the potential pitfalls, if any, to creating a fully-functional brain simulation? What happens if treatments or policies are created based on the simulated brain and those treatments prove deleterious or the models miscalculated? Could we plug a simulated brain into a body and create a new “person”?

I think this research is exciting and ground-breaking should it come to full fruition. On the other hand, I do not believe we should proceed without serious ethical discussions. This is not just cloning a sheep or a rat, this is creating a full simulation of the human brain that would ostensibly grow, develop, feel, and mature.

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What is Free Will? http://brainblogger.com/2009/05/22/what-is-free-will/ http://brainblogger.com/2009/05/22/what-is-free-will/#comments Fri, 22 May 2009 12:52:25 +0000 http://brainblogger.com/?p=2775 This post continues my discussion of free will and determinism in neuroscience. Due to the relatively brief nature of these posts, this discussion is incomplete. However, I hope it spurs additional discussion. I believe addressing free will and determinism allows us to understand the underlying theories and implications of neuroscience and social science research as well as the practical application of that research.

For this article, the main questions are: “Is behavior biologically determined?” and “Do humans have free will?” I will not address in this post the argument between compatibilism and incompatibilism. In response to comments and questions about my previous post, I thought it necessary to attempt to define free will before I write further posts on this general topic of free will and biological determinism in the neurosciences.

In reading some comments to my post one fairly common definition — at least an operational definition — of free will was randomness. In other words, in a psychology experiment, for example, free will is part of the unexplained variance — the randomness in the data. Equating free will with randomness — overtly or not — is something I have heard and read repeatedly.

However, I do not believe that free will can simply equal randomness. Randomness is chance. It is the flip of a coin or the roll of a die. Randomness is unpredictable. However, let’s go with the assumption that free will equals randomness. One of the simplest forms of randomness is a coin flip. That coin flip might seem random, at least the outcome might seem random, but suppose we understand the composition of the coin. We know it has a particular mass; we know the density of the metal as well as any variations in density throughout the coin. We know its precise coefficient of friction, its air resistance, its rotational velocity, and so forth. We understand everything about the chemistry and physics of the coin’s flip. With this comprehension, we can predict with 100% certainty the outcome of the flip. Based on our knowledge we can predict perfectly the outcome. However, our knowledge or predictions do not cause the outcome.

In other words, even with a perfect prediction of the outcome of the coin flip, that knowledge did not cause the randomness of the result. So, am I arguing that randomness is a good definition of free will? No. If we can understand all the chemistry and physics of the coin and its flight, we can then state that the flip of the coin merely appeared random but was in fact determined by the particular interaction between physics and chemistry. In other words, the outcome of the coin flip was determined by the physical world – by the materials of the coin and the interaction of those materials with our material world – even if our knowledge of the material world did not determine the outcome. Therefore, we can create a deterministic explanation for the seemingly random event.

This demonstrates that what appears random can be explained away as determined. Researchers even have deterministic and indeterministic explanations for quantum theory, which also indicates that defining free will as randomness is not sufficient. Thus, randomness is a poor definition of free will because if free will is nothing more than randomness, once we understand our material world perfectly we will perfectly explain all randomness, all previously unexplained variance. This is what some neuroscientists are trying to do with human behavior, although few are willing to take the hard stance of completely denying free will.

So what is free will? I’ll start with an example. Free will is standing out in the sunlight and denying that the sun is shining. Free will can be defined as choosing one’s actions or course. Free will also is frequently defined as indeterminism. What is interesting is that this definition meaning “not determinism,” relies on determinism to define free will. Why do many use determinism to define free will? Because determinism is easy to define — it is a concrete concept. Additionally, it is one of the major philosophical foundations of modern science, in part because we can easily create operational definitions for determinism.

In the biological sciences and neurosciences, in particular, determinism is inextricably tied to biology and materialism (i.e., biological determinism). Most neuropsychologists seek to explain behavior as determined by the interaction between biology and environment (many may have a soft deterministic view but they still want to know the causes of behavior). In forensic (legal) cases, neuropsychologists often clash with the legal system; psychology assumes biological determinism (i.e., causal determinism) whereas the legal system assumes free will (while it does not necessarily deny some form of determinism, the main emphasis is on free will).

In the end, I did not really define free will other than saying that it is not randomness and it is not determinism. Even defining free will as choosing one’s own course or actions is an incomplete definition because as demonstrated above, it is still possible to explain those choices as determined if we resort to reductionism of behaviors. This leads to one of the major problems with determinism — that it cannot really be falsified by science (after all, science does assume determinism to start) but that is a different discussion altogether. As David Hume once said (I’m paraphrasing), “[The nature of free will is] the most contentious question of metaphysics.”

In my next post I’ll address an alternative set of assumptions (i.e., beliefs or explanations) to determinism, particularly biological determinism as is found in neuroscience.

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Free Will and the Philosophy of Science http://brainblogger.com/2009/04/14/free-will-and-the-philosophy-of-science/ http://brainblogger.com/2009/04/14/free-will-and-the-philosophy-of-science/#comments Tue, 14 Apr 2009 13:32:30 +0000 http://brainblogger.com/?p=2599 Neuroscience and Neurology CategoryFor many years the discussion over the existence of free will was limited to philosophers and theologians. Scientists started talking about free will once science started separating as a discipline from philosophy. However, it wasn’t until the rise of functional neuroimaging that some neuroscientists started studying if the brain and deterministic brain processes could explain away free will. In short, some scientists want to discover whether or not free will is merely an illusion, an idea humans create out of an innate desire to feel in control.

IllusionIn a 2008 article in Nature Neuroscience, researchers believe that their findings indicate that free will is at best highly implausible. They stated they were able to accurately predict, using fMRI and statistical modeling, people’s responses up to 10 seconds before a response was made on a simple task where participants were asked to push a button with their left or right hand. Activity in the prefrontal and parietal cortices preceded response by up to 10 seconds. The researchers interpret their results as showing there is no evidence for free will. Because this brain activity occurs before people are aware of their response, the authors feel that free will is nothing more than an illusion. The mechanics of the brain determine our responses.

On the other hand, assuming the findings are valid and replicable, there are other interpretations. I’ll explain an alternative interpretation by explaining a little epistemology and the philosophy of science first. Modern science is founded on the philosophical assumptions of materialism, naturalism, and empiricism — among other ideas. Materialism assumes determinism. Determinism is mechanistic and denies free will.

Because determinism is assumed, it is not possible to really study free will using neuroscience methods because it’s saying and doing the following:

  • Believe that free will may or may not exist.
  • Use methods (e.g., scientific method) that assume that free will doesn’t exist.
  • Conduct free will research that apparently shows free will does not exist.
  • Interpret the results as showing that free will does not exist.

One fault with this research is that the authors assume determinism and mechanism of our material world and then they try to study something that does not exist according to the foundational assumptions of modern science. It is thus not surprising that they view their research findings as pointing towards the nonexistence of free will.

Why is it important to understand the philosophical assumptions that underline modern science, including neuroscience and psychology? In psychology, the question of free will is important because it can change how a psychologist views abnormal behavior (and even normal behavior). It can change how psychotherapy is conducted (e.g., personal responsibility versus repressed early experiences). If a psychologist takes a deterministic approach to science or therapy, her approach can be very different than someone who takes a non-deterministic (e.g., free will) approach.

In closing I’d like to throw out a couple questions for the readers. Is there room for assuming free will in neuroscience research? Are there other ways of approaching the question of free will, especially as it relates to science research?

Reference

Soon, C., Brass, M., Heinze, H., & Haynes, J. (2008). Unconscious determinants of free decisions in the human brain Nature Neuroscience, 11 (5), 543-545 DOI: 10.1038/nn.2112

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Cognitive Theories and Brain Damage http://brainblogger.com/2009/04/03/cognitive-theories-and-brain-damage/ http://brainblogger.com/2009/04/03/cognitive-theories-and-brain-damage/#comments Fri, 03 Apr 2009 16:46:33 +0000 http://brainblogger.com/?p=2603 Psychiatry and Psychology CategoryCognitive theorists postulate how information is processed. For example, is it like a computer where all the information is broken down into bits, processed, and then reassembled for output? Or is processing handled in a completely different manner? One prevalent way to test theories of cognitive psychology is by studying patients (whether human or animal) with brain damage. There are both advantages and disadvantages to using brain-damaged patients to test and construct cognitive theories.

MRIMany years ago Paul Broca made certain assumptions about language processing as the result of studying someone with a lesion in a specific area of the brain. The trend of studying patients with damaged brains continues today with cognitive neuropsychology. Theorists study subjects with lesions and see what is not working properly when compared to a normal subject. If a certain part of the brain is damaged and yields very specific deficits, theories can be shaped to account for that deficit. So, if for example, you have a patient with damage to the posterior part of the left inferior frontal gyrus and he or she has speech production problems (aphasia) and if you have another patient with damage to the posterior part of the superior temporal gyrus who produces fluent but meaningless speech, you know by double disassociation that speech production and comprehension are processed differently.

In a similar manner, brain damage thus makes falsification of theories fairly easy. If, for example, a researcher theorizes that there is no difference between how nouns and verbs are processed she could look at brain-damaged people to try and falsify her theory. In doing so she would discover that there are in fact people who can read nouns and write verbs but not speak verbs. This finding would probably send her back to adjust her theory. Even though these are great advantages there are some disadvantages to using brain-damaged patients to produce theories.

One disadvantage is that brain damage is rarely focal. It is rare to have only one small process interrupted and everything else intact. This means that if a researcher uses brain-damaged patients to help him create theories, there are many possible interaction effects and other confounds due to the simple physical nature of most lesions. Another disadvantage is the assumption that a damaged brain functions just like a normal brain except for the part that is damaged. In other words, theorizing based on brain-damaged patients is like having a computer that is missing capacitors from the motherboard and trying to figure out how a normal computer works. You may see that sometimes the computer randomly shuts off and when you run a program and add 1+1 you get 3.

It may be that the missing capacitors are responsible for the computer problems or they may affect the processor which then causes the problems, or there may just be a software glitch and the hardware doesn’t matter in that case. In short, there may be many explanations for the deficits caused by brain damage. This is one thing that Gestalt psychologists really point out — a possible disadvantage to studying brain-damaged patients. Is the whole greater than the simple sum of the parts? Basing theories on brain-damaged patients can be problematic because the damage can really affect the overall cognitive processing in subtle and unforeseen ways.

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Essential Tremor and Parkinson’s Disease http://brainblogger.com/2009/03/07/essential-tremor-and-parkinsons-disease/ http://brainblogger.com/2009/03/07/essential-tremor-and-parkinsons-disease/#comments Sat, 07 Mar 2009 15:24:10 +0000 http://brainblogger.com/?p=2376 Neuroscience and Neurology CategoryParkinson’s disease (PD) and essential tremor are both primarily movement disorders. The symptoms are commonly confused with each other, mainly because essential tremor is not as well known as PD even though essential tremor is more prevalent. High-profile people like Michael J. Fox and Muhammad Ali raised our awareness of PD in the 1990s just like Pres. Ronald Reagan did with Alzheimer’s disease in the 1980s. Because of this, essential tremor is not as well-known to the general public even though more people suffer from it than from PD.

The two disorders differ in etiology and symptoms. Scientists understand the cause of PD quite well. It manifests when there is a loss of about 80% of the dopamine-producing neurons in the substantia nigra, a small area within the brainstem. However, we do not know what causes the death of these dopamine-producing cells. The etiology of essential tremor is not understood as well. What we do know is that the mechanics of essential tremor, like PD, involve the deep nuclei and white matter of the brain, including the thalamus and striatum.

PDThe symptoms of PD include tremor, rigidity, akinesia, and postural instability. Bradykinesia (slowed movements) and bradyphrenia (slowed cognition) are also common symptoms. If tremor is present in PD (and it does not have to be), it is manifest mainly as a resting tremor. However, when someone with PD moves and tries to do something, the tremor usually goes away. In other words, there is less of an action tremor than a resting tremor. Emotional changes are also common; depression and facial masking (little facial expression of emotion) are particularly prevalent. With essential tremor it is more common to have just an action (or intention) tremor and a postural tremor. Both diseases are progressive (although some forms of essential tremor do not progress). Both diseases can be very debilitating. Additionally, patients with essential tremor are more likely to develop or have PD.

Treatment of PD usually starts with some form of levodopa, a precursor molecule the body can turn into dopamine. Treatment of essential tremor usually involves taking various pharmaceuticals, including beta-blockers or anti-seizure medications. Deep brain stimulation (DBS) of the subthalamic nucleus, globus pallidus, or thalamus are becoming more common treatments of both essential tremor and PD (and pleasure). DBS was approved for treatment of essential tremor in 1997 and for PD in 2002. While we still have a lot to learn about these two diseases, we have come a long way in understanding and treating them.

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What is Intelligence? http://brainblogger.com/2008/10/29/what-is-intelligence/ http://brainblogger.com/2008/10/29/what-is-intelligence/#comments Wed, 29 Oct 2008 13:32:08 +0000 http://brainblogger.com/?p=1766 Intelligence has been discussed throughout much of human history. Socrates gave one definition of intelligence: “I know that I am intelligent, because I know that I know nothing.” Intelligence over the years has been defined as such diverse things as understanding others, knowledge gained, who you surround yourself by, what you accomplish, and the ability to reason. Before the 19th century, intelligence was solely in the realm of philosophy. Franz Joseph Gall, who started the phrenology movement, sought to localize intelligence (among other things) in the brain, which was in turn measured on the skull. While many of the ideas of phrenology were inaccurate, the idea of quantifying individual differences and localizing those differences onto the brain was an important one. Over the years, researchers started using better methods of research and understanding individual differences.

Then in the early 20th century, a French researcher was asked by the French government to come up with a way to identify children who would and would not benefit from schooling. He developed the first modern intelligence test. This first intelligence test quantified attention, verbal skills, and memory. About 10 years later, Lewis Terman, a psychologist at Stanford, adapted it for use in the United States. These tests provided an Intelligence Quotient as the quantification of intelligence. It was quickly applied by the military to identify who would make good officers an who should be rejected from service. Charles Spearman, an English psychologist, developed the idea that many disparate components of intelligence all represented an underlying general factor of intelligence (g). This had a large impact on the idea of intelligence and on the development of future measures of intelligence.

LightbulbDavid Wechsler developed an intelligence test, largely based on Spearman’s idea of g; this test is the most widely used intelligence test in the United States. The most recent version measures verbal comprehension, perceptual reasoning, working memory, and processing speed. There is considerable controversy whether processing speed — which roughly is how quickly someone can perceive and process new information or perform an action — should be considered a measure of intelligence. Other people balk at assigning a single number to intelligence, especially when there is not a universally agreed upon definition of intelligence. Still others feel that traditional intelligence tests provide a too narrow view of intelligence. One such researcher, Howard Gardner, initially proposed that there are seven intelligences (this has since been modified to include at least two more), including bodily-kinesthetic, linguistic, interpersonal, visual-spatial, and so forth. A problem with his theory is that his intelligences are not easily measured (however, some people would not see this as a fault).

What do the readers think about intelligence? Do IQ tests provide a good measure of intelligence? In other words, is it a meaningful concept? Does Gardner’s theory fit better? Is intelligence even a useful concept to measure? Was Oscar Wilde correct when he said, “The intellect is not a serious thing, and never has been. It is an instrument on which one plays, that is all”?

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Rogue Limbs – Introduction to Alien Limb Syndrome http://brainblogger.com/2008/10/19/rogue-limbs-an-introduction-to-alien-limb-syndrome/ http://brainblogger.com/2008/10/19/rogue-limbs-an-introduction-to-alien-limb-syndrome/#comments Sun, 19 Oct 2008 17:57:35 +0000 http://brainblogger.com/?p=1711 There is a rare neurological condition called alien limb syndrome in which a person has one or more limbs that will often move without conscious control. Little is known about the exact cause of this rare and interesting disorder. The person usually can have conscious control of the limb at times but not always. A classic manifestation of this syndrome is when the left arm, for example, will reach out and grab objects, fiddle with clothing or other body parts, or just move straight up or out and stay there. When asked by a neurologist to perform a specific action with the good arm, the alien arm may often hinder or impede the action of the good arm. The arm then often needs to be wrestled back to a resting position by the other arm.

To the person with an alien limb, the limb really is foreign — it acts as if it were not their limb. Many people with alien limb syndrome name the limb or refer to it as “It.” The patients are sometimes upset that they don’t have control over the limb but most learn to just live with the rogue limb. However, not all people are aware of the alien limb’s movements until they look at the limb or until someone tells them about it.

BrainSo what causes someone to have an alien limb? The disorder is termed a syndrome because there is not one specific cause or even one specific symptom. There may be myriad causes and a constellation of symptoms. Lesions to a wide range of sites in the brain can result in an alien limb syndrome.

The most common neurological correlate is basal forebrain degeneration (i.e., atrophy of the bottom part of the frontal lobes). Damage to the corpus callosum — a wide swath of white matter connective fibers that provides much of the communication between both cerebral hemispheres — can also result in alien limb syndrome. Strokes or tumors are the most common cause of the lesions that produce this disorder. Widespread damage to the parietal lobe may also sometimes result in an alien limb syndrome. In cases of lesions to this posterior area of the brain, self-injurious behaviors are more common (e.g., the alien limb tries to strangle the person). There is no cure so neurologists and researchers will likely be fascinated by this disorder for many years to come.

Reference

Keith A. Josephs, Martin N. Rossor (2004). The alien limb. Practical Neurology, 4 (1), 44-45 DOI: 10.1111/j.1474-7766.2004.06-189.x

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Reduced Empathy Following Traumatic Brain Injury http://brainblogger.com/2008/09/24/reduced-empathy-following-traumatic-brain-injury/ http://brainblogger.com/2008/09/24/reduced-empathy-following-traumatic-brain-injury/#comments Thu, 25 Sep 2008 05:39:18 +0000 http://brainblogger.com/?p=1529 Empathy is the ability and quality that allows humans to feel and understand what others are experiencing. It literally means “with [em-] suffering [-pathos]” as in suffering along with someone else. Empathy is not just emotionally suffering; it is also cognitively understanding what another person is going through; walking in their shoes, per se. Empathy connects people with each other and helps bind societies together.

In one recent study in the Journal of the International Neuropsychological Society the authors found that 31% of normal adults exhibited low emotional empathy scores on the Balanced Emotional Empathy Scale (BEES). This number is not particularly surprising because it represents a fairly normal distribution of empathy scores (i.e., about 2/3 of people have average to high empathy scores). What is surprising is that among patients with traumatic brain injury (TBI), 61% had low scores on the BEES, meaning they had a lower ability to empathize with others. Further, the authors did not find a relationship between how severe the TBI was and ability to empathize. They also found no relationship between empathy scores and performance on neuropsychological tests. This again, supports the finding of no relationship between TBI severity and empathy score. Further, low empathy scores in TBI patients could not be predicted by scores on measures of emotion, such as the Beck Depression Inventory.

BrainThese results are interesting on a couple of levels. It appears that TBI, regardless of severity, disrupts the normal functioning of the brain such that there is a disruption of frontal and limbic areas and circuitry that are involved in empathy. This makes sense because the frontal lobes are commonly damaged in TBI. This partially explains why many TBI patients with frontal lobe injuries appear emotionally blunted or apathetic. Many TBI patients with frontal damage also have a harder time interacting appropriately with others. Thus TBI interrupts general social cognition.

Another interpretation is that those with low empathy to begin with are more likely to experience TBIs. This means that there could be personality or other differences that lead to risky behaviors that in turn result in TBIs. The authors did exclude TBI patients under the age of 22 (when brains and emotional regulation are still developing) to help reduce the number of TBIs resulting risky behaviors. However, without having pre- and post-TBI measures of empathy, this interpretation cannot be ruled out. In any case, researchers are finding more and more evidence that even mild traumatic brain injury can have varied and lasting effects on a person.

Reference

RODGER LL. WOOD, CLAIRE WILLIAMS (2008). Inability to empathize following traumatic brain injury Journal of the International Neuropsychological Society, 14 (02) DOI: 10.1017/S1355617708080326

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Involving Physicians in Military Interrogations http://brainblogger.com/2008/09/17/involving-physicians-in-military-interrogations/ http://brainblogger.com/2008/09/17/involving-physicians-in-military-interrogations/#comments Wed, 17 Sep 2008 13:50:19 +0000 http://brainblogger.com/?p=1486 A recent New England Journal of Medicine article questions the ethics of psychiatrists being involved in interrogations. In 2006 the American Psychiatric Association (APA), the American Medical Association (AMA), and the American Psychological Association (APA) issued statements that it is unethical for doctors and psychologists to be directly involved in the interrogation process. Directly involved also includes viewing the interrogation with the “intention of intervening.” Physicians are allowed to train interrogation personnel but are not supposed to tailor interrogation protocols to specific prisoners or detainees.

In 2006, the military outlawed harsh interrogation techniques such as waterboarding, hooding, and using military dogs. However, detainees can be kept in complete isolation for up to 30 days, which could result in post-traumatic stress. Some military psychiatrists and psychologists have been involved in teaching specific psychological concepts, such as learned helplessness, to military personnel. Physicians and psychologists do have a responsibility, not only ethically, but also mandated by the military to report inappropriate and coercive interrogations to the proper authorities. However, that means that the physicians have to be involved on some level in the interrogation, even if it only viewing it, which goes against the issued statements by the APA and AMA.

War campSome military psychologists have argued that they should be involved to make sure that the detainees and prisoners are treated well. In other words, they feel that if they were not there to supervise, the interrogations of the prisoners would be harsher than necessary. However, this position goes against what the professional organizations recommend. This leaves some military physicians and psychologists in a bind; on one hand they feel morally obligated to monitor the well-being of detainees but on the other hand, it is unethical for them to do so.

Many physicians believe that treating prisoners well, being kind to them is much more effective than harsh interrogation or even other more mild but aversive interrogation techniques. There is evidence so support that belief. Information given when under duress is often unreliable; social psychologists have been studying a related topic –- eyewitness testimony –- for a number of years. They have found that individuals under a lot of stress, such as having a gun pointed at them, are much more unreliable than outside observers. So, there is considerable theoretical evidence that treating prisoners as humanely as possible both inside and outside interrogations leads to the most reliable information.

Should medical and health care professionals be directly or indirectly involved in interrogation? If so, what should their roles be? If not, why shouldn’t they be involved? Do you agree with the position of the APA and AMA? Should physicians and psychologists even be involved in the general training of military interrogators?

Reference

J. H. Marks, M. G. Bloche (2008). The Ethics of Interrogation — The U.S. Military’s Ongoing Use of Psychiatrists New England Journal of Medicine, 359 (11), 1090-1092 DOI: 10.1056/NEJMp0806689

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