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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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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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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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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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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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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In 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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Many 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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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.

The 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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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.

David 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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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.

So 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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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.

These 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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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.

Some 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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When consumed, alcohol has similar effects on cells in the body. It can break down the lipids and proteins that form the walls of cells. Body tissue left in alcohol will dissolve over time (this is one reason why alcohol is sometimes used as a marinade or tenderizer for meat). Most of the time, the concentration of alcohol in the body is too low to do much, if any, damage to cells; however, over time as alcohol continues to be consumed it can have lasting effects on the body. This is one of the effects that leads to sclerosis of the liver; eventually the toxicity and solvent effects of alcohol are too much for the liver. In the brain, alcohol easily crosses the blood brain barrier, which serves to protect the brain from harmful substances (it also keeps out many good ones), and directly affects the neurotransmitters and receptors of neurons. At high enough concentrations (or over time) alcohol can weaken the blood brain barrier by damaging the tight junctions of blood vessels in the brain that form the barrier.

At high concentrations alcohol acts as a vasoconstrictor, increasing blood pressure. Over time, high blood pressure can severely affect the brain leading to stroke and other disorders such as vascular dementia. Volatile (rapid changes in) blood pressure (such as could hypothetically occur secondary to frequent binge drinking) has also been linked to Parkinson’s disease. On the other hand, a recent study found lower rates of Parkinson’s disease in people who had consumed alcohol versus abstainers (Paganini-Hill, 2001). The etiology of this effect is unknown.

Alcohol intake can also lead to vitamin deficiency, which can severely damage the brain (e.g., Korsakoff’s Syndrome), resulting in memory loss, emotional disturbance, gait problems, and ataxia. Additionally, alcohol is physiologically and psychologically addictive. So, does all of this mean that we should not drink alcohol? There certainly are good arguments against its consumption that possibly outweigh any possible positive health benefits it might have. However, if abstinence is not desired then drinking in moderation should certainly be encouraged.

Reference

Annlia Paganini-Hill (2001). Risk Factors for Parkinson’s Disease: The Leisure World Cohort Study Neuroepidemiology, 20 (2), 118-124 DOI: 10.1159/000054770

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Many children have been exposed to others having seizures at school. Experiences such as these can be frightening for the children viewing the event; they are not always sure what is going on. Sometimes those with epilepsy feel stigmatized by others. Sometimes as children they are made fun of by others. Experiences such as these can make people less likely to talk about the disorder with others. People with moderate to severe epilepsy also tend to have slightly lower IQs than average; on average, their intelligence would still be considered average but there are also other cognitive deficits associated with epilepsy. Many children with the disorder have many symptoms of ADHD — inattention, distractibility, and hyperactivity. Often they also have slower processing speed than average, meaning that they cannot process information as quickly and might even appear slower to others. This can impact performance at school, resulting in learning disorders and the need for special education classes, which can lead to further social stigmatization.

Problems also can develop at home when parents do not understand all the effects epilepsy can have (e.g., cognitive difficulties, emotional lability, and attention problems). Parents may not realize that their child is acting out because of how seizure activity interrupts the normal functioning of the brain. Parents may not link a child’s emotional problems to their seizures. Other parents might not realize that attention problems might be due to absence seizures. It is important for physicians and psychologists to correctly educate parents about the problems that might arise as a result of epilepsy. We have come a long way in our understanding of epilepsy, both from a scientific and general population perspective, but stigma and discrimination still occur too frequently.

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