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The role of the insula in many human behaviors

The role of the insula in many human behaviors

Following up on my lead on Antoine Bechara’s upcoming visit, it is worthnotinv one of the new trends in decision making research. In particular, working from an extension of the somatic market theory and the role of ventromedial prefrontal cortex (vmPfC), Bechara and colleagues have recently demonstrated how the role of the insula seems to play an important role in decision making involving risk and aversion.

In the article entitled Differential effects of insular and ventromedial prefrontal cortex lesions on risky decision-making, the researchers compared patients with lesions to vmPfC and the insula to healthy controls and lesion controls on the Cambridge Gamling Task (nice demo here). The authors note that:

The vmPFC and insular cortex patients showed selective and distinctive disruptions of betting behaviour. VmPFC damage was associated with increased betting regardless of the odds of winning, consistent with a role of vmPFC in biasing healthy individuals towards conservative options under risk. In contrast, patients with insular cortex lesions failed to adjust their bets by the odds of winning, consistent with a role of the insular cortex in signalling the probability of aversive outcomes. The insular group attained a lower point score on the task and experienced more ‘bankruptcies’.

The results thus confirmed previous findings of a role of the vmPfC in gambling tasks, while the surprising finding was that insular lesions would also have detrimental effects on decision making. in particular, while vmPfC patients responded to reduced likelihood ratios of the gambles, betting behaviour in insular patients did not show much response to decreasing probabilities. This is demonstrated nicely in the following figure:

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The effect of ratio on betting behaviour in the four groups of participants: healthy controls, vmPFC lesions, insular cortex lesions and the lesion control group.

Furthermore, over the course of the entire gambling task, insular patients suffered significantly more bankrupcies than both the vmPfC group and control groups. This does suggest that one role of the insula is guiding behaviour through aversive coding. In other words, it may be that the insula is responsible for loss aversion (as well as risk aversion, judging from the task).

The researchers further suggest that the findings were expected from the somatic marker theory:

The detrimental effect of insular cortex damage on emotional decision-making is also predicted by the Somatic Marker hypothesis (Damasio, 1994; Bechara and Damasio, 2005), which posits a crucial role for the insular cortex in holding the representations of bodily states associated with different choice options.

The results are also relevant to other studies, including Lawrence et al. (2009), who report that using the Iowa Gambling Task, choices from disadvantageous versus advantageous card decks produced activation in the medial frontal gyrus, lateral orbitofrontal cortex, and insula. So does the insula play a role in other forms of decision making, and is it a cause in pathological gambling? To date, no conclusive studies have emerged, which is why our own research has now turned to aversion-related activations in gambling, and the study of the dynamics (and overlap) between aversion related and reward related neural functions. The recent study by Clark et al demonstrates that the insula is a structure – long ignored – to take into considerations in decision making studies.

-Thomas

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broca.jpgNature is running a nice news article on the re-localization of Broca’s language area in the brain, and has as feature about it in their latest podcast.

Pierre Paul Broca originally described patient cases in which the patient suffered speech production deficits following injury to the left frontal hemisphere. However, a revisit to Broca’s original papers (see translations here and here), combined with a modern scanning of the preserved remains of Broca’s patients, has revealed that what has been called Broca’s area in modern times does not correspond to the areas implicated by Broca in his patient descriptions and neuroanatomical descriptions.

The story is interesting, but I’m amazed that the excitement is running so high. After all, lots of papers have already dethroned Broca’s (and Wernicke’s) area in the role of language processing. Take the example of the special issue of Cognition on language. Basically, what we know about language in the brain is beyond the talk (!) about Broca and Wernicke, and especially the models they suggested. Rather, both language comprehension and production require a larger neural symphony, and with substantial internal redundancy. IOW, Broca’s area can participate in comprehension, and Wernicke can play a part in production.

Nevertheless, the Nature news article is a good read, and I always recommend the Nature podcast.

-Thomas

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brainsurgery.jpgBrain tumors are a huge problem in neurosurgery. Not only do you have to take into consideration the delicate network of blood supply to the brain that can ultimately lead to further damage to the brain. In addition, the tumor is placed with in a meshwork of cognitive functions. Cutting too much on one side of the tumor can lead to amnesia, too much of another part can lead to aphasia.

To alleviate this problem, MRI is currently being used to identify the tumor through conventional structural scans. In addition functional MRI can be used to identify vital functional nodes that borders to the tumor. In this way, neurosurgery can use a better estimate of the tumor’s position and extent, as well as avoid functional centres. In all, the precision of neurosurgery has improved dramatically with the use of MRI.

In an article in Radiology, a study now shows that the use of structural and functional MRI in preoperative surgical planning both leads to more precise and more efficient surgery. As a brief resume in Medscape.com reports:

In six cases, the neurosurgeon reported that functional MRI results led to a more complete resection, whereas two patients required a smaller craniotomy than had been planned. The surgeons also noted that surgical time was reduced by 15 to 60 minutes in 22 patients. Invasive imaging that would have been required for four patients was avoided.

In practice this has a tremendous impact for the livesof the patients. With the use of preoperative MRI brain tumors can now be more fully ablated, and at the same time patients will have a lower chance of suffering unwanted dysfunctions. From the Radiology paper, we can see this in one female patients. From the description of the patient:

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Recurrent left parietal lobe anaplastic astrocytoma in 37-year-old right-handed woman. Surgery was not initially planned because of presumed involvement of receptive speech area. Left inferior and middle frontal gyral activation (yellow arrows) is consistent with dominant expressive speech area and is located at anterior border of more cephalad component of lesion. Left superior and middle temporal gyral activation (green arrows) is consistent with dominant receptive speech area and abuts inferior border of temporal component of lesion, with superior temporal gyral activation component lying anteroinferior to lesion. Biopsy was performed, and no postoperative neurologic deficits were documented.

-Thomas

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alcohol.gifAdolescence is a period of dramatic transformation in the healthy human brain, leading to both regional and general brain volume changes. Recent high-resolution Magnetic Resonance Imaging (MRI) studies emphasize the effects of ongoing myelination, indicating a substantial maturation process (see Figure 1). The period of adolescence is often defined as spanning the second decade of life, although some researchers expand their definition of adolescence to include the early 20s as well. Research into brain maturation in adolescence is particularly important, given that it is normally considered the peak period of neural reorganization that contributes to normal variation in cognitive skills and personality Additionally, it is seen as the period of major mental illness onset, such as schizophrenia. Despite growing evidence for pronounced changes in both the structure and function of the brain during adolescence and early adulthood, few studies have explored this relationship directly using in vivo imaging methods. Thus, little is still known about the relationship between adolescent behaviour and outcomes, and maturational effects on morphological and functional aspects of the brain.

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Figure 1Brain development during adolescence

The psychological and social changes of that occur during adolescence include a higher level or orientation towards and identification with peers, group socialism and personality consolidation. A main social behavioural change is the tendency to use alcohol and other stimulants. In European countries and especially Denmark, 60% of all adolescents report having had their first alcoholic whole drink before age 15, the majority reporting a debut at around age 12 (see Figure 2). Today, alcohol is considered a normal part of adolescent culture.

 

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Figure 2Age of alcohol use debut, as measured by the first consumption of a full alcoholic unit. Note that the majority of debuts are around 12 years. Furthermore, note the relatively high number (8%) reporting a <9 year old debut. (x-axis numbers indicate age of reported first full drink of alcoholic beverage; “yngre end 9” = “younger than 9”; “jeg har ikke drukket” = “I have not yet tried alcohol”)

The effects of prolonged regular alcohol consumption in adults are today considered well documented. Studies of extreme cases such as Wernicke’s encephalopathy and foetal alcohol syndrome have shown that alcohol at critical periods or over time can have severe effects on significant modification and damage of brain structure, physiology and function. In adults, heavy alcohol consumption results in atrophy of grey and white matter, particularly in the frontal lobes, cerebellum, and limbic structures. Heavy drinking also raises the risk of ischemic and hemorrhagic stroke.

Adolescents tend to drink larger quantities on each drinking occasion that adults, possibly a combination of lower sensitivity to some of the unpleasant effects of intoxication and altered patterns of social interaction, including a willingness to indulge in more risky activities. However, it has been suggested that adolescents may be more sensitive to some of alcohol’s harmful effects on brain function. Research now suggests that, even over the shorter time frame of adolescence, drinking alcohol can harm the liver, bones, endocrine system, and brain, and interfere with normal growth. Studies in humans have found that alcohol can lower the levels of growth- and sex hormones in both adolescent genders.

Recent studies using animal models have demonstrated that the adolescent brain is even more sensitive to alcohol consumption. Alcohol inhibits normal neurogenesis, the process in which neurons are created. The magnitude of this effect has been related to the level of consumption; higher levels of consumption (e.g. binge consumption) had the most severe effects on the brain. Furthermore, alcohol impairs spatial memory function in adolescent animals more than adults, a result that is thought to be mediated by a larger inhibitory effect of alcohol on neural transmission in adolescence.

The long-term effects of alcohol consumption on brain maturation are yet poorly understood in human adolescence. Studies report that a history of high alcohol consumption in adolescence has been associated with reduced hippocampal volumes (see Figure 3), and with subtle white-matter microstructure abnormalities in the corpus callosum. In order to understand the effects of alcohol on the brain these findings must be compared to several factors pertaining to alcohol consumption in young adults, including 1) onset of alcohol use; 2) amount of alcohol consumed regularly; 3) type of alcohol consumption (regular use or binge drinking). In addition, a number of confounding factors need to be addressed and controlled between different study groups, including 1) general cognitive function; 2) the effects of gender and pubic stage; 3) gender-related preferences for alcoholic beverages; and 4) the effects of gene-related differences in neurotransmitter function.

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Figure 3Hippocampus volume differences in adolescents with alcohol use disorder (AAU, right) compared to healthy adolescents (left). Volume estimation is corrected for general brain size.

So who says alcohol is not damaging? We know it is in adults. We know it is in prenatal development. Why not during adolescence? Even more so; during this period of brain development so much is happening; the continuation of brain development; pruning and consolidation of brain, cognition and personality; all combined with the coctail of changes resulting from hormonal changes. Add alcohol, and in heavy doses in binge drinking, and you’ve got a recipe for brain dysfunction and detrimental brain development.

In most cultures, alcohol is seen as acceptable, even for adolescents. Alcohol is possibly even more problematic in countries such as Denmark, since it is not illegal for children and adolescents to drink alcoholic beverages (although it is strangely enough illegal for them to buy it; i.e. they have to get it from their parents or another >15 year old). Statistically, Denmark ranges among the countries that has the earliest alcohol debut and the highest mean weekly/monthly alcohol consumption in adolescence. In general, alcohol is more socially and culturally accepted in the Western world (or all cultures?). But given that alcohol has such damaging effects should we allow it if it turns out to have detrimental effects on brain development and cognitive functions?

You can put it another way: given that you know this, would you allow your teenage son or daughter to drink alcohol? If you knew that her or his brain would respond negatively (both long and short term) to the alcohol, would you let it happen? Thick twice

-Thomas

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motherbrain1.jpgHaving a baby has a large impact on how we live our lives (trust me). But whereas men may react with amazement, wonder, even jealousy of being left aside, little actually happens to our bodies after birth. The changes that happen in women are far more obvious, not only during pregnancy but after birth also. The production of milk, and the possibility of conditional learning of milk production to the child’s crying is just one example of how body, brain and mind get tuned into caretaking.

Furthermore, studies of oxytocin, a mammalian hormone that acts as a neurotransmitter in the brain, has been implicated in the bonding of the mother-infant attachment bond. Oxytocin is present in both sexes and is thought to be involved in social bonding, stress-reduction and orgasm, just to mention some. but the hormone seems to play a specific role in how mothers react to their newborns, and the establishment of a sound dyadic attachment. In this way, the brains of mothers change, both as a result of hormonal expression (loads of additional oxytocin) and the social interaction with the infant.

But did you know that some of the neurons in mothers’ brains actually stem from their babies? In other words: some of a mother’s brain cells are actually from the offspring.

This is just what a team of researchers from Singapore have found and published in the journal Stem Cells. It’s well known in this literature that fetal cells can enter the blood of circulation during pregnancy and remain there for many years after birth. These cells can, just as regular stem cells, develop into different kinds of tissue, including bone marrow, liver an spleen cells. But whether these cells can cross the blood-brain barrier has been less certain.

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The expression of fetal stem cells in the mother’s cortex at 4 months after birth. Figure 1-H from the article.

This is exactly what the researchers found. By labelling fetal stem cells they discovered that these cells had indeed crossed the blood-brain barrier and moved into the brain. Furthermore, at measurement four days after pregnancy these cells had developed into neurons, astrocytes, oligodendrocytes or macrophage-like cells. In other words, they developed just as any other stem cell.

So babies gets into their mothers’ minds in more than through hormonal and psychological mechanisms.

However, what is actually the function of these neurons is more unclear. Does the workings of fetal neurons have any significance for their relationship, or any particular mental function in mothers? This is indeed an opening field, and an eye-opener to many people (including myself when I first read it). No results have been reported in either direction as of yet.

What has been studied, however, is how these fetal stem cells can actually play a supporting role in the mother’s brain in the case of pathology. In addition to documenting that fetal stem cells enter the mother’s brain, the researchers added a condition involving brain lesion of the mother’s brain. What they found was just as surprising: after a lesion to the brain, more fetal cells were found in the lesioned region. So the baby’s cells seem tuned into helping the mother regain herself in the case of injury.
Mind-blowing as this finding may be, little is still known about this phenomenon. The development, mechanism, function and evolution of this process is just beginning to be explored. But it already raises a whole range of questions: can we measure a difference between mother’s and “non-mother’s” brains, both structurally and functionally? Does this “fetomaternal microchimerism” lead to any advantages (i.e. survival) in mothers? What is the range of variation in this kind of expression: are there “good” and “bad” fetuses? Are mothers of many children better off in any respect of those with fewer children? Or is this process just a question of striking the energy balance, the child “paying back” what it deprived the mother of during pregnagcy?

So a portion of yourself resides somewhere in your mother’s brain (and body). Children are indeed the result of their parents, but now it seems that children pay back, too.

-Thomas

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save-brain2.jpgDoes talking in your mobile phone influence the workings of your brain? Yes, claims a new study in Neuropsychologia of healthy volunteers. But it’s not only bad, it seems; some cognitive functions become better during mobile phone radiation.

Mobile phone radiation and health concerns have been raised since the 1990s, especially following the enormous increase in the use of wireless mobile telephony throughout the world. This is because mobile phones use electromagnetic waves in the microwave range. These concerns have induced a large body of research (both epidemiological and experimental, in non-human animals as well as in humans). Concerns about effects on health have also been raised regarding other digital wireless systems, such as data communication networks.

Although previous studies have shown mixed and often conflicting results, these studies have been criticized for having a low statistical power. The current study included 120 subjects to improve the statistical power of the analyses; 58 males and 62 females from 18 to 70 years. Mind you, such a spread in age could actually be a confounding variable, and an age effect should have been included in the analysis. To that, the current study does not seem to have controlled for age and gender effects on the age sample.

The researchers gave the subjects a number of different cognitive tasks tapping into cognitive functions such as reaction time, encoding, verbal comprehension, and working memory. Radiofrequency radiation was induced through a regular Nokia mobile phone placed on a helmet that subjects wore during cognitive testing. The study was a double-blinded setup, so that neither researchers nor the subjects knew if the cellular phone was transmitting (or emitting radiofrequency radiation). Measures were taken to make sure that neither sound or heating would lead subjects to detect when the phone was transmitting. Subjects performed the tests (different versions of the test each time) during radiofrequency stimulation (both sham and real stimulation).
What was found was that the performance during radiofrequency exposure, compared to sham condition, changed theperformance on several tests. While the performance on reaction time decreased during exposure, performance on the Trail Making test B, which loads working memory, was increased during exposure. As the researchers write:

The results of this study provide statistical evidence of a cognitive difference in performance between the real and sham field [mobile phone] exposure conditions. The negative effects of [radiofrequency] exposure on [reaction time, RT] performance indicate that the more basic functions were adversely affected by exposure. In contrast, the improved RT for the working memory task suggests that [radiofrequency] exposure has a positive effect on tasks requiring higher level cortical functioning, such as working memory.

The results are also very interesting because several reports now support the view that using a cellular phone while driving leads to a reaction time comparable to that of having several alcoholic drinks. Through this study it seems that it’s not only the talking in the phone that pulls your reaction time down; it’s also the mere radiation itself.

But are the conclusions warranted? For one thing: the cognitive measures being made are rather crude. The reactions time measures should be less problematic, but as for concluding that working memory increases due to a Trail Making B test score only is really invalid. The Trail B is indeed a measure of how people can switch from one serial counting mode to another (numbers or alphabet). Working memory is really much more than keeping track of only one number or letter back. What should be applied is a so-called parametric n-back task (PDF). In addition, a better test battery should be applied. Although the current focus has been on reaction time, it now seems likely that effects on higher-order cognitive functions may take place, too. However, in order to make firm conclusions of such, we need better cognitive test batteries.

What, then, happens to our cognitive brains after prolonged exposure to radiofrequency waves? Here, we can only speculate, or as the authors point out:

The implications of this study can only be directed towards the effects of short-term exposure of [mobile phone radiofrequency radiation] on cognition. Further longitudinal research is required to determine the effects that long-term use of [mobile phones] (years) may have on health and cognition.

It’s still early days for studies on mobile phones, radiation and brain funcitoning. Many studies have used a less than optimal sample size and problematic experimental designs. Nevertheless these results seem to point out that just being exposed to radiofrequency radiation from a cellular phone induce changes in the brain’s workings. And now I start wondering whether my subjects in the MR scanner also change during scanning…

-Thomas

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Recently, a team in Cambridge has developed a diagnostic tool for prosopagnosia, a rare disorder of face perception where the ability to recognize faces is impaired, although the ability to recognize objects may be relatively intact. While this work has made it easier to sort out between those who are truly prosopagnosic and those who have a more global agnosia, a recent report shows that prosopagnosia is much more common that you would think.

An impressive 2 percent of the population may have some fom of prosopagnosia! That means that millions of people are not only poor but disastrous at recognizing faces, even from famous people.

You can read more about the story at ScienceDaily, visit the faceblind.org website, or read the papers yourself from Ken Nakayama's homepage

So next time you meet a person whos name you've forgotten, don't worry. At least you're not prosopagnosic!

-Thomas 

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The visual word form area (VWFA) is one of the most contested concepts of modern neuroscience. Its proponents claim that a dedicated slice of cortex in the occipitotemporal region of the brain – probably centered on the fusiform gyrus – underlie the ability to read. The most radical version of this hypothesis states that the VWFA is a specialized module – an idea that implicates some sort of genetical determinism. Since writing only has been around for some 6000 years many researchers doubt that there have been enough time for such a module to evolve. Instead, they expect reading to piggybackride on other, perhaps more general, visual processes.

The April 20 issue of Neuron contains a case study of man surgically treated for epilepsy that bears on these questions. As a consequence of excision of cortical tissue posterior to the putative VWFA this patient developed a case of pure alexia where, whereas before surgery he took ~600 ms to read a word, regardless of word lenght, after surgery his reading slowed to ~1000 ms for three-letter words and increased by ~100 ms per additional letter.

Crucially, postsurgical fMRI tests showed that the VWFA no longer responded more to words than to other objects, even when words were contrasted with viewing a simple fixation point. The authors suggest that this lack of activation is explained by the fact that postsurgically the VWFA is no longer receiving its normal input. Instead, a more widespread activation pattern, including frontal, parietal, and temporal sites, appear to "take over", resulting in a letter-by-letter reading strategy.

While the study clearly demonstrates that the VWFA plays some kind of (important) role in reading, it doesn't really illuminate what type of function the VWFA performs. And, at the same time, it cannot be said to settle the question of modularity, since the patient was a 46-old man who, of course, has had amble time to develop a reading skill from learning. As Alex Martin notes in a great accompanying resumé, the study do, however, leaves unresolved "the vexing problem of how to account for the intersubject consistency in the general location of the VWFA and other category-related regions in ventral occipitotemporal cortex. One possibility is that the VWFA performs a visual processing function that predisposed it to being co-opted for reading." But there may also be other reasons. In any case, it is a very nice study that will prove important for further debates on both reading and modularity.

Reference

Gaillard, R. et al. (2006): Direct intracranial, fMRI, and lesion evidence for the causal role of left inferotemporal cortex in reding. Neuron 50: 191-204.

Martin, A. (2006): Shades of Déjerine – forging a causal link between the visual word form area and reading. Neuron 50: 173-175.

-Martin

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Traumatic brain injury distorts the brainFrom time to time I receive emails from people who have relatives or other loved ones that suffer from a neurological or psychiatric condition. I respond to these the best that I can. Today, I'd like to share with you one such response. This is why neuroscience is important; it opens up a better understanding of diseases and treatments. Is your loved one suffering from a vegetative state – is he unconscious all the time, even though being awake – or is he in a minimally conscious state – actually emerging into awareness? Even worse: is he in a locked-in state – being fully aware but unable to communicate, and treated as unconscious?

The email below is anonymized in order to avoid identification. The text is otherwise unedited.

Hello, my name is RD. My 27 year old son, P was in a car accident 3 years ago. He was age 23 at the time of the accident. P suffered a traumatic brain injury. He now lives in a nursing home. In his medical records he is diagnosed as persistent vegetative state. I would call it minimally conscious state, especially these past several months.

We, his family have been very active in his life. I have searched everywhere I can think of for help, in-depth information, clinical trials, anything that may help him. He is aware of his surroundings. He is using his arms now, where 6 months ago he couldn't. He plays ball with his little girl. She was 5 months old when he had his accident. She plays pic-a boo with him. He smiles…especially when someone who he hasn't seen for a while comes to see him, his uncles for instance.

I am looking for someone to take interest in his condition, to see if he can be help. I just pray that someone will give him a chance. I know he has the potential to improve. We just need to be pointed in the right direction. Can you help or do you know who someone who can?

And here is my response:

Dear RD,

Thank you for your email and please excuse my much belated reply.

I am deeply sympathetic to your son's condition and your problem. We are all moved by these tragic accidents. Through my previous work as a clinical neuropsychologist, I have seen people suffering from the same condition that your son is now.

My own shortcomings to be of any serious help to you is that I am living in Copenhagen, Denmark. Although you do not mention explicitly, I think you are living in the US. The medical treatment of post-traumatic amnesia, ranging from coma through vegetative state and to minimally conscious states, is still being improved from day to day. In countries such as the US and Denmark the treatment should be similar, on average. However, there may be places that are more focused and knowledgeable on these cases.

On your feelings that your son is actually better than vegetative state, I would suggest trying to find professionals that deal with the diagnosis of these problems daily. You should always bear in mind four (opposing) facts:

  • Vegetative state patients display signs and behaviours that makes us think that they are aware, conscious and responding. However, if a patient is truly in a vegetative state these signs are automatic responses, and not signs of conscious mental life
  • Vegetative state is often misdiagnosed (publications by e.g. Steven Laureys in Belgium). Many patients are at a higher level of function, such as minimally conscious or locked-in
  • Although a diagnosis is set at vegetative state, the condition of a patient might still improve. The rule is often that that the longer a person stays in a coma or vegetative state the worse the diagnosis. Saying that, one should never lose hope. We do not fully understand the mechanisms behind loss of consciousness, and even less about the awakening from such states.
  • Should a person regain consciousness after a vegetative state, one should always remember that the loss of consciousness had a specific and dramatic cause. Although consciousness may be restored (even as episodes) the brain is often significantly damaged. The person might still be unable to speak, attend, see etc. Many psychological and cognitive functions may be severely distorted or non-functioning

You do not mention where your son's diagnosis has been set, or where in the US you live, but I will suggest some names below. Unfortunately, I have no personal correspondence with Fins or Schiff, but know them through the scientific literature I read. Steven Laureys I know a bit, but I would suggest going to Schiff or Fins first, or the place (university / hospital) they are situated.

Joseph Fins at the Center for Bioethics, Colombia University (homepage)
Nicholas D. Schiff at the Department of Neurology and Neuroscience, Weill Medical College of Cornell University (E-mail)

Steven Laureys (Belgium, for further US directions) at the Cyclotron Research Centre (E-mail)

I hope this could be of any help to you and your family.

Sincerely,
Thomas

References

Laureys S. (2005). Science and society: death, unconsciousness and the brain. Nat Rev Neurosci, 6(11), 899-909

Laureys S. (2005). The neural correlate of (un)awareness: lessons from the vegetative state. Trends Cogn Sci

Laureys S, Pellas F, Van Eeckhout P, Ghorbel S, Schnakers C, Perrin F, Berre J, Faymonville Me, Pantke Kh, Damas F, Lamy M, Moonen G, and Goldman S. (2005). The locked-in syndrome : what is it like to be conscious but paralyzed and voiceless? Prog Brain Res, 150, 495-511

Laureys S, Perrin F, Schnakers C, Boly M, and Majerus S. (2005). Residual cognitive function in comatose, vegetative and minimally conscious states. Curr Opin Neurol, 18(6), 726-733

– Thomas

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