[VIDEO] Kid Loses Half His Brain

In consonance with the last posting, I came across this segment of an American kid who lost half his brain/skull in a shooting incident:

Thugs left man with half a head

I don't often read tabloids, but I noticed this intriguing report in The Sun lately:

Thugs left man with half a head

By STAFF REPORTER

Published: 11 Sep 2009

VICIOUS thugs who punched this man so hard he was left with HALF A HEAD have got off scot free.

Horrified Steve Gator had to have the front of his skull removed by stunned surgeons after his head was smashed against a pavement in the sickening attack. And now the 26-year-old has been told that the teen attackers who disfigured him will escape justice after his case was dropped.

Steve, of Romford, Essex, was attacked after confronting one of the yobs who had been taunting him about his cousin. Another of the violent louts hit him so hard that he was sent flying and struck his head on the path. Steve plunged into a coma for two weeks as his shattered mum and distraught family kept a bedside vigil at Queen's Hospital, Romford.

His brain quickly began swelling and surgeons were forced to remove the front half of his skull just hours after he was admitted.

Grief-stricken mum Nina Gator was warned her son had just a terrifying 15 per cent chance of survival. Two days later cops charged a pair of teenage boys with the savage attack which shocked the neighbourhood. Steve, who has had to quit his job, was left seriously brain damaged and now suffers frequent seizures, has difficulty talking, and his memory is seriously impaired. Mrs Gator, who is his main carer, last night blasted the shock move. The 47-year-old said: "I can't believe it. Everyone is entitled to their day in court."

CPS lawyers claim they needed more proof before going ahead with the case. But Mrs Gator stormed: "Our boy is walking around with half a head - what more evidence do they need? "His sparkle is totally gone. He used to be so independent but he can't work any more and he can't drive." She added: "He's got half a head and he's completely lost his confidence. There's absolutely nothing protecting his brain now it's just under his skin."

Just from looking at the picture, it seems obvious that with this traumatic brain injury (TBI) his frontal lobes are practically destroyed and quite possibly the front parts of his midbrain. The frontal lobe is an extremely important structure responsible for a variety of functions. It is the 'Command HQ' for emotions, and controls and regulates functions such as memory, language, movement, and problem-solving. It is also responsible for more subtle things like judgment, planning, reasoning, spontaneity or impulse control, and some effects on social and sexual behaviour. As such, the frontal lobe administrates much of our very personality and sense of identity. It is also the largest 'lobe' structure, meaning that there is more of it to carry a greater risk of damage. As the story mentions, Gator's "sparkle is totally gone". It is tempting to draw parallels with the tale of Phineas Gage, another individual dubiously famed for frontal lobe damage.

A friend, The Neurocritic, pointed out that Gator may need several cranioplasties in order to rebuild his skull, and highlighted a recent Neurosurgical Focus literature review that discusses the types of post-operative complications associated with the surgical procesure underwent by Gator. Known as a decompressive craniectomy, and consisting of a partial removal of the skull in order to allow the swelling brain to expand without being squeezed, we start with contusion blossoming; the surgery leaves massive bruises which can be observed via pre-op and post-op CT scans.

Lesions - a mass lesion may develop on the opposite side of the brain to the injury or elsewhere in the brain. As Gator's frontal lobes were destroyed, it is possible that a lesion may develop around the back end and possibly affect the parietal lobes, which deals generally with perception, orientation and recognition.

Herniation - a small protrusion (or more) of neural tissue may remain in the early period after swelling subsides, sometimes through the cranial defect as is observed with 'normal' skin hernias. Gator has no such defect though, as the front of the skull was smashed.

Subdural Effusions - a collection of pus beneath the outer lining of the brain. This condition usually results from bacterial meningitis, but because craniectomies affect the circulation of cerebrospinal fluid (CSF) it is possible that buildups may accumulate. Similar to blood clots. Hygromas may also occur, which are buildups of CSF without blood. To counteract these, a craniectomy should be accompanied with a duraplasty, a reconstructive operation on the dura mater, the outermost and fibrous membrance covering the brain and spinal cord. Duraplasties have been observed to lower the incidence of subdural effusions occurring.

Infection - this may seem a rather obvious effect of any medical procedure, to guard against, but craniectomies (bone removal) will necessitate cranioplasties (bone reconstruction). As such, opening old scars and exposing the brain upto or after a month after the incident runs the risk of contracting infection and delaying healing. The review suggests a minimum wait of 3 months before replacing the bone, and that storage of the bone in a freezer can also increase the risk of infection.

Hydrocephalus - "water on the brain", refers to accumulations of CSF in neural cavities. This is unfortunately a common occurrence beyond a month after the injury, and will need specialised procedures (shunt treatment) to deal with it if it occurs.

Syndrome of the Trephined - another unfortunate common occurrence after decompressive craniectomies, of which common symptoms include dizziness, headaches, concentration difficulties, mood disturbances, irritability, and memory problems. Because Gator's particular situation involved the destruction of his frontal lobes, he will unfortunately suffer much worse symptoms than these. However, in general terms when the motor functions are affected, this then becomes known as motor trephine syndrome.

Bone resorption - when one undergoes a decompressive craniectomy, you're likely to have stray bone fragments swimming around and there's around a 50% chance that bone resorption will occur, which is when bone cells (known as osteoclasts) break down the bone and release minerals like calcium directly into the blood.

Persistent vegetative state - clearly the saddest effect of all extreme brain injuries. While decompressive craniectomies are effective at ameliorating intra-cranial pressure and reducing the risk of death, they offer no guarantee of restoring brain function once the patient suffers a TBI. The risks of surviving into a vegetative or minimally conscious state after undergoing craniectomy range upwards of 15-20%.

It may be that Steve Gator's clinicians need to be vigilant and ensure that his treatment is as risk-free as possible. And of course, wishing him all the best to recover well.
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Stiver, S. (2009). Complications of decompressive craniectomy for traumatic brain injury Neurosurgical FOCUS, 26 (6) DOI: 10.3171/2009.4.FOCUS0965

Ain't Taking This Lying Down..!

Apologies for the lack of activity in recent months, I have been absorbed in a number of promising projects as well as taking a much-needed vacation.

An interesting report in New Scientist magazine suggests that insults are handled better when lying down rather than sitting or standing up. According to the article, University students who were insulted while seated exhibited neural activity consonant with "approach motivation", which describes to desire to approach and explore. This activity appeared absent in a control group insulted while lying down. Eddie Harmon-Jones, a cognitive scientist at Texas A&M University, interprets this as suggesting that one might be more inclined to attack if one were in the upright state, whereas while lying down we may be more inclined to brood.

At first glance this seems a little odd to me. Brooding is quite different to receiving insults and possibly reacting to them. Brooding means a certain amount of thinking and contemplation is occurring. It isn't the done thing to offer or accept anecdotal evidence as important fact, but from personal experience I've sometimes become more enraged over an incident by brooding about it (while lying down) than I have reacted to insults while sitting or standing upright. Would that mean my reactions contradict this research? The real value of psychological research lies in the ability to translate insights and findings into our lives and observe how relevant or useful they are, and I also have to consider these things personally. I downloaded and read the paper for this experiment; technically it is not an actual paper but a 'short report', a brief description of the subject and experimental method followed by conclusions. A mini-paper. Here's an extract:

"Body movements affect emotional processes. For example, adopting the facial expressions of specific emotions (even via unobtrusive manipulations) affects emotional judgments and memories (Laird, 2007). Manipulated body postures can affect behavior: slumped postures lead to more ‘‘helpless behaviors’’ (Riskind & Gotay, 1982). Simple body postures may also affect other emotive responses and the neural activations associated with them."

That's from the very first paragraph, and to me it seems to get more unreal every time I think about it. I don't dispute that body postures can affect neural activation (anything can affect neural activation, that's kind of what the brain does in the first place, reacting and responding to stimuli) but it seems overstated a bit much. The link between body posture and affectability on emotional reaction looks tenuous when compared with something as fundamental as the availability of oxygen and the human requirement to inhale it to live. But let's take a look at the study: 23 females and 23 males (n = 46) were randomly assigned to write a polemical essay featuring their views on a hot topic (e.g. smoking in public, abortion, etc.) and were told assessment would be carried out by another participant. After attaching EEG sensors, participants were randomly assigned to the upright or lying positions on a reclining chair while hearing themselves being rated on six characteristics including intelligence (1 = unintelligent, 9 = intelligent). Needless to say, participants heard negative reviews of themselves and fumed.

To be more specific, all 'reclined' participants heard negative reviews of themselves while only half 'uprights' heard negative. The other half heard slightly positive reviews. It's good to add a little variety to these things to account for different causes and effects, but I think the total sample size here was too small. Gender effects were accounted for too; males and females were randomly assigned to the two conditions, and male participants heard male-voiced feedback with females hearing female-voiced feedback. For future research, switching gender-voice feedback would make an interesting manipulation.

The results showed that for those in the upright position, the left prefrontal cortex (PFC) was substantially activated more than those who were reclining. Even though both sets of participants expressed similar levels of anger in response to the negative feedback, the left PFC has been linked to anger and approach motivation. This suggests a marked reduction in approach motivation when lying down.

What this means in reality remains under question: Does body posture really affect emotional reactions that much? Similar levels of anger existed between both groups, but those who were lying down appeared less inclined to do something about it? How might those students have reacted with the absence of inhibitory factors? I know that this is preliminary research but these are just some of the questions that need to be researched and accounted for.

Why? Because although some people may consider a study like this to be "fluff psychology" and a little boring, clinicians need to take these types of things a little more seriously when you consider that a large proportion of serious neuroscience is carried out with reclining participants in fMRI-scanners. So I agree with the conclusion of Harmon-Jones' paper; that research is required to help evaluate neuroimaging techniques requiring supine positions. There may not be much to it, but it's worth an exploration.
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Harmon-Jones, E., & Peterson, C. (2009). Supine Body Position Reduces Neural Response to Anger Evocation Psychological Science DOI: 10.1111/j.1467-9280.2009.02416.x

If You Had Half a Brain..

A great story made its way onto the interwebz lately. The Daily Mail reports:

"A 10-year-old girl born with half a brain has both fields of vision in one eye, scientists said today. The youngster, from Germany, has the power of both a right and left eye in the single organ in the only known case of its kind in the world.

"University of Glasgow researchers used Functional Magnetic Resonance Imaging (fMRI) to reveal how the girl’s brain had rewired itself in order to process information from the right and left visual fields in spite of her not having a whole brain."

BBC News goes further with:

"In the case of the German girl, her left and right field vision is almost perfect in one eye. Scans on the girl showed that the retinal nerve fibres carrying visual information from the back of the eye which should have gone to the right hemisphere of the brain diverted to the left ... 'Despite lacking one hemisphere, the girl has normal psychological function and is perfectly capable of living a normal and fulfilling life. She is witty, charming and intelligent.'"

Get that? The only known case in the world where brain plasticity (the ability of the brain to reorganise itself after injury) is displayed for all to see. Plasticity doesn't always work this way, there are many cases where plasticity effects haven't achieved the mark of restoring all or most of the impaired brain function. Epilepsy patients, for example, who undergo a hemispherectomy (removal of a half of a brain) in order to prevent the onset of severe seizures, among other things tend to lose an entire field of vision in both eyes; they only see people and objects in one half of their visual field, as in the illustration below:



Neither was this a case of brain injury; the anonymous girl (known only as 'AH') failed to adequately develop her cerebral right hemisphere in the womb. As a result, she is without a right-brain and also without the use of her right eye. She also has a slight left-hemiparesis (weakness affecting half of the body) but close to normal vision in both hemifields of her normal left eye.

In a study published by the Proceedings of the National Academy of Sciences (PNAS), a team led by Lars Muckli of the University of Glasgow used fMRI to investigate how the visual cortex had remapped itself. In a healthy individual, the cerebral cortex contains "maps" for vision, sound, motion and touch, which develop and modify over time dependent on several factors including genetic cues and neural activity. In the mammalian brain (that is, human brain) the visual cortex is made up of distinct sections dealing with vision, the main one being an area known simply as 'V1', the primary visual cortex. 'V2' deals with quarterfield representations in the area of vision, effectively dealing with the 'up' and 'down' areas of both the right and left hemispheres of vision, while 'V3' is a structure in front of V2 that, among other things, performs a supporting role for V2. There is also the question of retinotopic maps, a direct mapping of the spatial arrangement of the retina, located in visual structures including the cortex and thalamus.

As per materials provided by the University of Glasgow, "visual information is gathered by the retina at the back of the eye and images are inverted when they pass through the lens of the pupil so that images in your left field of vision are received on the right side of the retina, and images from the right are received on the left." The part of the retina close to the nose is known as the nasal retina whereas the other part is referred to as the temporal retina, being in proximity to the temples. Both halves transmit received information through separate nerve fibres. In a normal situation, the nerve fibres of the nasal retina cross over in the optic chiasm, a brain structure located at the bottom of the brain near the hypothalamus, and are processed by the hemisphere on the opposite side. The nerve fibres of the temporal retina remain in the same hemisphere (ipsilateral), meaning that the left and right visual fields described earlier are processed by opposite sides of the brain.



[DIGRESSION]Vision is not the only modality to be processed in this strange way. It actually reflects the larger processing activities of the intact brain which tends to process all other modalities in opposite sides of the brain. To wit, touch and hearing for example that is "entered" into the right side of the body (right body, right ear) are processed by the left-brain, and touch/hearing entered into the left body/ear is processed by the right-brain. This is generally referred to as contralateral processing, when input is processed by the 'opposite' half of the brain. Those inputs processed by the 'same' side of the brain is known as ipsilateral processing. For more information, please read about Basic Visual Pathways.[/DIGRESSION]

The MRI scan displays the complete lack of a right-hemisphere: The optic chiasm is shown here (top l-r) in the transverse and enlarged transverse planes, and (bottom l-r) in the coronal and saggital planes. A rudimentary optic nerve is pointed out in the enlargement by the green arrow but with no discernible optic tract, and it can also be seen how the left-hemisphere is spilling over into the right-domain. The vacant right-hemisphere is filled with cerebrospinal fluid (CSF).

In AH's fascinating case, it was found that the nasal retinal nerve had connected to her left-brain. A possible interpretation for AH's condition is suggested by the authors: The lack of a right-brain prevented an opposite connection from being made, which led the optic nerve fibers to "connect" with ipsilateral structures instead.

Remembering that normal cases require a crossing in the optic chiasm, and AH's connections were essentially ipsilateral, how exactly does AH see both visual fields with only one eye? After all, if the entire right hemisphere is missing, AH should see only the left hemifield. The answer lies with the Lateral Geniculate Nucleus (LGN), a structure that is embedded deep in the thalamus and which processes visual information from the retina. In AH, both the nasal and temporal retina would need to be mapped onto the LGN to allow for the processing of both hemifields. Again a similar suggestion of ipsilateral projections were presented as being the solution, instead of the usual contralateral connections, and that a mirror-symmetric representation of the hemifields would be received and processed by the thalamus. Similar cases have been seen in achiasmatic dogs where optic nerve fibres terminated in the ipsilateral LGN.

'Islands' were also found to have formed in the left-hemisphere to deal especially with processing of the left hemifield, to compensate for the missing right-brain activity.

The loss of AH's right-hemisphere was discovered at age 3 when she was treated for brief seizures and twitching taking place on her left side. It is speculated that the right-brain failed to develop between Day 28 and Day 49 of embryonic development. Despite the situation, she is able to engage quite capably in activities that require a fair amount of balance, such as riding a bicycle or roller-skating. Truly an extraordinary case in more ways than one.

For a professional view, please see Dr. Steven Novella's entry on this case.
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Muckli, L., Naumer, M., & Singer, W. (2009). Bilateral visual field maps in a patient with only one hemisphere Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0809688106

Image: CT Brain Art

New Scientist magazine currently has a gallery up featuring beautiful art made from real live CT scans of different body parts. Radiologist Kai-hung Fung digitally manipulates images of CT scans so as to make them look more appealing. One of his shots featuring the inside of the nose won the 2007 International Science and Engineering Visualisation Challenge.

Here is a shot featuring the brain:



It is a view of the brain from above it. One can see the complex network of arteries and veins (dark blue) and the base of the skull is shown in green.

Michael Jackson: Buried Without His Brain

After witnessing the media blaze related to Michael Jackson's recent death, I started hearing a number of reports that Jackson would be buried without his brain. Rather an odd thought as I watched the live memorial along with millions of other people around the globe, that the body in the gold-plated coffin wasn't an entire specimen. According to one such report, Jackson's brain is being held for further testing to determine the extent to which it was damaged by years of painkillers and other medications.

After scouting through the interwebz for a more scientific explanation, I discovered that Vaughan Bell had written up a good explanation on his excellent Mind Hacks blog. I hope he won't mind me nicking it, but I think it's that good that it deserves repetition:

According to press reports Michael Jackson will be buried without his brain because it is still 'hardening'. Although this may seem unusual, the 'hardening' process is actually a standard part of any post-mortem examination where the brain is thought to be important in the cause of death, such as in suspected overdose.

It involves removing the brain from the skull and leaving it to soak in a diluted mixture of formaldehyde and water called formalin. This soaking process usually takes four weeks and the brain genuinely does harden.

A 'fresh' brain is a pinkish colour and has the consistency of jelly, gello or soft tofu meaning it is difficult to examine and the various internal structures are often hard to make out.

After soaking the brain, it has the consistency and colour of canned mushrooms making it easier to slice, examine and photograph. However, because the brain is so soft to start with, it can't just be dropped in a tank of fixing solution, because it will deform under its own weight.

To solve the problem it is usually suspended upside down in a large bucket of formalin by a piece of string which is tied to the basilar artery.

After it has 'hardened' or 'fixed' it is sliced to look for clear damage to either the tissue or the arteries. Small sections can also be kept to examine under the microscope.

Because this part of the post-mortem takes several weeks preparation it is usually only carried out with the family's permission as the body may need to be buried without it, or the burial delayed until the procedure is finished.

This also means that this form of post-mortem brain examination is usually only carried out where there is a feeling that examining the brain can help clarify the cause of death - which is what pathologists are often most concerned with.

In cases such as Michael Jackson's, where the effects of drugs are suspected to play a part, pathologists will be looking for evidence of both sudden-onset and long-term brain damage. If they find it, they'll be trying to work out how much it could have been caused by drug use and how much it contributed to the death.

So now you know.

Can Alzheimer's Be Cured?

An excellent article over at Scientific American. As I eventually hope to be involved with Alzheimer's in my career, I found it so good that I fancied reproducing it here on this blog.

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P. Murali Doraiswamy is the head of biological psychiatry at Duke University and is a Senior Fellow at Duke’s Center for the Study of Aging. He’s also the co-author of The Alzheimer’s Action Plan, a guide for patients and family members struggling with the disease. Mind Matters editor Jonah Lehrer chats with Doraiswamy about recent advances in Alzheimer’s research and what people can do to prevent memory loss.

What do you think are the biggest public misconceptions of Alzheimer's disease?

The two biggest misconceptions are “It’s just aging” and “It’s untreatable, so we should just leave the person alone.” Both of these misconceptions are remnants of an outdated view that hinders families from getting the best diagnosis and best care. They were also one of the main reasons I wanted to write this book.

Although old age is the single biggest risk for dementia, Alzheimer’s is not a normal part of aging. Just ask any family member who has cared for a loved one with Alzheimer’s and they will tell you how different the disease is from normal aging. Alzheimer’s can strike people as young as their forties; there are some half a million individuals in the United States with early-onset dementia. Recent research has pinpointed disruptions in specific memory networks in Alzheimer’s patients, such as those involving the posteromedial cortex and medial temporal lobe, that appear distinct from normal aging.

The larger point is that while Alzheimer’s is still incurable it’s not untreatable. There are four FDA-approved medications available for treating Alzheimer symptoms and many others in clinical trials. Strategies to enhance general brain and mental wellbeing can also help people with Alzheimer’s. That’s why early detection is so important.

Given the rapid aging of the American population - by 2050, the Alzheimer's Association estimates there will be a million new cases annually - what are the some preventative steps that people can take to prevent or delay the onset of the disease?

Unfortunately, there isn’t yet a magic bullet for prevention. You can pop the most expensive anti-aging pills, drink the best red wine, and play all the brain games that money can buy, and you still might get Alzheimer’s. While higher education is clearly protective, even Nobel Laureates have been diagnosed with the disease, although it’s likely their education helped them stave off the symptoms for a little bit.

My approach is more pragmatic - it’s about recognizing risks and designing your own brain health action plan. The core of our program is to teach people about the growing links between cardiovascular markers (blood pressure, blood sugar, body weight and BMI, blood cholesterol, C-reactive protein) and brain health. A population study from Finland has developed a fascinating scale that can predict 20-year risk for dementia – sort of a brain aging speedometer. Obesity, smoking, lack of physical activity, high blood pressure, and high cholesterol are some of the culprits this study identified. So keeping these under control is crucial.

Depression is another risk factor for memory loss, so managing stress and staying socially connected is also important. B vitamins may prevent dementia in those who are deficient and there are some simple blood tests that can detect this. For the vast majority of people, however, there are no prescription medications that have been proven to prevent dementia. This means that a brain-healthy lifestyle is really our best bet for delaying the onset of memory loss.

In the near future we will likely have prevention plans that are personalized based on genetic, metabolic and neurological information. In familial Alzheimer’s disease, pre-implantation genetic diagnosis has already been used to successfully deliver babies free of a deadly Alzheimer causing mutation—though only time will tell if deleting such dementia risk genes in humans has other consequences.

Your book talks about a new technique that allows doctors to image amyloid plaques in the brain. How will these change the diagnosis of the disease?

Amyloid PET scans are in the late stages of validation testing to see if they can improve the accuracy of clinical diagnosis. The Alzheimer’s brain is defined by beta-amyloid plaques and tangles but, at present, these can only be definitively diagnosed with an autopsy. If an amyloid PET scan is “plaque negative” that will tell a doctor that Alzheimer’s is unlikely to be the diagnosis and help reassure the family. Early findings suggest that people who carry risk genes are more likely to have plaque positive scans even before they develop symptoms - suggesting that the scans could possibly be useful for predicting future risk. If true, this might eventually lead to a change in diagnostic terminology where “preclinical” Alzheimer’s is diagnosed purely based on biomarker and scan findings long before memory symptoms start. Therapies to treat Alzheimer’s by blocking amyloid plaques are already in trials but are currently given blindly to patients without knowing their brain plaque status—raising their risk for side effects and treatment failure. So this scan may also help drug development by helping select the most appropriate subjects for treatment and then monitoring treatment effects. Amyloid accumulation with aging is seen in many animal species and the scan offers us a tool to study what role plaque plays in normal brain aging. So this could do for the brain what colonoscopy did for the gut!

Will science ever find a cure for Alzheimer's?

It’s an incredibly tough puzzle to crack but the pace of research is so great that new drug targets are being reported daily. I think a form of cure is more likely to come from delaying the onset rather than by growing new brain cells to repair lost tissue. Realistically speaking there are several fundamental questions we don’t fully understand and have yet to answer: What causes the disease? Why do plaques and tangles form? Why are the memory centers the first to be destroyed? On the positive side, there are several dozen drugs in clinical trials.

What recent scientific advances in treating or understanding Alzheimer's are you most excited about?

I’m most excited about diagnostic advances. By using a combination of biomarkers, genetic tests and new brain scans, we are inching very close to predicting not only who will develop Alzheimer’s but the exact age when they may start developing symptoms. This offers huge opportunities for conducting prevention trials. Of course, it also brings a whole host of ethical challenges, since our diagnostic and predictive abilities are advancing far faster than our ability to prevent Alzheimer’s.

On the treatment side, there are several developments that I am excited about. The interactions between vascular disease and memory loss suggest that at least some aspects of Alzheimer’s may be modifiable through diet and exercise. Dimebon, a drug that improves mitochondrial function, has yielded promising results and is in final stages of testing. In addition, therapeutic strategies which target the brain’s own ability to repair itself – for example, by delivering nerve growth factor through viral vectors – are in clinical trials. Until we have a cure, however, it’s really important to focus on improving the quality of life of people with Alzheimer’s.