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Zika virus (ZIKV), an arbovirus transmitted by mosquitoes of the Aedes genus, was first isolated in 1947 in the Zika forest of Uganda from a sentinel monkey. It has always been considered a minor pathogen. From its discovery until 2007 only 14 sporadic cases – all from Africa and Southeast Asia – had been detected. In 2007, however, a major outbreak occurred in Yap Island, Micronesia, with 73% of residents being infected.
The importance of a healthy diet for proper functioning of the brain is increasingly being recognized. Week in, week out studies appear recommending a high intake of certain foods in order to achieve optimal brain function and prevent brain diseases. Although it is definitely no punishment for the most of us to increase our chocolate consumption to boost brain function, the most important period during which nutrition affects our brain may already be behind us.
Are we at the birth of a new culture in the western world? Are we on the verge of a new way of thinking? Both humanistic and scientific thinkers suggest as much.
To mark this month’s release of Martin R. Turner and Matthew C. Kiernan’s Landmark Papers in Neurology, we spoke with the two editors, to discuss their thoughts on neurology – past and present. We asked about the origins of neurology, the understanding of neurological diseases, milestones in the field, why historical context is so important – and their predictions for the future…
Each year in July, I greet a new group of post-doctoral psychiatric trainees ('residents,' 'registrars') for a year's work in our psychiatric outpatient clinic. One of the rewards of being a psychiatric educator is witnessing the professional growth of young clinicians as they mature into seasoned, competent, and humanistic psychiatrists.
It was midnight and I had just slumped into bed, exhausted after one of my first days on-call as a new intern, and still adjusting to life in a new apartment. As my nagging reflections on the day were just beginning to subside, insistent knocking at my door jolted me back to alertness. Dragging myself out of bed to open the door, I was surprised to see a diminutive elderly lady who appeared quite perturbed.
In the wake of the development of advanced neonatal intensive medical care, more and more children born very preterm manage to beat the previously tough odds and survive the perils of infections and respiratory distress that are some of the common problems in the group. While this is one of the success stories of modern medicine, long-term follow-up of premature-born pediatric cohorts show that the obstacles don’t cease with the need of intensive medical care.
How would we know if a medieval person had a neurological disorder? If we did know, would it be possible to pinpoint the type of condition? What insight can we gain about the practical impact of disorders on medieval life? Fortunately, a physical record survives that provides a reliable window into the health of medieval people—or, at least, those who were able to write.
The brain is a product of its complex and multi-million year history of solving the problems of survival for its host, you, in an ever-changing environment. Overall, your brain is fairly fast but not too efficient, which is probably why so many of us utilize stimulants such as coffee and nicotine to perform tasks more efficiently. Thus far, no one has been able to design a therapy that can make a person truly smarter.
Can you imagine a concert hall full of chimpanzees sitting, concentrated, and feeling 'transported' by the beauty of Beethoven’s Ninth Symphony? Even harder would be to imagine a chimpanzee feeling a certain pleasure when standing in front of a beautiful sculpture. The appreciation of beauty and its qualities, according to Aristotle’s definition, from his Poetics (order, symmetry, and clear delineation and definiteness), is uniquely human.
Imagine the unimaginable. Suffering from Alzheimer’s Disease (AD), the person with whom you shared most of your life has forgotten who you are, and even worse, can no longer remember their own experiences, their relationships, and how to behave appropriately in everyday situations. But although most of their long-term memory is heavily impaired, they may continue to relate astonishingly well to autobiographically relevant pieces of music.
At one point in the recent film The Imitation Game the detective assigned to his case asks Alan Turing whether machines could think. The dialogue that follows is perhaps not very illuminating philosophically, but it does remind us of an important point: the computer revolution that Turing helped to pioneer gave a huge impetus to interest in what we now call the mind-body problem. In other words, how is the mind related to the body? How could a soggy grey mass such as the brain give rise to the extraordinary phenomenon of consciousness?
Our actions, thoughts, perceptions, feelings, and memories are underpinned by electrical activity, which passes through networks of neurons in the brain. As a child grows and gains new skills their brain changes rapidly and brain networks are formed and strengthened with learning and experience.
Does coffee enhance marijuana? A study published recently in the Journal of Neuroscience (Vol 34 (19):6480-6484, 2014) by neuroscientists from the Integrative Neurobiology Section of the National Institute on Drug Abuse, a branch of the National Institutes of Health, has finally provided a definitive answer: Yes, No, and it depends.
I read this after listening the fabulous Bookrageous Podcast which read and discussed the book for their book club and then interviewed the author. It is a fascinating look at what is happening inside our minds when we read. The author, Peter Mendelsund, is a book designer for Knopf in the US but also has […]
Head hits cause brain damage, but not always. Should we ban sport to protect athletes? Exposure to electromagnetic fields is strongly associated with cancer development. Should we ban mobile phones and encourage old-fashioned wired communication? The sciences are getting more and more specialized and it is difficult to judge whether, say, we should trust homeopathy, fund a mission to Mars, or install solar panels on our roofs. We are confronted with questions about causality on an everyday basis, as well as in science and in policy.
Causality has been a headache for scholars since ancient times. The oldest extensive writings may have been Aristotle, who made causality a central part of his worldview. Then we jump 2,000 years until causality again became a prominent topic with Hume, who was a skeptic, in the sense that he believed we cannot think of causal relationships as logically necessary, nor can we establish them with certainty.
The next major philosophical figure after Hume was probably David Lewis, who proposed quite a controversial account saying roughly that something was a cause of an effect in this world if, in other nearby possible worlds where that cause didn’t happen, the effect didn’t happen either. Currently, we come to work in computer science originated by Judea Pearl and by Spirtes, Glymour and Scheines and collaborators.
All of this is highly theoretical and formal. Can we reconstruct philosophical theorizing about causality in the sciences in simpler terms than this? Sure we can!
One way is to start from scientific practice. Even though scientists often don’t talk explicitly about causality, it is there. Causality is an integral part of the scientific enterprise. Scientists don’t worry too much about what causality is – a chiefly metaphysical question – but are instead concerned with a number of activities that, one way or another, bear on causal notions. These are what we call the five scientific problems of causality:
Phrenology: causality, mirthfulness, and time. Photo by Stuart, CC-BY-NC-ND-2.0 via Flickr.
Inference: Does C cause E? To what extent?
Explanation: How does C cause or prevent E?
Prediction: What can we expect if C does (or does not) occur?
Control: What factors should we hold fixed to understand better the relation between C and E? More generally, how do we control the world or an experimental setting?
Reasoning: What considerations enter into establishing whether/how/to what extent C causes E?
This does not mean that metaphysical questions cease to be interesting. Quite the contrary! But by engaging with scientific practice, we can work towards a timely and solid philosophy of causality.
The traditional philosophical treatment of causality is to give a single conceptualization, an account of the concept of causality, which may also tell us what causality in the world is, and may then help us understand causal methods and scientific questions.
Our aim, instead, is to focus on the scientific questions, bearing in mind that there are five of them, and build a more pluralist view of causality, enriched by attention to the diversity of scientific practices. We think that many existing approaches to causality, such as mechanism, manipulationism, inferentialism, capacities and processes can be used together, as tiles in a causal mosaic that can be created to help you assess, develop, and criticize a scientific endeavour.
In this spirit we are attempting to develop, in collaboration, complementary ideas of causality as information (Illari) and variation (Russo). The idea is that we can conceptualize in general terms the causal linking or production of effect by the cause as the transmission of information between cause and effect (following Salmon); while variation is the most general conceptualization of the patterns of difference-making we can detect in populations where a cause is acting (following Mill). The thought is that we can use these complementary ideas to address the scientific problems.
For example, we can think about how we use complementary evidence in causal inference, tracking information transmission, and combining that with studies of variation in populations. Alternatively, we can think about how measuring variation may help us formulate policy decisions, as might seeking to block possible avenues of information transmission. Having both concepts available assists in describing this, and reasoning well – and they will also be combined with other concepts that have been made more precise in the philosophical literature, such as capacities and mechanisms.
Ultimately, the hope is that sharpening up the reasoning will assist in the conceptual enterprise that lies at the intersection of philosophy and science. And help decide whether to encourage sport, mobile phones, homeopathy and solar panels aboard the mission to Mars!
How does the brain work? It’s a question on a lot of people’s minds these days, especially with the launch of massive new research efforts like the American BRAIN Initiative and the European Human Brain Project. It’s also a systems question because after all, the brain is a key part of the nervous system, like the skull is a key part of the skeletal system or the heart is a key part of the circulatory system. The basic approach to understanding how any system works has been clear since Greek and Roman times two thousand years ago: understand what the system does, make a parts list, describe how each part works, and then determine how the parts interact to carry out the various functions of the system.
Science is based on observing nature and testing resulting hypotheses to understand functional mechanisms. And major progress comes from the most general hypotheses—theoretical frameworks at the systems level: paradigms. Famous examples include Copernicus organizing the sun and planets with the earth rather than the sun at the center, Mendeleev arranging the basic chemical elements of all matter into a periodic table, and Watson and Crick’s model of the molecular basis of heredity—in terms of how the four nucleotide building blocks of DNA are arranged spatially in a double helix.
Systems neuroscience does not have a comparable theoretical framework, leaving it in a pre-Watson and Crick, or maybe even better, a pre-Darwin state of affairs. The solution is simple, obvious, and attainable—but essentially ignored in current “big science” approaches to neuroscience. Watson and Crick’s model of DNA led 50 years later to the sequencing of the human genome. At first, this project was widely criticized as frivolous, but it proved to be seminal in many ways, not the least of which is establishing the scope of the problem—the basic overall organization of the chromosomes—and allowing the relatively fast and cheap assaying of genome-wide expression patterns on a tiny chip. Getting the structural sequence was only the first step, but it was a necessary step, allowing all of functional, mechanistic understanding to follow logically, in a classic hypothesis-driven way.
Stained human neocortical pyramidal cell. Photo by Bob Jacobs, Laboratory of Quantitative Neuromorphology Department of Psychology Colorado. CC BY-SA 3.0 via Wikipedia.
The analogous solution for neuroscience is figuring out the basic wiring diagram of the nervous system, and this has to start with the connectome, essentially a table of connections between the parts. From this connectome a blueprint of the nervous system can be developed, like the architectural drawings for an office building, the plans for an airliner, or the schematics for a motherboard. The basic circuit diagram is like a skeleton, a basic framework for understanding the function of the nervous system. It is hard to imagine building and fixing a modern skyscraper, airplane, or computer without detailed and accurate schematics—and the same applies to understanding mechanisms underlying brain function and fixing problems scientifically.
Everybody knows that the brain is the most complex object on earth, so a viable strategy for solving the wiring diagram is essential. The approach here is also obvious—start with the simplest level of analysis, and progress to deeper and deeper levels. The simplest level is the wiring diagram between basic parts, and there are about 500 of them in mammals. This is analogous to displaying the airline routes between major cities around the world. The next level is the wiring diagram at the level of neuron types that make up each part—there are probably 2,500 to 5,000 neuron types in mammals. And the next level after that is the wiring diagram between all of the individual nerve cells that make up each of the neuron types—hundreds of millions to billions in mammals. The simplest, most general level can be solved now with current technology in rodents. Why not do it, and develop more efficient technology at the same time—just like the history of the genome project. Developing effective ways to interact between animal connectomes based on histology at cellular resolution and human connectomes based on MRI—and correlating both with genomic information—is the wave of the future. Great progress in diagnosing, treating, and understanding the etiology of nervous system diseases can be expected by correlating the results of genome-wide association studies with connectome-wide association studies.
Headline image credit: Diagram of brain synapses. Image by Allan Ajifo, aboutmodafinil.com. CC BY 2.0 via Wikimedia Commons.
Imagine you are in class and your friend has just made a fool of the teacher. How do you feel? Although this will depend on the personalities of those involved, you might well find yourself laughing along with your classmates at the teacher’s expense. The experience of sharing an emotion with your friends (in this case the fun of getting one over on the teacher) will probably strengthen your friendship further. But in a class of one hundred students, there are likely to be one or two who have trouble understanding the joke.
The ability to infer and understand other peoples’ emotions and beliefs plays an important role in human social relationships. However, for individuals with autism spectrum disorder (ASD) — a developmental disorder that affects approximately 1% of the population and for which there is no established treatment — this can be challenging. While high-functioning individuals with ASD may be able to compensate for difficulties in inferring others’ beliefs, they often continue to have trouble understanding others’ emotions, and this leads to impaired social functioning.
Increasing evidence suggests that oxytocin — a neuropeptide that promotes social behavior and bonding in humans and in animals — can improve emotion recognition in ‘typically developing’ individuals, i.e. those without ASD. Notably, oxytocin improves the ability to infer others’ emotions more than the ability to identify their beliefs. Oxytocin has also been shown to improve social behavior in individuals with autism and to partially reverse patterns of brain dysfunction thought to be responsible for the deficits. This has led to the suggestion that oxytocin could be used to develop medications for currently untreatable psychiatric conditions characterized by social impairments.
However, studies to date have only investigated the ability of oxytocin to improve recognition of basic emotions such as fear or happiness. These differ from “social” emotions such as embarrassment and shame, which require us to represent the mental state of another. Moreover, most existing studies have provided participants with so-called “direct cues” as to others’ emotions, such as their facial expressions or tone of voice. However, these cues are not always available in real life and the ability to identify others’ emotions using only indirect cues is itself important for social functioning. We therefore decided to investigate whether oxytocin would also improve the ability of individuals with ASD to recognise social emotions, even in the absence of direct cues.
To do so, we modified a cartoon-based task called the “Sally-Anne task,” which is commonly used to test for understanding of other peoples’ false beliefs, and used MRI scans to measure brain activity in subjects with and without ASD as they performed the task. In the standard version, participants are shown a cartoon in which one protagonist (Sally) places a ball in a box and then leaves the room. In her absence, another protagonist (Anne) moves the ball to a second box to the right of the first, and Sally then returns. At the end of the story, participants are asked the following questions: “Is the ball in the left-hand box?” to test comprehension of the story, and “Does Sally look for her ball in the left-hand box?” to test for understanding of Sally’s false belief about the location of the ball. To examine participants’ ability to infer others’ emotions, we introduced a third question: “How does Anne feel when Sally opens the left-hand box?”. Given that Ann’s gain effectively depends on Sally’s loss, the emotions involved will be complex social emotions: Ann, for example, might gloat upon realizing that she has fooled Sally by moving the ball.
We discovered that individuals with ASD are less accurate than IQ-matched controls in inferring social emotions in the absence of direct cues such as facial expressions. Moreover, individuals with ASD showed lower activity than controls in two brain regions that contribute to this ability, namely the right anterior insula and superior temporal sulcus. Individuals with ASD who had a normal IQ were not significantly impaired in inferring others’ beliefs; however, they did show lower brain activity than controls in a region implicated in this process, the dorsomedial prefrontal cortex.
In order to determine whether oxytocin could improve the ability of individuals with ASD to identify others’ social emotions, we conducted a double-blind trial. We administered a single dose of either oxytocin or placebo in the form of an intranasal spray to subjects with ASD and to matched controls. As predicted, oxytocin increased the accuracy with which individuals with ASD were able to identify others’ social emotions in the absence of direct cues, and also enhanced their originally-diminished brain activity in the right anterior insula. This increase in activity was not observed in other brain regions or during attempts to understand others’ beliefs, suggesting that oxytocin acts specifically on the ability to infer social emotions.
Ultimately therefore, the results of our behavioral experiments and brain activity studies lend support to the idea that intranasal oxytocin could potentially form the basis of a treatment for at least some of the social impairments in ASD.
How rapidly does medical knowledge advance? Very quickly if you read modern newspapers, but rather slowly if you study history. Nowhere is this more true than in the fields of neurology and psychiatry.
It was believed that studies of common disorders of the nervous system began with Greco-Roman Medicine, for example, epilepsy, “The sacred disease” (Hippocrates) or “melancholia”, now called depression. Our studies have now revealed remarkable Babylonian descriptions of common neuropsychiatric disorders a millennium earlier.
There were several Babylonian Dynasties with their capital at Babylon on the River Euphrates. Best known is the Neo-Babylonian Dynasty (626-539 BC) associated with King Nebuchadnezzar II (604-562 BC) and the capture of Jerusalem (586 BC). But the neuropsychiatric sources we have studied nearly all derive from the Old Babylonian Dynasty of the first half of the second millennium BC, united under King Hammurabi (1792-1750 BC).
The Babylonians made important contributions to mathematics, astronomy, law and medicine conveyed in the cuneiform script, impressed into clay tablets with reeds, the earliest form of writing which began in Mesopotamia in the late 4th millennium BC. When Babylon was absorbed into the Persian Empire cuneiform writing was replaced by Aramaic and simpler alphabetic scripts and was only revived (translated) by European scholars in the 19th century AD.
The Babylonians were remarkably acute and objective observers of medical disorders and human behaviour. In texts located in museums in London, Paris, Berlin and Istanbul we have studied surprisingly detailed accounts of what we recognise today as epilepsy, stroke, psychoses, obsessive compulsive disorder (OCD), psychopathic behaviour, depression and anxiety. For example they described most of the common seizure types we know today e.g. tonic clonic, absence, focal motor, etc, as well as auras, post-ictal phenomena, provocative factors (such as sleep or emotion) and even a comprehensive account of schizophrenia-like psychoses of epilepsy.
Epilepsy Tablet and the Dying Lioness, reproduced with kind permission of The British Museum.
Early attempts at prognosis included a recognition that numerous seizures in one day (i.e. status epilepticus) could lead to death. They recognised the unilateral nature of stroke involving limbs, face, speech and consciousness, and distinguished the facial weakness of stroke from the isolated facial paralysis we call Bell’s palsy. The modern psychiatrist will recognise an accurate description of an agitated depression, with biological features including insomnia, anorexia, weakness, impaired concentration and memory. The obsessive behaviour described by the Babylonians included such modern categories as contamination, orderliness of objects, aggression, sex, and religion. Accounts of psychopathic behaviour include the liar, the thief, the troublemaker, the sexual offender, the immature delinquent and social misfit, the violent, and the murderer.
The Babylonians had only a superficial knowledge of anatomy and no knowledge of brain, spinal cord or psychological function. They had no systematic classifications of their own and would not have understood our modern diagnostic categories. Some neuropsychiatric disorders e.g. stroke or facial palsy had a physical basis requiring the attention of the physician or asû, using a plant and mineral based pharmacology. Most disorders, such as epilepsy, psychoses and depression were regarded as supernatural due to evil demons and spirits, or the anger of personal gods, and thus required the intervention of the priest or ašipu. Other disorders, such as OCD, phobias and psychopathic behaviour were viewed as a mystery, yet to be resolved, revealing a surprisingly open-minded approach.
From the perspective of a modern neurologist or psychiatrist these ancient descriptions of neuropsychiatric phenomenology suggest that the Babylonians were observing many of the common neurological and psychiatric disorders that we recognise today. There is nothing comparable in the ancient Egyptian medical writings and the Babylonians therefore were the first to describe the clinical foundations of modern neurology and psychiatry.
A major and intriguing omission from these entirely objective Babylonian descriptions of neuropsychiatric disorders is the absence of any account of subjective thoughts or feelings, such as obsessional thoughts or ruminations in OCD, or suicidal thoughts or sadness in depression. The latter subjective phenomena only became a relatively modern field of description and enquiry in the 17th and 18th centuries AD. This raises interesting questions about the possibly slow evolution of human self awareness, which is central to the concept of “mental illness”, which only became the province of a professional medical discipline, i.e. psychiatry, in the last 200 years.
The consequences of traumatic brain injury (TBI) are sizable in both human and economic terms. In the USA alone, about 1.7 million new injuries happen annually, making TBI the leading cause of death and disability in people younger than 35 years of age. Survivors usually exhibit lifelong disabilities involving both motor and cognitive domains, leading to an estimated annual cost of $76.5 billion in direct medical services and loss of productivity in the USA. This issue has received even more intense scrutiny in the popular media with respect to sports-related concussions where there is a proposed link between having suffered multiple injuries, regardless of severity, with later neurodegeneration. At present, there is a dearth of evidence to either support or undermine the role of sports concussions in the later development of neurodegenerative processes, much less the influence of those brain injuries on the normal aging process.
As most people agree that no two concussions are alike, they all share at least one feature in common; they all involve the near instant transfer of kinetic energy to the brain. The brain absorbs kinetic energy as a result of acceleration forces, while deceleration forces cause it to release kinetic energy when colliding with the skull. Coup contrecoup injury is one of the most ancient and best supported biomechanical models of traumatic brain injury induction. Acceleration/deceleration forces can either be transferred to the brain in a straight line passing through the head’s centre of gravity or in a tangential line and arc around its centre of gravity. Shearing and stretching of axons are common manifestations of inertial forces applied to the brain and this type of damage is commonly referred to as traumatic axonal injury. Although robustly demonstrated in both animal and post-mortem models of TBI, neuroimaging techniques limitations, however, have long prevented us from accurately tracking projecting axonal assemblies, also called white matter fibers, in living humans. The recent emergence of a magnetic resonance imaging (MRI)-based tool called Diffusion Tensor Imaging (DTI) can reveal abnormalities in white matter fibers with increasing sensitivity. DTI has quickly gained in popularity among TBI researchers who have long sought to characterize the neurofunctional repercussions of traumatic axonal injury in living humans. One particularly appealing clinical application of DTI is with athletes who have sustained sports concussion in whom conventional MRI assessments typically turn out negative despite the persistence of long-lasting, cumulative neurofunctional symptoms. First applied to young concussed athletes, a follow-up DTI study conducted in our laboratory revealed subtle white matter tracts anomalies detected in the first few days after the injury and again 6 months later. Interestingly, these young concussed athletes were all asymptomatic at follow-up and performance on concussion-sensitive neuropsychological tests had returned to normal.
In parallel, our group became increasingly interested in the characterization of the remote neurofunctional repercussions of concussion sustained decades earlier in late adulthood former elite athletes. Quantifiable cognitive (i.e. memory and attention) and motor function alterations were found on age-sensitive clinical tests, a finding that significantly contrasts with the full recovery typically found within a few days post-concussion in young, active athletes on equivalent neurofunctional measures. This finding was the first of many demonstrations that a remote history of sports concussion synergistically interacts with advancing age to precipitate brain function decline. These neuropsychological tests performance alterations specific to former concussed athletes were soon after found to correlate significantly with markers of structural damage restricted to ventricular enlargement and age-dependent cortical thinning. However, besides the significant interaction of age and a prior history of concussion on cortical thinning, former concussed athletes could not be differentiated from age-matched unconcussed teammates using highly sophisticated measures of grey matter morphometry. White matter integrity disruptions therefore appeared as a likely candidate to explain the observed significant ventricular enlargement found in former concussed athletes. We thus turned to state-of-the-art DTI metrics to conduct the first study of white matter integrity with older but clinically normal retired athletes with a history of sports-related concussions. A particular emphasis was put on bringing together former elite athletes who were free from confounding factors such as clinical comorbidities, drug/alcohol abuse, and genetic predisposition that are too often confusing the long-term effects of concussions on brain health. Our results show that aging with a history of prior sports-related concussions induces a diffuse pattern of white matter anomalies affecting many major inter-hemispheric, intra-hemispheric as well as projection fiber tracts. Of crucial clinical significance with relation to our previous findings on former concussed athletes, we found ventricular enlargement to correlate significantly with widespread alterations of key markers of white matter integrity including not only peri-ventricular white matter tracts, but also an extensive network of fronto-parietal connections. Most of all, these white matter integrity losses were found to be associated with altered neurocognitive functions including memory and learning.
Taken together with previous functional and structural characterizations of the remote effects of concussion in otherwise healthy older former athletes, the pattern of white matter alterations, being more pronounced over fronto-parietal brain areas, more closely resemble what has been observed in normal aging. From this interpretation, we suggest that concussion induces a latent microstructural injury that synergistically interacts with the aging process to exert late-life brain decline in both structure and function.
Want to help your students focus better during independent writing time? A recent NY Times piece by Daniel J. Levitin may hold the key to making this happen in your classroom.
The earth is filled with many types of worms, and the term “planarian” can represent a variety of worms within this diverse bunch of organisms. The slideshow below highlights fun facts about planarians from Oné Pagán’s book, The First Brain: The Neuroscience of Planarians, and provides a glimpse of why scientists like Pagán study these fascinating creatures.
In taxonomic terms, planarians belong to a large class of organisms called Vermes, the Latin term for “worm.” Platyhelminthes, or “flatworms,” represent a phylum within the class of Vermes, though the Platyhelminthes are broken down into four additional categories. One of these categories includes the Turbellarians—flatworms that are free-living and non-parasitic. Turbellarians are then arbitrarily distinguished based on their size, creating two further divisions: the microturbellarians (worms that are shorter than 1 mm) and macroturbellarians (worms that are longer than 1 mm). There are two types of macroturbellarians, the triclads and polyclads. Though “planarian” is a general term used to describe many types of flatworms, it is most often used in reference to triclads.
Triclads are small worms. They do not typically exceed one inch in length, but many of these worms are even smaller than that. Though these planarians can usually be seen with the naked eye, they are often studied under a microscope for closer observation. The two distinctive bumps that you can see on both sides of a planarian’s head, even without a microscope, are called auricles. Though they are commonly mistaken for ears, auricles do not pick up sounds in the environment, and instead contain many chemoreceptors that help planarians sense both nourishing and toxic substances in their surrounding environment.
Planarians are an ancient species. But like other invertebrates, it’s hard for planarians to fossilize because their bodies lack hard bones. Planarians’ tendency to autolyze—or dissolve head first—when they die makes the process of fossilization even more difficult. Though the fossil record for these organisms is a bit scarce, scientists have identified a fully intact turbellarian fossil from the Eocene period about 40 million years ago. Scientists have also found what they interpret as fossilized flatworm tracks from the Permian period (300 million years ago).
Planarians possess the incredible capability to regenerate cells that are damaged or removed. Though the scope of regeneration varies from species to species, many planarians are capable of full regeneration. This means that if you chop up a planarian into several pieces—the current record is 279 sections—each piece can regenerate into a full grown worm, assuming that this piece of the worm is placed in an environment with adequate nourishment. Even the isolated tip of a tail from a planarian can develop into a full grown worm that possesses a brain and central nervous system.
In the early 20th century, scientists began looking for organisms with which they could test the principles of Mendelian genetics. Most people are aware that fruit flies (Drosophila melanogaster) became a common test subject because of their short lifespans and ability to produce large quantities of offspring in a short period of time. However, planarians also became a great model organism for scientists to use. Though the planarian nervous system is simple, these flatworms display an immense array of complex behaviors—making planarians an ideal candidate with which scientists can study how the brains of more complex organisms, such as humans, function.
Planarians are not only test subjects for scientists to study. These are also creatures of popular culture, making appearances in several movies and TV shows. For example, in an episode of Fringe, Dr. Bishop offers Agent Dunham a smoothie with chopped pieces of planarians—a gesture meant to pay homage to the memory transfer experiments conducted by McConnell. Planarians have also appeared in the first movie of the Twilight saga, in addition to episodes of The Big Bang Theory and Dr. Who.
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Images: The first five photos in this slideshow have been used courtesy of Dr. Masaharu Kawakatsu. Photo six is copyrighted (2003) by the National Academy of Sciences, USA and has been used with permission.
Scientists, using epidural stimulation over the lumbar spinal cord, have enabled four completely paralyzed men to voluntarily move their legs.
Kent Stephenson is one of the four. This stimulation experiment wasn’t supposed to work for him; he is what clinicians call an AIS A. This is a measure of disability, formally the American Spinal Injury Association Impairment Scale (AIS), that rates impairment from A (no motor or sensory function) to D (ability to walk). Kent, a mid-thoracic paraplegic, has what is considered a “complete” injury. Kent’s doctors told him it was a waste of time to pursue any therapy; per the dogma, A’s don’t get better. Well, the young Texan, who was hurt five years ago on a dirt bike, didn’t get the message. He likes to cite a fortune cookie he got shortly after his injury. It said, “Everything’s impossible until somebody does it.”
Kent had the stimulator implanted. A few days later they turned it on. No one expected it to do anything. Researchers were only looking for a baseline measurement to compare Kent’s function later, after several weeks of intense Locomotor Training (guided weight supported stepping on a treadmill).
Kent tells the story: “The first time they turned the stim on I felt a charge in my back. I was told to try pull my left leg back, something I had tried without success many times before. So I called it out loud, ‘left leg up.’ This time it worked! My leg pulled back toward me. I was in shock; my mom was in the room and was in tears. Words can’t describe the feeling – it was an overwhelming happiness.”
Kent was the second of the four. Rob Summers, three years ago, was the first to pioneer the concept that complete doesn’t mean what it used to; epidural stimulation could make the spinal cord more receptive to nerve signals coming from the senses or the brain. Seven months after he was implanted with a stimulator unit, he initiated voluntary movements of his legs. The other two subjects, Andrew Meas and Dustin Shillcox, also started moving within days of the implant. Summers probably could have initiated movement early on too, but the research team didn’t test for it – they had no reason to believe he could do it.
Here’s lead author of the Brain paper, Claudia Angeli, Ph.D., to explain. She is a senior researcher at the Human Locomotor Research Center at Frazier Rehab Institute, and an assistant professor at the University of Louisville’s Kentucky Spinal Cord Injury Research Center (KSCIRC).
“First, in the Lancet paper [regarding the first stimulation subject] it was just Rob, just one person. Yes, it was proof of concept, yes it went great. But now we are talking about four subjects. That’s four out of four showing functional recovery. What’s more, two of the four are categorized as AIS A – no motor or sensory function below the lesion level, with no chance for any recovery.”
The other two patients are classified AIS B: no motor function below the lesion but with some sensory function.
Left to right is Andrew Meas, Dustin Shillcox, Kent Stephenson, and Rob Summers, the first four to undergo task-specific training with epidural stimulation at the Human Locomotion Research Center laboratory, Frazier Rehab Institute, as part of the University of Louisville’s Kentucky Spinal Cord Injury Research Center, Louisville Kentucky.
How does this work? The epidural stimulation supplies a continuous electrical current, at varying frequencies and intensities, to specific locations on the lower part of the spinal cord. A 16-electrode spinal cord stimulator, commonly used to treat pain, is implanted over the spinal cord at T11-L1, a location that corresponds to the complex neural networks that control movement of the hips, knees, ankles and feet.
The leg muscles are not stimulated directly. The epidural stimulation apparently awakens circuitry in the spinal cord. “In simple terms,” says Dr. Angeli, “we are raising the excitability or gain of the spinal cord. Let’s say you have an intent to move. That signal originates in the brain and gets through to the spinal cord but the cord is not aware enough or excited enough to do anything with that intent. When we add the stimulation, the spinal cord networks are made a little more aware, so when the intent comes through, the cord is able to interpret it and movement becomes voluntary.”
The theory behind spinal cord stimulation is that these spinal cord networks are smart: they can remember and they can learn. The current work builds on decades of research. Susan Harkema, Ph.D. (University of Louisville) and V. Reggie Edgerton, Ph.D. (University of California Los Angeles) have led the effort. Dr. Harkema is Principal Investigator for the epidural stimulation projects and Director of the Christopher & Dana Reeve Foundation’s NeuroRecovery Network. Dr. Edgerton, a member of the Reeve Foundation’s International Research Consortium on Spinal Cord Injury, is a basic scientist whose work attempts to understand human locomotion and how the brain and spinal cord adapt and change in response to various interventions, including activity, training and stimulation.
Dr. Harkema says plans are in place to implant eight more patients in the next year. Four will mirror the first group, matched by age, level of injury, time since injury, etc. (Gender, by the way, is not a factor; men with spinal cord injury happen to outnumber women four to one.) Another four patients will be stimulated specifically to control heart rate and blood pressure. Dr. Harkema said one of the first four had issues with low blood pressure. When the stimulator was on, though, the pressure was raised, even without contracting any muscles. They want to assess that sort of autonomic recovery in greater detail.
The research team is aware that epidural stimulation can enhance autonomic function in paralyzed subjects; indeed, the first four subjects report improved temperature control, plus better bowel, bladder, and sexual function. Data is being collected to present that part of the stimulation story in another paper.
Does this mean anyone with a spinal cord injury with an implanted stimulator can move? Not necessarily, says Dr. Harkema. “But what I want people to know about this study is that we need to change our attitude about what a complete injury is, challenge the dogma that in AIS A patients there is no possibility of recovery. The view is that it is not a worthwhile investment to offer even intense rehabilitation to people with complete injuries. They’re not going to recover. But the message now is that there is a tremendous amount available. These individuals have potential for recoveries that will improve their health and quality of life. Now we have a fundamentally new strategy that can dramatically affect recovery of voluntary movement in those with complete paralysis, even years after injury.”
Brain provides researchers and clinicians with the finest original contributions in neurology. Leading studies in neurological science are balanced with practical clinical articles. Its citation rating is one of the highest for neurology journals, and it consistently publishes papers that become classics in the field.
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Image credit: Video and image both used with permission from the Christopher and Dana Reeve Foundation.
I recently painted a self-portrait on a modified washing machine. The installation's called "Brainwashing Machine" and it's accompanied by a laundry rack with brain-socks, brain-undies, a brain hoodie as well as suitable washing powders like "Cerebral Soft" and "Panic Oxi". Enjoy!
Imagine that you return from work to find that a thief has broken into your home. The police arrive and ask if they may dust for finger and palm prints. Which would you do? (A) Refuse permission because palm reading is an antiquated pseudoscience or (B) give permission because forensic dermatoglyphics is sometimes useful for identifying culprits. A similar question may be asked about the photographs of the external surface of Albert Einstein’s brain that recently emerged after being lost to science for over half a century. If asked whether details of Einstein’s cerebral cortex should be identified and interpreted from the photographs, which would you answer? (A) No, because to conduct such a study would engage in the 19th century pseudoscience of phrenology or (B) Yes, because the investigation could produce interesting observations about the cerebral cortex of one of the world’s greatest geniuses and, in light of recent functional neuroimaging studies, might also suggest potentially testable hypotheses regarding Einstein’s brain and those of normal individuals. Lest you think this is a straw man (or Aunt Sally) exercise, more than one pundit has recently invoked the phrenology argument against studying Einstein’s brain. For example, one blogger opines, “I hope no one cares about Einstein’s brain. By this I mean his brain anatomy.” The three of us who were privileged to describe the treasure-trove of recently emerged photographs opted for B.
We did so because various data support studying the variation and functional correlates of folds (gyri) on the surface of the human brain and the grooves (sulci) that separate them. For example, David Van Essen hypothesizes that tensions along the connections between cells that course beneath the surface of the brain explains typical patterns of convolutions on its surface. Disruptions in the development of these connections in humans may result in abnormal convolutions that are associated with neurological problems such as autism and schizophrenia. Representations in sensory and motor regions of the cerebral cortex may change later in life as shown by imaging studies of Braille readers, upper limb amputees, and trained musicians, and sometimes these adaptations are correlated with superficial neuroanatomical features such as an enlargement in the right precentral gyrus (called the Omega Sign because of its shape) associated with movement of the left hand in expert string-players. Indeed, Einstein’s right hemisphere has an Omega Sign (labeled K in the following photograph, for knob), which is consistent with the fact that he was a right-handed string-player who took violin lessons between the ages of 6 and 14 years. The aforementioned blogger supports his opposition to studying Einstein’s cerebral cortex with the observation that “assuming causality with correlation” is “a cardinal sin of science”. However, this old saw does not mean that correlated features are necessarily causally unrelated. The functional imaging literature on the cerebral cortices of musicians and controls suggests that Einstein’s Omega Sign and his history as a violinist were probably not an unrelated coincidence.
Superior view of Einstein’s brain, with frontal lobes at the top. The shaded convolution labeled K is the Omega Sign (or knob), which is associated with enlargement of primary motor cortex for the left hand in right-handed experienced string-players.
The investigation of previously unpublished photographs of Einstein’s brain reveals numerous unusual cortical features which suggest hypotheses that others may wish to explore in the histological slides of Einstein’s brain that surfaced along with the photographs. For example, Einstein’s brain has an unusually long midfrontal sulcus that divides the middle frontal region into two distinct gyri (labeled 2 & 3 in the following image), which causes his right frontal lobe to have four rather than the typical three gyri. An extra frontal gyrus is rare, but not unheard of. Einstein’s frontal lobe morphology is interesting because the human frontal polar region expanded differentially during hominin evolution, is involved in higher cognitive functions (including thought experiments), and is associated with complex wiring underneath its surface. These data suggest that the connectivity associated with Einstein’s prefrontal cortex may have been relatively complex, which could potentially be explored by investigating histological slides that were prepared from his brain after it was dissected.
Tracing from photograph of the right side of Einstein’s brain taken with the front of the brain rotated toward viewer. Unusual sulcal patterns are indicated in red; rare gyri are highlighted in yellow.
The microstructural organization in the parts of the cerebral cortex that are involved heavily in speech (Broca’s area and its homologue) were shown to be unique in their patterns of connectivity and lateralization in the genius Emil Krebs, who spoke more than 60 languages. That study, however, did not include information about the gross external neuroanatomy in the relevant regions. Functional neuroimaging technology is making it possible to explore the functional relationships between variations in external cortical morphology, subsurface microstructure including neuronal connectivity, and cognitive abilities. In other words, scientists should now be able to analyze form and function cohesively from the external surface of the cerebral cortex into the depths of the brain. Pseudoscience this is not.
Brain provides researchers and clinicians with the finest original contributions in neurology. Leading studies in neurological science are balanced with practical clinical articles. Its citation rating is one of the highest for neurology journals, and it consistently publishes papers that become classics in the field.
Subscribe to the OUPblog via email or RSS. Subscribe to only health and medicine articles on the OUPblog via email or RSS. Image credits: Both images are authors’ own. Do not reproduce without prior permission from the authors.
