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Viewing: Blog Posts Tagged with: neurology, Most Recent at Top [Help]
Results 1 - 15 of 15
1. Randomized controlled trials: Read the “fine print”!

Most randomized controlled trials (RCTs) can appear deceptively simple. Study subjects are randomized to experimental therapy or placebo—simple as that. However, this apparent simplicity can mask how important subtle aspects of study design—from patient selection to selected outcomes to trial execution—can sometimes dramatically affect conclusions.

The post Randomized controlled trials: Read the “fine print”! appeared first on OUPblog.

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2. Can neuroscience explain consciousness?

Long excluded from serious consideration within psychology and the neurosciences, consciousness is back in business. A new journal Neuroscience of Consciousness will catalyse this new understanding by publishing the best new research, review, and opinion on how our "inner universe" comes to be.

The post Can neuroscience explain consciousness? appeared first on OUPblog.

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3. Q & A: Neurology’s past, present, and future

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…

The post Q & A: Neurology’s past, present, and future appeared first on OUPblog.

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4. The music next door

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.

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5. Predicting future cognition in preterm children with MRI

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.

The post Predicting future cognition in preterm children with MRI appeared first on OUPblog.

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6. Scrutinizing the script of the medieval ‘Tremulous Hand of Worcester’

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 post Scrutinizing the script of the medieval ‘Tremulous Hand of Worcester’ appeared first on OUPblog.

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7. What stays when everything goes

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.

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8. 50 shades of touch

Disgusting or delighting, exciting or boring, sensual or expected, no matter what you think about it, 50 Shades of Grey is certainly not a movie that passes by without leaving a mark on your skin. Based on E.L. James’ novel (honestly, somehow even more breathtaking than the movie), it tells the story of the complicated relationship between the dominant multi-millionaire Christian Grey, and the newly graduated, inexperienced, and shy, Ana Steele.

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9. Purple Day: a day for thinking about people with epilepsy

Purple Day started with the curiosity and of a girl in eastern Canada, in the province of Nova Scotia, who had epilepsy. It soon became a world-wide success. Purple Day is now an international initiative and effort dedicated to increasing awareness about epilepsy around the globe. Why is it so important to create awareness around people with epilepsy?

The post Purple Day: a day for thinking about people with epilepsy appeared first on OUPblog.

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10. Oxytocin and emotion recognition

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.

MRI of brain by bykst. Public Domain via Pixabay.
MRI of brain by bykst. Public Domain via Pixabay.

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.

Heading image: Oxytocin-neurophysin by Edgar181. Public domain via Wikimedia Commons.

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11. Neurology and psychiatry in Babylon

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.

babylon large
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.

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12. 10 things you didn’t know about Parkinson’s Disease

By Charley James


Did you know that 7-13 April is Parkinson’s Awareness Week 2014? To mark the occasion, here are 10 facts you might not have known about Parkinson’s Disease. Go on, improve your awareness!

1.     Parkinson’s Disease is named after British surgeon James Parkinson, who in 1817 wrote An Essay on the Shaking Palsy. Whilst Parkinson was the first to observe and describe the symptoms in a number of patients, it was actually Jean-Martin Charcot, a French neurologist, who would later coin the name ‘Parkinson’s Disease’.

2.     There is not yet a cure for Parkinson’s Disease, but there are very effective – almost miraculous – treatments for the symptoms. Of all the neurological disorders, Parkinson’s is one of the most treatable.

3.     Symptoms are often on only one side of the body, or are asymmetric; this asymmetry persists throughout life.

4.     Communication may be hindered by a softness of voice, decreased articulation, monotone speech, loss of normal inflection, and a decline in facial animation and expression.

5.     Progression of Parkinson’s disease varies from person to person; it may be slow and in some cases may never lead to significant impairment.

6.     There is no single laboratory test a doctor can order to confirm whether a person has Parkinson’s disease. There are, however, four “Cardinal Symptoms”, the combination of any two being enough for diagnosis:

(a) Resting tremor
(b) Bradykinesia (slowness of movement)
(c) Rigidity
(d) Postural Instability

7.     While it is recognised that depression, apathy, and anxiety can be frequent “partners” of Parkinson’s, it is not uncommon for people to find inspiration and new meaning in their lives after their diagnosis.

508px-Neus18.     Physicians may use the Hoehn and Yahr scale to report the degree of disease progression, and the Unified Parkinson’s Disease Rating Scale to describe the severity of the symptoms and signs.

9.     Exposure to paraquat, a pesticide, triples a person’s risk of getting Parkinson’s Disease.

10.     Loss of the sense of smell may be one of the earliest symptoms, sometimes preceding the onset of the disease by many years.

Charley James works in marketing for Oxford University Press. Her father’s experience of Parkinson’s Disease motivated her to write about the condition in support of Parkinson’s Awareness Week 2014. She wrote this blog with the help of Navigating Life with Parkinson’s Disease, The Parkinson’s Disease Treatment Book, and Parkinson’s Disease: Improving Patient Care.

Parkinson’s UK is the Parkinson’s Disease research and support charity. They bring people with Parkinson’s, their carers and families together via their network of local groups, their website and free confidential helpline. Specialist nurses, supporters and staff provide information and training on every aspect of Parkinson’s.

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Image credits: (1) James Parkinson’s 1817 work ‘An Essay on the Shaking Palsy’. Public domain via Wikimedia Commons; (2) Nose. Author information missing. CC-BY-SA-2.0 via Wikimedia Commons.

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13. Examining photographs of Einstein’s brain is not phrenology!

By Dean Falk, Fred Lepore, and Adrianne Noe


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.

Dr Dean Falk is the Hale G. Smith Professor of Anthropology at Florida State University and a Senior Scholar at the School for Advanced Research in Santa Fe, New Mexico. Dr Fred Lepore is Professor of Neurology and Ophthalmology at Robert Wood Johnson Medical School in Piscataway, New Jersey. Dr Adrianne Noe is Director of the National Museum of Health and Medicine in Silver Spring, Maryland. You can read their paper, ‘The cerebral cortex of Albert Einstein: a description and preliminary analysis of unpublished photographs’ in full and for free. It appears in the journal Brain.

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 credits: Both images are authors’ own. Do not reproduce without prior permission from the authors.

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14. David Marsden: The Father of Movement Disorders

The final monumental work of the late Professor David Marsden – Marsden’s Book of Movement Disorders – is due for publication this month, almost thirty years on from when the project was initially conceived. In homage to the ‘father of movement disorders’, his friend and colleague, Ivan Donaldson, has written a personal reflection on great contribution and influence David had on the field of movement disorders.

By Ivan Donaldson


When, at the tender age of 34 years, Christopher David Marsden was appointed as inaugural Professor of Neurology at Kings College Hospital and the Institute of Psychiatry in London, the now well-established neurological subspecialty of movement disorders did not exist. I first met him two years after he took up this chair and was so seduced by his enthusiasm, depth of knowledge, and friendly manner, that I went to work with him. He had already developed two research laboratories, one devoted to investigating the physiological mechanisms underlying posture, balance, and movement in health and disease; and the other to elucidating the underlying brain biochemistry. At the same time he was running a very busy neurology clinic.

Prior to then, knowledge of the diseases, which fascinated him so much, was to a large extent descriptive. David sought to find their causes, the mechanisms by which they had their ill effects, and effective therapies for them. In addition, he strongly advocated that a number of muscular spasms, which had previously been thought to have a psychological basis, were actually organic. He recognised that several apparently unrelated conditions, such as writers’ cramp, facial grimacing, and spasmodic movements of the neck, were really different focal expressions of the same underlying disorder, namely dystonia. Subsequent scientific discoveries, including genetics, proved him to be correct. He was instrumental in persuading the UK Parkinson’s Disease Society to establish a ‘brain bank’, which has led to many important scientific studies that have greatly increased our knowledge of the condition.

The importance of movement disorders was also given a boost when in 1987 David was appointed to the prestigious chair of Clinical Neurology at the Institute of Neurology and National Hospital for Neurology and Neurosurgery at Queen’s Square, London. There he was instrumental in establishing a new research unit into human movement and balance, directly funded by the Medical Research Council, and he helped set up functional neuro-imaging. He travelled widely and became a visiting professor at over 40 institutions worldwide.

Source: Journal of Neurology, Neurosurgery & Psychiatry

In 1986 he and Stanley Fahn had established the International Movement Disorder Society and the movement disorder journal, of which they became the editors. This journal broke new ground by using video — the perfect medium in which to demonstrate disordered movement. The field of movement disorders, consisting of conditions in which disturbance of movement does not result from weakness, was born. Although there were other pioneers, the depth, breadth, and quality of David’s original contributions and his pivotal role in promot

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15. Elementary Brain Dysfunction in Schizophrenia

Robert Freedman, MD, is Professor and Chair of Psychiatry at the University of Colorado and the Editor-in-Chief of the American Journal of Psychiatry.  His new book, The Madness Within Us: Schizophrenia as a Neuronal Process, is a discussion of these two aspects of the illness.  Freedman outlines the emerging understanding of schizophrenia as a neurobiological illness.  In the excerpt below we learn about the basic brain dysfunction in schizophrenia.

The earliest observers of how people with schizophrenia seemed to react to their environment noted a peculiarity in the ability of persons with schizophrenia to appear unaware of the environment and yet overly responsive to it.  Eugen Bleuler first developed the concept of an attentional dysfunction in schizophrenia in his essay on attention in schizophrenia…

Rachel not only hears voices but she hears noises as well, noises that her family members also hear but have learned to ignore.  She hears screaming all the time, and she sometimes wanders the neighborhood to find out who is screaming.  When my colleague Merilyn Waldo suggested to her that it might be traffic, she told us that her mother had said the same thing.  There is a busy corner near the front of her house, and there are always cars stopping and then accelerating away.  My wife and I experienced the very same perceptual abnormality ourselves on the night we brought our first son home from the hospital.  We put the baby to bed and tried to sleep ourselves, but I heard screaming.  I checked on the baby, and he was asleep.  Then my wife heard it too.  We checked again.  Then we listened at the door.  The screaming must be coming from another apartment, and we wondered if we should call the police to alert them to child abuse, but we knew that no other couples with babies lived in the building.  Finally, when the traffic on the highway in front of the building stopped at 2 a.m., we understood how two very anxious, hypervigilant new parents can misinterpret the world around them.

For Rachel, the problem is not a single stressful night.  It is a lifelong problem, which she has struggled with since she was a teenager, long before the onset of her illness at 28.  She could never concentrate at school.  The least noise captured her attention.  As she put it, “My mind has to be here, it has to be there, I can’t concentrate on anything.”  Unlike a typical child with attention-deficit disorder (ADD), whose attention is rarely captured, her attention was captured by everything, from the traffic squeaking to the refrigerator cycling on and off, to the neighbor’s ongoing argument next door.  As a result, she could concentrate on very little.

Paul, on the other hand, seems to be aloof in his environment.  When he was first ill and worried about snakes, I wondered if their voices arose out of noises around him in the dormitory.  He acknowledged that the noise of the dormitory was exquisitely painful, but he could not connect it to the snakes.  Now he seems withdrawn.  When I walk out to get him in the waiting room, he seems oblivious to the people around him.  He has constructed a psychological shell around himself, a solution many patients use to shield themselves from their otherwise overwhelming environment.

The most dramatic experience of the phenomenon of seeming to ignore the environment is catatonia, a rarely seen syndrome in schizophrenia today.  The patient gradually stops responding to environmental stimuli and then eventually stops moving altogether.  In the most advanced cases, the person suddenly freezes.  If he is moved passively, then he may retain the position into which he is moved, a symptom termed “waxy flexibility.”  These patients can often be drawn back to awa

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