Archive for the ‘Brain studies’ Category

the brain is so very awesome…

In Brain imaging, Brain studies, Neurogenesis, Neuropsychology, Neuroscience on Thursday, 17 April 2014 at 15:39


Phillip Seymour Hoffman did not have choice or free will and neither do you.

In ADHD, Anxiety, Brain imaging, Brain studies, Child/Adolescent Psychology, General Psychology, Medicine, Mood Disorders, Neuropsychology, Neuroscience, Psychiatry on Tuesday, 11 March 2014 at 12:37

one of the best things about this subject that i’ve read in a long time.  give it a read. it makes you think.

Phillip Seymour Hoffman did not have choice or free will and neither do you..

take your vitamins!

In Brain studies on Monday, 26 November 2012 at 16:37


things that dumb you down…

In Brain studies, Neuroscience on Saturday, 24 November 2012 at 06:21


and another one:


computerized neuropsychological assessment…

In Brain imaging, Brain studies, Neuropsychology, Neuroscience on Friday, 23 November 2012 at 16:45

this has to be coming soon.  and i will be thrilled.  can you imagine how many opportunities for further research there will be???  yay!



Brain Scans Predict Reading Skills

In Brain imaging, Brain studies, Education on Wednesday, 21 November 2012 at 13:42

Brain Scans Predict Reading Skills

New research shows that the growth of long-range connections between brain regions predicts how well a child will learn to read.

By Dan Cossins | October 9, 2012

Our ability to read depends on the communication between distant areas of the brain, such as those involved in vision, hearing, and language. Research published this week (October 8) in the Proceedings of the National Academy of Sciences reveals that the growth pattern of connections between these areas can predict how a child’s reading skills will develop—a finding that could lead to teaching strategies most appropriate for kids at different stages of development.

Neuroscientists at Stanford University in California studied the reading skills of 55 children, aged 7 to 15, over a 3-year period. They also took MRI scans of the children’s brains at least 3 times during that period to visualize the growth of two major white-matter tracts—bundles of nerve fibers that connect brain regions. They found that differences in the growth of these tracts predicted variations in reading ability.

White-matter growth is governed by two processes: pruning, in which extraneous nerve fibers and neuronal connections are eliminated, and myelination, in which nerve fibers in the tracts are surrounded by fatty tissue that increases the speed with which they transmit electrical signals. Both are in part determined by experience, so they happen at different times in different people.

“We think the relative timing of pruning and myelination differs between strong and weak readers,” Stanford’s Jason Yeatman, one of the study authors, told Nature. “In good readers, both processes are unfolding together at an even rate. In poor readers, the two processes are out of sync. You have rapid, early growth, and the tracts develop before [the children] even start learning to read.”

Yeatman added that in future it might be possible to see when pruning is taking place, a period in which children may find it easier to learn to read, and tailor lessons accordingly.

Retrieved from: http://www.the-scientist.com/?articles.view/articleNo/32776/title/Brain-Scans-Predict-Reading-Skills/

Development of White Matter and Reading Skills

Jason D. YeatmanRobert F. DoughertyMichal Ben-Shacharand Brian A. Wandell

White matter tissue properties are highly correlated with reading proficiency; we would like to have a model that relates the dynamics of an individual’s white matter development to their acquisition of skilled reading. The development of cerebral white matter involves multiple biological processes, and the balance between these processes differs between individuals. Cross-sectional measures of white matter mask the interplay between these processes and their connection to an individual’s cognitive development. Hence, we performed a longitudinal study to measure white-matter development (diffusion-weighted imaging) and reading development (behavioral testing) in individual children (age 7–15 y). The pattern of white-matter development differed significantly among children. In the left arcuate and left inferior longitudinal fasciculus, children with above-average reading skills initially had low fractional anisotropy (FA) that increased over the 3-y period, whereas children with below-average reading skills had higher initial FA that declined over time. We describe a dual-process model of white matter development comprising biological processes with opposing effects on FA, such as axonal myelination and pruning, to explain the pattern of results.

This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1206792109/-/DCSupplemental.

Retrieved from: http://www.pnas.org/content/early/2012/10/04/1206792109.abstract


The Mind of Oliver Sacks

In Brain studies, Neuropsychology, Neuroscience on Monday, 19 November 2012 at 12:41

The Mind of Oliver Sacks.

Optogenetics illuminates pathways of motivation through brain

In Brain imaging, Brain studies, Neuroscience on Monday, 19 November 2012 at 12:40

Optogenetics illuminates pathways of motivation through brain.

Mending the Brain Through Music

In Brain imaging, Brain studies, Neuropsychology, Neuroscience on Wednesday, 7 November 2012 at 07:45

Mending the Brain Through Music

Bret S. Stetka, MD, Concetta M. Tomaino, MA, DA, LCAT

Editor’s Note: 
From a Darwinian perspective, music is a mystery. It’s unclearwhether the human ability to appreciate a catchy melody conferred some specific evolutionary advantage or was a by-product of more general adaptations involving sound and pattern processing. But what is known is that evidence of music has been found in every documented human culture[1,2] — and that nearly all of us have at least some innate capacity to recognize and process song. The human brain houses a staggeringly complex neuronal network that can integrate rhythm, pitch, and melody into something far greater with, it turns out, significant therapeutic potential.

Research and clinical experience increasingly support music as medicine. Accessing and manipulating our musical minds can benefit numerous psychiatric, developmental, and neurologic conditions, often more effectively than traditional therapies. Dr. Concetta M. Tomaino, along with noted neurologist and author Dr. Oliver Sacks, cofounded the Institute for Music and Neurologic Function to study the effects of music on the brain and neurologic illness in particular. In light of increasing interest in music therapy and accumulating data supporting the approach, Medscape spoke with Dr. Tomaino about how the brain perceives music and the role of the Beatles in treating neurologic disease.


Medscape: Thanks for speaking with us today, Dr. Tomaino. The Institute for Music and Neurologic Function has been integral to our understanding of how the brain processes music, and how music can be used as therapy in certain neurologic conditions. Can you give us some background on the Institute and discuss your role and work there?

Dr. Tomaino: The Institute was incorporated in 1995 to bridge the worlds of neuroscience and clinical music therapy. It grew out of the work of both myself and Dr. Oliver Sacks, with support from CenterLight Health System (formerly Beth Abraham Family of Health Services).

I’m a music therapist by training, with a master’s degree and doctorate in music therapy but also with a strong neuroscience background. Back in the 1970s, I was working in a nursing home and was amazed at how people with end-stage dementia, with little to no cognitive ability or awareness of their surroundings, could still process familiar music. I started wondering whether music could be used as a specific therapy to arouse cognition in patients with severe dementia.

When I came to Beth Abraham in 1980, Oliver Sacks was the attending neurologist and had been asking similar questions about the postencephalitic patients he wrote about in Awakenings, wondering how music and arts affected people who’d lost brain function through disease or trauma. And so we sought each other out and became good friends.

We worked together, him using music to test patients and me clinically applying music to help people recover or improve function. Both of us realized that there was something important going on here, and in the mid-1980s, we began seeking out scientists who could help us study the effects of music on brain function. In 1985, Oliver’s book The Man Who Mistook His Wife for a Hat became popular, and I was president of the American Association for Music Therapy. Our administration took notice of the attention both Oliver and I were receiving from the media and asked whether there was something they could help us do to expand upon our ideas. And so the Institute was formed as a center dedicated to studying music and brain and bridging the clinical and neuroscience communities.

Medscape: Can you speak about the origins of music therapy and how it’s been used over the years?

Dr. Tomaino: The therapeutic aspects of music have been noted in societies for thousands of years; however, interest really grew around the time of World War II, in part because the Works Progress Administration (WPA) program started bringing musicians into veterans hospitals. Doctors and nurses observed that people who seemed to be totally unresponsive would come to life when music was played. The hospital staff wanted to bring more musicians in, but training was needed to prepare them to better understand the conditions and needs of the patients. The approach gained attention, and eventually music therapy came together as a profession in the late 1940s. We now have a certification board, and the American Association for Music Therapy oversees academic and clinical training approaches.

The scope of music therapy has become very broad. It’s been studied and shown effective in psychiatric illness; developmental issues; and medical conditions, including pre- and postoperative settings. However, Dr. Sacks’ and my interests and contributions to the field have been in the area of neurologic function.

Medscape: In which neurologic conditions has music therapy shown the greatest effectiveness?

Dr. Tomaino: There are so many, but one of the most recognized areas is motor initiation in patients with neuromuscular and movement disorders, such as Parkinson disease (PD). Patients with PD often have a slowness of movement and a shuffling gait. Music, specifically highly rhythmic music, has been shown — and there’s quite a bit of supporting data here — to help them in training and coordinating their movements and gait. Music also enhances the length of their stride and improves balance.

Later in the course of PD, cognitive and short-term memory decline are common; in this case, music has been shown to be an effective mnemonic tool, a memory enhancer for remembering basic information — phone numbers, people, addresses, things like that (I’ll get to other forms of dementia in a second). My work and that of some colleagues has also shown that singing and using music to enhance voice and communication is also beneficial for people with PD.

Medscape: Is music therapy used preventatively or symptomatically to address the cognitive component of PD?

Dr. Tomaino: Ideally, it’s started early to help prevent memory decline and create new associative memories early in the disease — linking acquaintances, places, and events, for example, in order to prevent or slow future memory problems and enhance recall. Recent research is really enhancing our knowledge of neuroplasticity. Forming these associations — these new neuronal connections — appears to be neuroprotective.

Recalling Words and Memories

Medscape: Another area researched at the Institute is using music therapy to help patients with nonfluent aphasias recover speech — patients who comprehend language and know what they want to say, but just can’t find the words. How successful has this approach been?

Dr. Tomaino: These are patients who have had damage, such as a stroke, to the Broca region of the brain, in the left frontal lobe. Some do have mild cognitive impairment, but mostly they fully understand what’s being said to them — at least, that’s the case in the patients we work with.

We apply several techniques depending on the patient’s residual skills: for example, can they sing a simple song and tap their finger along with the rhythm. We cue them to sing along with familiar lyrics from memory and help prompt word retrieval by leaving pauses within the lyrics — you leave out a few lyrics in a familiar Beatles song and have the patient try to find the words without losing the beat. This helps a great deal. As the person improves, we move toward a more traditional form of melodic intonation therapy (MIT), focusing on the tone and rhythm or normal speech phrases rather than singing lyrics to songs.

Traditional MIT, developed by a team at the Boston Veterans Affairs Hospital in 1973, is being studying by such neuroscientists as Gottfried Schlaug at Harvard Medical School. A simple, 2-tone sequence — a high and a low pitch — is used to pattern the inflection of speech. It has 4 levels, beginning with humming and tapping short phrases and gradually moving toward a Sprechstimme, or a more normal rhythmic speech with little melodic change.

Patients are asked to repeat single words with the beat and tones, gradually increasing to more complex phrases, such as “Good morning, how are you today?” [Editor’s Note: Imagine each syllable alternating between 2 tones.] The repetition overlaid on the music helps reinforce the patterns of normal speech and helps patients recover words and fluency. Neuroimaging studies indicate compensatory changes in the right frontal lobe areas.

Music therapy is also used to as a psychotherapeutic application in mental illness and can help alleviate stress and anxiety. This has an impact on neurologic function as well; for example, multiple sclerosis symptoms can be exacerbated by stress. Preliminary research shows that music can be an excellent tool for self-relaxation and stress management in these patients. And one of the most fascinating areas in which music is used is dementia and amnesia.

Medscape: Dr. Sacks has written about a number of patients who, despite exhibiting severe amnesia, can remember song lyrics perfectly. What does this say about the neuronal pathways involved in musical memory vs say, declarative memory, our ability to consciously recall information? And what is the therapeutic potential here?

Dr. Tomaino: They are most likely primarily processed by separate brain systems. So a person with dementia or amnesia may not consciously recognize a familiar song, but something in their subconscious knows it’s familiar. There are feelings, emotions, or moments of history in there somewhere. And if they listen to those songs, we’re realizing that sometimes these feelings or the emotions are so strong that they trigger fleeting glimpses of pieces of memory. If we can work with those fleeting moments and build upon them, maybe stronger connections can be made and more memories experienced.

Medscape: Do the memories and recollections last once the music has stopped?

Dr. Tomaino: It depends on the patient. I’ve had a few patients with short-term memory problems in whom using music, and progressing from older memories forward, have then been able to recall recent events. In people with Alzheimer-type dementia, who have seemingly lost the ability to recall past events, music with strong emotional ties and meaning can lead to enduring remembrances and recall.

Medscape: Several case reports — including a recent documentary clip that went viral on YouTube — have demonstrated how effective music can be in helping patients with dementia open up and engage with their environment. How much of this is an actual heightened sense of awareness vs reflexive neurologic activity in response to the music?

Dr. Tomaino: It’s both, depending on the individual. Initially, it’s more reflexive and reactive. But if the musical interventions are provided on a regular basis and for longer periods — 15 minutes, 20 minutes, an hour — we find that their short-term memory and attention improve over time.

We did some studies years ago that were funded by the New York State Department of Health and engaged people with mid- to late-stage Alzheimer disease in music therapy sessions for 1 hour, 3 times a week for 10 months. We found that over time, their awareness of other people improved significantly. Some even recognized those people by name, increased their group interactions, and demonstrated improvement in memory and awareness — they once again knew when it was lunch time.

So yes, in patients with dementia, things that you think are lost forever are retrievable over time with this kind of stimulation. I believe there is now scientific evidence showing this — that when somebody’s engaged in an activity that’s meaningful, it involves regions of their frontal cortex that stimulate short term memory and attention. Then if you can hold somebody’s attention with something that’s meaningful for a long period, the very mechanisms that are breaking down in somebody with dementia are actually being enhanced and activated.

Medscape: Interesting. So, music-based therapies work via a variety of musical qualities, with aspects like rhythm, melody, and emotional familiarity having much different effects, respectively?

Dr. Tomaino: Right. There are totally different mechanisms at work here. The emotional and personal connection is important in dementia, whereas in PD, we’re looking at the person’s ability to perceive and feel the beat. In patients with PD, rhythm is so important and unique to the patient. Instead of just picking a beat and using a metronome, we experiment with different rhythms and rhythmic styles to see what the person responds best to. They have to feel the pulse in order for that pulse to drive their motor function. So when we talk about “music therapy,” we’re talking about components of music, such as rhythm, tone, melody, harmony, song — all of these qualities can be used together or individually to affect the patients with certain conditions.

Who Benefits Most?

Medscape: I’m curious about how an individual’s degree of engagement with music before therapy affects the outcome. Does a person’s musical skill or appreciation come into play? Does a classical violinist benefit most from music therapy? A music critic? A Deadhead?

Dr. Tomaino: Anybody can benefit from music therapy, but their background in music can help or hurt them. Most humans have an affinity for sound and can process it in highly complex ways. However, in certain diseases people may lose this ability, and in fact sound may get so distorted that they have a negative response to it, even if they’d loved music before their injury. This is especially evident in people with damage to the right temporal lobe: These patients often lose their perception of pitch. In fact, I think in Musicophilia, Dr. Sacks writes about a classically trained, professional musician who, after localized brain damage, is a quarter tone off in his perception of pitch.

Medscape: That’s right. And he ended up just tuning his piano up a quarter step!

Dr. Tomaino: Yes! So that’s where the music therapist really has to look at what a person is able to perceive. This patient’s perceptive problem probably wouldn’t have bothered someone who couldn’t tell the difference. With a professional musician, you can imagine that their neural connections to sound and perception are greatly enhanced.

For example, we treated a percussionist who’d had a stroke. The traditional therapy would be to work with the nonaffected side to encourage the intact side of the brain to take over function. For example, a right-handed person would be taught to perform tasks with the left hand. But because percussionists and musicians, by nature of their craft, presumably have stronger bilateral neural representation, we convinced the physical therapist to try working with the affected side of the brain and body. The person was able to regain function. By encouraging the patient to use the affected limb, we try to restore as much function as possible to this limb rather than compensate with the other side.

Medscape: We know that certain areas of the brain are highly dedicated to certain aspects of perception and information processing. The left frontal and temporal lobes are highly involved in speech recognition and production. The occipital cortex processes visual information. But music and sound perception and processing seems to involve numerous regions all over the brain. Can you speak about how the brain perceives and processes music, and how this lends itself to therapeutic applications?

Dr. Tomaino: There are some areas of the brain that are known to be involved in specific aspects of sound processing, mainly through looking at people who have lost certain abilities through certain brain lesions. As I mentioned earlier, patients with a lesion in the right temporal lobe often experience loss of pitch perception. We know that singing is dominant in the right temporal lobe; however, syntax of both speech and music is left dominant. And there are areas on both sides of the brain that inform and coordinate with each other when it comes to music, because music isn’t just one specific skill. That said, music processing is incredibly complex, and as far as I know, a complete map of the areas responsible for music and sound processing doesn’t yet exist.

This complexity is probably why music is so beneficial as a therapeutic tool. It’s processed bilaterally: in the cortex and subcortically, where it stimulates evolutionarily primitive areas of brain function, such as the cerebellum and the basal ganglia. So when a person does have a deficit, there is still some part of the brain functioning properly that is involved in music processing and can be stimulated through sound.

Another interesting aspect here is that in patients with damage to higher cortical regions — those with frontal temporal dementia (FTD) — their appreciation for music may change. Oliver wrote about a classically trained musician who didn’t care for any other types of music; after developing FTD, he starting liking rock and roll.

Functional imaging studies, such as those by Dr. Schlaug that I mentioned earlier, are really helping us understand neural plasticity as well as which areas of the brain are involved in what. You can first isolate the components of music, studying where pitch is processed, and beat, and melody. Then you can put them all together, and it becomes very complex. With functional imaging, it became possible to literally watch the brain work in real time while it listens to music.

Acting, Painting, Listening

Medscape: In reading Musicophilia, one of the things that really fascinated me was the idea that our memory for music is far more high-fidelity than it is for nonmusical creative sensory stimuli. Our recollections of visual art and narrative are often distorted or approximated; however, musical memories and dreams have been proven highly accurate in pitch, melody, mood, and rhythm. How does this distinguish music therapy from other forms of creative arts-based interventions, such as art and drama therapy?

Dr. Tomaino: I should admit that I used to be biased when I sat on the board for the creative arts therapy coalition, because I knew that music — especially the components of music, such as rhythm — could directly affect brain function rather than requiring the interpretation by the arts therapist. I think the big difference is the other arts therapies tend to work psychotherapeutically. And in fact, many music therapists work psychotherapeutically, which can be very effective.

But myself, Dr. Sacks, and a few of our colleagues became interested in the neurologic underpinnings of music and how sound itself could arouse and stimulate basic brain functioning. Whereas art and drama tend toward the emotions and personal associations — a sense of self and ego, and all those areas of psychotherapy — the specific components of music can actually affect brain function in a very measurable, functional way.

Because of this, music therapy is one of the therapies still available to people with devastating diseases, such as Alzheimer disease and neuromuscular conditions, in whom the other creative arts therapies would no longer have a therapeutic benefit. Music can bypass upper-brain processes and higher cognition, as well as stimulate some of the fundamental lower and midbrain areas.

I should say that although we don’t treat psychiatric patients at our facility, so often neurologic and psychiatric illnesses — as well as medical illnesses — are intertwined. So the psychotherapeutic component of our music-based interventions are very important to our patients too.

Medscape: How widely accessible is music therapy, and how many therapists are there in the United States?

Dr. Tomaino: There are close to 6000 music therapists in the United States. It’s not that many, when you think about how many people could benefit from it.

Medscape: Short of having access to a music therapy resource for referral, how can clinicians incorporate music therapy techniques into their practice?

Dr. Tomaino: It’s really great that something so effective is available to everyone. Although it is always important to seek out a professional music therapist first, there are therapeutic applications of music that others can make use of: for example, using personalized music to help someone with Alzheimer disease feel connected, or using rhythmic cues to help increase stride and gait in someone with PD.

And we haven’t even touched on children. Professionals who are working with children with autism-spectrum disorders should really seek out music therapy because it’s been very, very successful with this population. It can be so important in developing early language and motor skills, as well as self-identity and social skills.

I could also see a psychiatrist or social worker who’s having a hard time having a patient open up asking them to bring their favorite piece of music in; it could be an effective entry point into forming a relationship. Speech therapists who have a patient with aphasia can ask the persons to sing.

Likewise, a physical or occupational therapist can use rhythmic cues to help with motor problems. It’s amazing how little rhythm is used in rehabilitation especially in helping people with PD move more effectively. Just remember that each patient responds to different musical cues and rhythms, which requires time to navigate. I’ve talked to a few neurologists who will put on a Sousa march and expect a patient to immediately get up and walk!

Editor’s Note: The American Music Therapy Association’s Website maintains a list of music therapists in the United States, many of whom provide Skype services for remote patients.

Retrieved from: http://www.medscape.com/viewarticle/773401?src=mp

mental weight lifting…

In Brain imaging, Brain studies, Fitness/Health on Monday, 5 November 2012 at 13:45

Mental strain helps maintain a healthy brain

Posted By Daniel Pendick On November 5, 2012

When it comes to keeping healthy and fit, living a mentally active life is as important as regular physical exercise. Just as your muscles grow stronger with use, mental exercise keeps your mental skills and memory in tone.

Are certain kinds of “brain work” more effective than others? I put that question to Dr. Anne Fabiny, chief of geriatrics at Cambridge Health Alliance and an assistant professor of medicine at Harvard Medical School.

Any brain exercise is better than being a total mental couch potato. But the activities with the most impact are those that require you to work beyond what is easy and comfortable. Playing endless rounds of solitaire and watching the latest documentary marathon on the History Channel may not be enough. “If it’s too easy,” Dr. Fabiny says, “it’s not helping you.”

Four brain-health strategies

As I write in the November 2012 Harvard Men’s Health WatchDr. Fabiny recommends four complementary strategies for keeping your brain healthy.

Be a lifelong learner: You spend the first half of your life building dense networks of connections between brain cells. Scientists call that “cognitive reserve.” Continuing to learn new things builds and maintains these connections.

Strain your brain: Think of all mental activities as a continuum. Watching a TV documentary would be on the passive, mildly challenging end of the spectrum, while learning how to converse in a new language would be on the active, very challenging end. When it comes to cognitive reserve, mentally challenging tasks have the biggest impact. “Be open to new experiences that cause you to see the world and do things differently,” Dr. Fabiny says.

Get uncomfortable: One stereotype of aging is that young people are bold explorers but older people are timid homebodies who “know what they like.” Stereotype though it may be, it is easy to get in a rut. Getting out of your comfort zone from time to time challenges your mental skills. An example of this would be traveling to a city that you haven’t been to before, which forces you to navigate unfamiliar surroundings.

Be social: Social isolation, aging researchers have discovered, puts people at risk of losing some of the brain reserves they have built up over a lifetime. There are many ways to be social. One good way is working as a volunteer in a social setting, which allows you to have contact with a variety of people and puts you in new situations.

Don’t forget your body

Healthy brain aging should involve the rest of the body, too. There is abundant evidence that physical activity that gets your pulse thumping helps the mind as well as the heart.

And if that exercise involves mental skill and balance, like racquet sports or a walking round of golf, it’s even better. As you vanquish your opponents on the court or green, you might also notice an improved ability to keep score in your head.

Related Information: Improving Memory: Understanding age-related memory loss

Retrieved from: http://www.health.harvard.edu/blog/mental-strain-helps-maintain-a-healthy-brain-201211055495?utm_source=twitter&utm_medium=socialmedia&utm_campaign=110512-pjs1_tw


NIMH · In-sync Brain Waves Hold Memory of Objects Just Seen

In Brain imaging, Brain studies, Neuroscience, Uncategorized on Monday, 5 November 2012 at 12:47

NIMH · In-sync Brain Waves Hold Memory of Objects Just Seen.

recipe for a younger brain…

In Brain imaging, Brain studies, Fitness/Health on Friday, 2 November 2012 at 07:11

Two Things Needed for a Younger Brain

Henry S. Lodge, M.D.

When I was in medical school, we were taught that you got all your brain cells by the time you were two years old. And by age 30, you start to lose them. Cognitive aging was simply the slow, steady loss of brain cells that occurred as you age. Well, it turns out this was wrong! Scientists around the world have demonstrated that your brain can continue to grow throughout your life — growing new cells, forming new connections, and rewiring existing ones. But this only happens if you use it. An idle brain will wither and decay, which leads to the decline in cognitive function that we once accepted as being part of the normal aging process.

There are two great roads to rejuvenating your brain, and they might surprise you:
 Exercise. MRI studies show marked growth in new brain tissue after three months of regular exercise. This growth is not just in the parts of the brain that control movement. It’s also evident in the areas responsible for memory, decision-making, and judgment.

 Social Connectedness. Your brain grows and thrives in direct proportion with the meaningful social connections you have — meaning your engagement with friends, family, and your community. People who are lonely and depressed actually lose brain tissue overtime and show marked reductions in cognitive function. But people who stay connected with others and give back to their communities improve their chances of staying vibrant and sharp well into their later years.

There’s a wonderful scientific study going on that’s a great example of the power of staying connected. A program called Experience Corps is putting older people in schools as reading tutors for young kids. The kids are doing better, of course. But the tutors are doing better too — a lot better! All markers of health are improving — blood pressure and weight are going down, and mood and energy are going up. What’s also interesting is that a wide range of blood tests that measure inflammation (linked to long-term risks of heart attack, stroke, and common cancers) also show improvement with social connection and emotional involvement!

Are you surprised at the control we can have over our brain health? Could this prompt you to make different lifestyle choices?

Retrieved from: http://forums.webmd.com/3/mens-health-community/forum/818?ecd=soc_tw_110112_am_community_youngerbrain

How Your Eyes Deceive You

In Brain studies, Neuroscience on Thursday, 1 November 2012 at 07:09

How Your Eyes Deceive You

Neuroscience News

Researchers at the University of Sydney have thrown new light on the tricks the brain plays as it struggles to make sense of the visual and other sensory signals it constantly receives.

The research has implications for understanding how the brain interprets the world visually and how the brain itself works.

People rely on their eyes for most tasks – yet the information provided by our visual sensing system is often distorted, unreliable and subject to illusion.

In a just published article in Proceedings of the National Academy of Science, Dr Isabelle Mareschal and Professor Colin Clifford, from the University’s School of Psychology and The Vision Centre, report a series of groundbreaking experiments tracing the origins of the tilt illusion to the cells of the primary visual cortex. This is where the first stage of vision processing takes place before the conscious mind takes over.

“We tend to regard what we see as the real world,” said Dr Mareschal.

“In fact a lot of it is distortion, and it is occurring in the early processing of the brain, before consciousness takes over. Our work shows that the cells of the primary visual cortex create small distortions, which then pass on to the higher levels of the brain, to interpret as best it can.”

A common example of this that is often exploited by artists and designers is known as the tilt illusion where perfectly vertical lines appear tilted because they are placed on an oriented background.

“We wanted to test at what level the illusion occurs in the brain, unconscious or conscious – and also to see if the higher brain is aware of the illusions it is receiving and how it tries to correct for them,” she explains.

“The answer is that the brain seeks more contextual information from the background to try to work out the alignment of the object it is seeing.”

The team subjected volunteers to a complex test in which they indicated the orientation of a vertical line, perceived as constantly tilting from side to side, against a fuzzy background that was also changing.

“These illusions happen very fast, perhaps in milliseconds,” Dr Mareschal says. “And we found that even the higher brain cannot always correct for them, as it doesn’t in fact know they are illusions.”

This is one reason why people’s eyes sometimes mislead them when looking at objects in their visual landscape.

Normally, Dr Mareschal explains, it doesn’t matter all that much – but in the case of a person driving a car fast in traffic, an athlete performing complex acrobatic feats, a pilot landing an aircraft or other high-speed uses of sight, the illusion may be of vital importance by causing them to misinterpret the objects they ‘see’.

The brain uses context, or background, to interpret a host of other visual signals besides the orientation of objects. For example, it uses context to tell colour, motion, texture and contrast. The research will help study how the brain understands these visual cues adding to our overall understanding of brain function.

In this tilt illusion, the lines in the centre of the image appear tilted counterclockwise, but they are actually vertical. Image adapted from University of Sydney image.

The Vision Centre is funded by the Australian Research Council as the ARC Centre of Excellence in Vision Science.

Contact: Verity Leatherdale – The University of Sydney

Source: The University of Sydney press release

Image Source: Neuroscience News image adapted from press release image

Original Research: Abstract for “Dynamics of unconscious contextual effects in orientation processing” by Isabelle Mareschal and Colin W. G. Clifford in Proceedings of the National Academy of Science Published online before print April 23, 2012, doi: 10.1073/pnas.1200952109

Retrieved from: http://neurosciencenews.com/how-your-eyes-deceive-you-neuroscience-optical-illusion/

Area of the Brain that Processes Empathy Identified

In Brain imaging, Brain studies, Neuropsychology, Neuroscience on Sunday, 28 October 2012 at 08:49

Area of the Brain that Processes Empathy Identified

ScienceDaily (Oct. 24, 2012)

An international team led by researchers at Mount Sinai School of Medicine in New York has for the first time shown that one area of the brain, called the anterior insular cortex, is the activity center of human empathy, whereas other areas of the brain are not. The study is published in the September 2012 issue of the journal Brain.

Empathy, the ability to perceive and share another person’s emotional state, has been described by philosophers and psychologists for centuries. In the past decade, however, scientists have used powerful functional MRI imaging to identify several regions in the brain that are associated with empathy for pain. This most recent study, however, firmly establishes that the anterior insular cortex is where the feeling of empathy originates.

“Now that we know the specific brain mechanisms associated with empathy, we can translate these findings into disease categories and learn why these empathic responses are deficient in neuropsychiatric illnesses, such as autism,” said Patrick R. Hof, MD, Regenstreif Professor and Vice-Chair, Department of Neuroscience at Mount Sinai, a co-author of the study. “This will help direct neuropathologic investigations aiming to define the specific abnormalities in identifiable neuronal circuits in these conditions, bringing us one step closer to developing better models and eventually preventive or protective strategies.”

Xiaosi Gu, PhD, who conducted the research in the Department of Psychiatry at Mount Sinai, worked with researchers from the United States and China, to evaluate Chinese patients, at Beijing Tiantan Hospital, who were shown color photographs of people in pain. Three patients had lesions caused by removing brain tumors in the anterior insular cortex; nine patients had lesions in other parts of the brain and 14 patients (the controls) had neurologically intact brains. The research team found that patients with damage restricted to the anterior insular cortex had deficits in explicit and implicit empathetic pain processing.

“In other words, patients with anterior insular lesions had a hard time evaluating the emotional state of people in pain and feeling empathy for them, compared to the controls and the patients with anterior cingulate cortex lesions.” said Dr. Jin Fan, corresponding author of this study and an assistant professor at the Department of Psychiatry at Mount Sinai.

According to Dr. Gu, this study provides the first evidence suggesting that the empathy deficits in patients with brain damage to the anterior insular cortex are surprisingly similar to the empathy deficits found in several psychiatric diseases, including autism spectrum disorders, borderline personality disorder, schizophrenia, and conduct disorders, suggesting potentially common neural deficits in those psychiatric populations.

“Our findings provide strong evidence that empathy is mediated in a specific area of the brain,” said Dr. Gu, who now works at University College London. “The findings have implications for a wide range of neuropsychiatric illnesses, such as autism and some forms of dementia, which are characterized by prominent deficits in higher-level social functioning.”

This study suggests that behavioral and cognitive therapies can be developed to compensate for deficits in the anterior insular cortex and its related functions such as empathy in patients. These findings can also inform future research evaluating the cellular and molecular mechanisms underlying complex social functions in the anterior insular cortex and develop possible pharmacological treatments for patients.

The study was funded by the National Institute of Health, the James S. McDonnell Foundation and a Brain and Behavior Research Foundation NARSAD young investigator award.

Retrieved from: http://www.sciencedaily.com/releases/2012/10/121024175240.htm?utm_source=twitterfeed&utm_medium=linkedin&utm_campaign=Feed%3A+sciencedaily%2Fmind_brain%2Fdisorders_and_syndromes+%28ScienceDaily%3A+Mind+%26+Brain+News+–+Disorders+and+Syndromes%29



Anterior insular cortex is necessary for empathetic pain perception

Xiaosi Gu,  Zhixian Gao, Xingchao Wang, Xun Liu,  Robert T. Knight,  Patrick R. Hof, and

Jin Fan


Empathy refers to the ability to perceive and share another person’s affective state. Much neuroimaging evidence suggests that observing others’ suffering and pain elicits activations of the anterior insular and the anterior cingulate cortices associated with subjective empathetic responses in the observer. However, these observations do not provide causal evidence for the respective roles of anterior insular and anterior cingulate cortices in empathetic pain. Therefore, whether these regions are ‘necessary’ for empathetic pain remains unknown. Herein, we examined the perception of others’ pain in patients with anterior insular cortex or anterior cingulate cortex lesions whose locations matched with the anterior insular cortex or anterior cingulate cortex clusters identified by a meta-analysis on neuroimaging studies of empathetic pain perception. Patients with focal anterior insular cortex lesions displayed decreased discrimination accuracy and prolonged reaction time when processing others’ pain explicitly and lacked a typical interference effect of empathetic pain on the performance of a pain-irrelevant task. In contrast, these deficits were not observed in patients with anterior cingulate cortex lesions. These findings reveal that only discrete anterior insular cortex lesions, but not anterior cingulate cortex lesions, result in deficits in explicit and implicit pain perception, supporting a critical role of anterior insular cortex in empathetic pain processing. Our findings have implications for a wide range of neuropsychiatric illnesses characterized by prominent deficits in higher-level social functioning.

Retrieved from: http://brain.oxfordjournals.org/content/135/9/2726

crazily creative…

In Brain imaging, Brain studies, Neuropsychology, Neuroscience on Sunday, 21 October 2012 at 09:38

Link Between Creativity and Mental Illness Confirmed in Large-Scale Swedish Study

ScienceDaily (Oct. 16, 2012)

People in creative professions are treated more often for mental illness than the general population, there being a particularly salient connection between writing and schizophrenia. This according to researchers at Karolinska Institutet, whose large-scale Swedish registry study is the most comprehensive ever in its field.

Last year, the team showed that artists and scientists were more common amongst families where bipolar disorder and schizophrenia is present, compared to the population at large. They subsequently expanded their study to many more psychiatric diagnoses — such as schizoaffective disorder, depression, anxiety syndrome, alcohol abuse, drug abuse, autism, ADHD, anorexia nervosa and suicide — and to include people in outpatient care rather than exclusively hospital patients.

The present study tracked almost 1.2 million patients and their relatives, identified down to second-cousin level. Since all were matched with healthy controls, the study incorporated much of the Swedish population from the most recent decades. All data was anonymized and cannot be linked to any individuals.

The results confirmed those of their previous study, that certain mental illness — bipolar disorder — is more prevalent in the entire group of people with artistic or scientific professions, such as dancers, researchers, photographers and authors. Authors also specifically were more common among most of the other psychiatric diseases (including schizophrenia, depression, anxiety syndrome and substance abuse) and were almost 50 per cent more likely to commit suicide than the general population.

Further, the researchers observed that creative professions were more common in the relatives of patients with schizophrenia, bipolar disorder, anorexia nervosa and, to some extent, autism. According to Simon Kyaga, Consultant in psychiatry and Doctoral Student at the Department of Medical Epidemiology and Biostatistics, the results give cause to reconsider approaches to mental illness.

“If one takes the view that certain phenomena associated with the patient’s illness are beneficial, it opens the way for a new approach to treatment,” he says. “In that case, the doctor and patient must come to an agreement on what is to be treated, and at what cost. In psychiatry and medicine generally there has been a tradition to see the disease in black-and-white terms and to endeavour to treat the patient by removing everything regarded as morbid.”

Simon Kyaga, Mikael Landén, Marcus Boman, Christina M. Hultman, Niklas Långström, Paul Lichtenstein. Mental illness, suicide and creativity: 40-Year prospective total population studyJournal of Psychiatric Research, 2012; DOI: 10.1016/j.jpsychires.2012.09.010

Retrieved from: http://www.sciencedaily.com/releases/2012/10/121016084934.htm

the brain in love…

In Brain imaging, Brain studies, Well-being on Sunday, 21 October 2012 at 09:30

Love, Sex, Relationships and the Brain

Does neuroscience hold the key to a lifetime of passionate love?

Published on October 18, 2012 by Melanie A. Greenberg, Ph.D. in The Mindful Self-Express

Let me not to the marriage of true minds Admit impediments. Love is not loveWhich alters when it alteration finds, Or bends with the remover to remove:O no! it is an ever-fixed mark That looks on tempests and is never shaken;It is the star to every wandering bark,Whose worth’s unknown, although his height be taken. Shakespeare, Sonnet 116

The qualities of true, romantic love have inspired playwrights, poets, and philosophers throughout the ages. Love is an ideal; an inspiration — a feeling of passion and commitment that adds richness and joy to life. A loving relationship provides a secure base from which to grow, expand and explore the world. Yet, until recently, we did not know for sure whether romantic love could last, or whether it inevitable transformed into companionate love — enduring friendship characterized more by shared interests, commitments and values than passion and excitement. Or, even more disappointing, perhaps love inevitably fades and couples stay together in miserable or passionless relationships because of social convention, convenience, and duty.

Are Kids Relationship Ruiners?

Research suggests that all of these patterns are possible. First, the bad news! Researchers at Bar Ilan University in Israel studied couples with children from pregnancy to 14.5 years after the child’s birth in two overlapping large-scale studies.  Overall, marital satisfaction decreased following the birth of the first child and continued to decline steadily, reaching an all-time low when the kids became teenagers. The more kids, the greater the decline in marital satisfaction. Dissatisfied couples did not inevitably divorce, however. Marital dissatisfaction was not significantly related to breaking up, except if husbands had especially low satisfaction during the first child’s transition to school.  Those couples with stronger relationships to begin with had less decrease in satisfaction.  The take home message is that marriage with kids is not just a bed of roses. While children can provide much pleasure and meaning, they can also take time away from couple bonding activities, place stress and emotional demands on parents, and lead to fights over parenting strategies and division of labor. Financial stress and a routine of errands and driving kids around can further erode relationship glamor and romance. Parents may be too tired for sex or even, conversation.  Thus, romantic love between parents, if left untended will diminish in intensity during childrearing years, most of the time. Shared commitment to parenthood, pride in kid’s achievements, and involvement in kids’ social, academic, and sporting activities can provide alternative sources of fulfillment and friendship during these years. When kids leave the home and couples have more time together, they can often rebuild closeness and intimacy.

Can Romantic Love Last?

At the other end of the spectrum,brain imaging studies provide proof that romantic love can last, at least for around 5-12 percent of couples, according to researcher Art Aron, the romantic love guru from Stony Brook University, in New York, whose studies look inside the brains of couples in love.  In a touching side-note, Aron often collaborates in these studies with his wife of 37 years, Elaine Aron, also a researcher at Stony Brook.

The Brain in Love

A groundbreaking study by Aron and his colleagues, published last year in the journal Social Cognitive and Affective Neuroscience sought to uncover the mysteries of how our brains process love. The researchers recruited couples that had been together more than 20 years as well as those recently fallen in love. After completing questionnaires assessing closeness, romantic love intensity, and sexual frequency, the couples entered brain scanning machines. Using functional magnetic resonance imaging to look inside the brain in real-time, the researchers compared the reactions of new, and long-time lovers, while they viewed pictures showing faces of their loved ones, and faces of close friends, and long-time acquaintances. This methodology was used to make sure that the brain effects seen were due to romantic love, rather than to affection or familiarity. Results showed that indeed, love can last, and has a unique physiological profile in the brain.  The brain scans of both long-term and recent couples showed activity in the ventral tagmental area (VTA), an area with high dopamine concentration, which is associated with reward and motivation. Partner pictures produced distinct and more powerful responses than friend and acquaintance pictures. Romantic partners, therefore, appear to have unique and lasting reward value! Also, those long-term couples that reported the highest levels of romantic love and closeness on questionnaires had levels of brain VTA activity similar to those of newly in love partners.

Sex and the Brain

This study also revealed some interesting findings related toattachment and sexuality. Compared to new partners, long-term partners showed activity in brain areas associated with attachment that demonstrated greater calmness and less tension. Thus, long-term partners may become more securely attached and less likely to fear abandonment.  Higher sexual frequency was associated with greater activity in the posterior hippocampus — an area associated withhunger, cravings, and obsession. Thus, romantic love appears to be different than sexual attraction, although this may be a component of it. Taken together these findings suggest it is important to build a strong romantic bond early on, so that love can withstand the challenges ofaging and family development. Since we know that our brains can change in adulthood and possess neuroplasticity, it is also likely that we can rebuild and renew love in relationships that have deteriorated.

How Do We Keep the Spark of Love Alive?

Research findings suggest we can rebuild or enhance love in relationships by:

  1. Generosity – Being helpful and considerate in small and large ways, doing our fair share of chores, stepping in to allow our partner to take a break.
  2. Positivity – Focusing on and communicating about our partner’s positive qualities. Showing appreciation and affection on a regular basis.
  3. Attachment – Allowing our partners to turn to us and depend on us when they are vulnerable; providing a secure emotional base and reassurance of worth.
  4. Expansion – Helping our partners to expand their worlds by engaging in novel and challenging activities together and bringing in our own passion for life.

My next post will provide concrete tools for using these research-based strategies to strengthen your own romantic relationships.

About The Author 

Melanie Greenberg, Ph.D. is a Clinical Psychologist, and expert onMindfulness, Attachment. & Relationships with expertise in the Gottman approach and Emotion-Focused Therapy for couples. Dr Greenberg provides workshops and speaking engagements for organizations and nonprofits, and coaching and therapy for individuals and couples in person or via skype.

Visit my website:


Retrieved from: http://www.psychologytoday.com/blog/the-mindful-self-express/201210/love-sex-relationships-and-the-brain


adhd…a longitudinal follow-up

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Brain imaging, Brain studies, Neuropsychology, Neuroscience, Psychiatry, School Psychology on Tuesday, 16 October 2012 at 07:34

Men Diagnosed with ADHD as Children had Worse Outcomes as Adults, Study Says

ScienceDaily (Oct. 15, 2012) — Men who were diagnosed as children with attention-deficit/hyperactivity disorder (ADHD) appeared to have significantly worse educational, occupational, economic and social outcomes in a 33-year, follow-up study that compared them with men without childhood ADHD, according to a report published Online First by Archives of General Psychiatry, a JAMA Network publication.

ADHD has an estimated worldwide prevalence of 5 percent, so the long-term outcome of children with ADHD is a major concern, according to the study background.

Rachel G. Klein, Ph.D., of the Child Study Center at NYU Langone Medical Center in New York, and colleagues report the adult outcome (follow-up at average age of 41 years) of boys who were diagnosed as having ADHD at an average age of 8 years. The study included 135 white men with ADHD in childhood, free of conduct disorder (probands), and a comparison group of 136 men without childhood ADHD.

“On average, probands had 2½ fewer years of schooling than comparison participants … 31.1 percent did not complete high school (vs. 4.4 percent of comparison participants) and hardly any (3.7 percent) had higher degrees (whereas 29.4 percent of comparison participants did). Similarly, probands had significantly lower occupational attainment levels,” the authors note. “Given the probands’ worse educational and occupational attainment, their relatively poorer socioeconomic status at [follow-up at average age of 41 years] is to be expected. Although significantly fewer probands than comparison participants were employed, most were holding jobs (83.7 percent). However, the disparity of $40,000 between the median annual salary of employed probands and comparisons is striking.”

In further comparisons of the two groups, the men who were diagnosed with ADHD in childhood also had more divorces (currently divorced, 9.6 percent vs. 2.9 percent, and ever been divorced 31.1 percent vs. 11.8 percent); and higher rates of ongoing ADHD (22.2 percent vs. 5.1 percent, the authors suspect the comparison participants’ ADHD symptoms might have emerged during adulthood), antisocial personality disorder (ASPD, 16.3 percent vs. 0 percent) and substance use disorders (SUDs, 14.1 percent vs. 5.1 percent), according to the results.

During their lifetime, the men who were diagnosed with ADHD in childhood (the so-called probands) also had significantly more ASPD and SUDs but not mood or anxiety disorders and more psychiatric hospitalizations and incarcerations than comparison participants. And relative to the comparison group, psychiatric disorders with onsets at 21 years of age or older were not significantly elevated in the probands, the study results indicate.

The authors note the design of their study precludes generalizing the results to women and all ethnic and social groups because the probands were white men of average intelligence who were referred to a clinic because of combined-type ADHD.

“The multiple disadvantages predicted by childhood ADHD well into adulthood began in adolescence, without increased onsets of new disorders after 20 years of age. Findings highlight the importance of extended monitoring and treatment of children with ADHD,” the study concludes.

Retrieved from: http://www.sciencedaily.com/releases/2012/10/121015162407.htm



Brain Gray Matter Deficits at 33-Year Follow-up in Adults With Attention-Deficit/Hyperactivity Disorder Established in Childhood

Erika Proal, PhD; Philip T. Reiss, PhD; Rachel G. Klein, PhD; Salvatore Mannuzza, PhD; Kristin Gotimer, MPH; Maria A. Ramos-Olazagasti, PhD; Jason P. Lerch, PhD; Yong He, PhD; Alex Zijdenbos, PhD; Clare Kelly, PhD; Michael P. Milham, MD, PhD; F. Xavier Castellanos, MD

Arch Gen Psychiatry. 2011;68(11):1122-1134. doi:10.1001/archgenpsychiatry.2011.117.


Context  Volumetric studies have reported relatively decreased cortical thickness and gray matter volumes in adults with attention-deficit/hyperactivity disorder (ADHD) whose childhood status was retrospectively recalled. We present, to our knowledge, the first prospective study combining cortical thickness and voxel-based morphometry in adults diagnosed as having ADHD in childhood.

Objectives  To test whether adults with combined-type childhood ADHD exhibit cortical thinning and decreased gray matter in regions hypothesized to be related to ADHD and to test whether anatomic differences are associated with a current ADHD diagnosis, including persistent vs remitting ADHD.

Design  Cross-sectional analysis embedded in a 33-year prospective follow-up at a mean age of 41.2 years.

Setting  Research outpatient center.

Participants  We recruited probands with ADHD from a cohort of 207 white boys aged 6 to 12 years. Male comparison participants (n = 178) were free of ADHD in childhood. We obtained magnetic resonance images in 59 probands and 80 comparison participants (28.5% and 44.9% of the original samples, respectively).

Main Outcome Measures  Whole-brain voxel-based morphometry and vertexwise cortical thickness analyses.

Results  The cortex was significantly thinner in ADHD probands than in comparison participants in the dorsal attentional network and limbic areas (false discovery rate < 0.05, corrected). In addition, gray matter was significantly decreased in probands in the right caudate, right thalamus, and bilateral cerebellar hemispheres. Probands with persistent ADHD (n = 17) did not differ significantly from those with remitting ADHD (n = 26) (false discovery rate < 0.05). At uncorrected P < .05, individuals with remitting ADHD had thicker cortex relative to those with persistent ADHD in the medial occipital cortex, insula, parahippocampus, and prefrontal regions.

Conclusions  Anatomic gray matter reductions are observable in adults with childhood ADHD, regardless of the current diagnosis. The most affected regions underpin top-down control of attention and regulation of emotion and motivation. Exploratory analyses suggest that diagnostic remission may result from compensatory maturation of prefrontal, cerebellar, and thalamic circuitry.

Retrieved from: http://archpsyc.jamanetwork.com/article.aspx?articleid=1107429

The Unfulfilled Promises of Psychotropics

In Brain studies, Medication, Neuropsychology, Neuroscience, Psychiatry, Psychopharmacology on Sunday, 14 October 2012 at 11:33

The Unfulfilled Promises of Psychotropics

By Richard Kensinger, MSW

I remember thinking over 40 years ago when I began my clinical career, that with the rapid advances made in psychotropic agents, psychotherapy would become a venture of the past. A recent editorial published in Schizophrenia Bulletindispels my myth of becoming unemployed.

Psychopharmacology is in crisis. The data are in, and it is clear that a massive experiment has failed: despite decades of research and billions of dollars invested, not a single mechanistically novel drug has reached the psychiatric market in more than 30 years. Indeed, despite enormous effort, the field has not been able to escape the “me too/me (questionably) better” straightjacket. In recent years, the appreciation of this reality has had profound consequences for innovation in psychopharmacology because nearly every major pharmaceutical company has either reduced greatly or abandoned research and development of mechanistically novel psychiatric drugs. This decision is understandable because pharmaceutical and biotechnology executives see less risky opportunities in other therapeutic areas, cancer and immunology being the current pipeline favorites. Indeed, in retrospect, one can wonder why it took so long for industry to abandon psychiatry therapeutics. So how did we get here and more importantly, what do we need to do to find a way forward?

The discovery of all three major classes of psychiatric drugs, antidepressants, antipsychotics, and anxiolytics, came about on the basis of serendipitous clinical observation. At the time of their discoveries, the mechanisms by which these molecules produce their effects were unknown, and it was only later that antipsychotics were shown to be D2 receptor antagonists, antidepressants monoamine reuptake inhibitors, and anxiolytics GABA receptor modulators. It is interesting and perhaps instructive to consider whether any of these classes of drugs could have been discovered by current drug discovery strategies. For example, what genetic or preclinical data exist that point to the D2 dopamine receptor as a likely target for antipsychotic activity? Presently there are no genetic data that suggest that this receptor is expressed or functions abnormally in psychotic disorders (emphasis added). And without the benefit of the prior clinical validation, it is difficult to see how preclinical data alone would point to the D2 receptor as an interesting potential target for the treatment of psychotic disorders. The same can be said for monoamine transporters with respect to depression where, like psychosis, there are no animal models based on disease pathophysiology and no compelling preclinical data pointing to these as potential targets for antidepressant drugs. This raises a troubling question: if in retrospect the three major classes of currently prescribed psychiatric drugs would likely never have been discovered using current drug discovery strategies, why should we believe that such strategies are likely to bear fruit now or in the future?

Given that there cannot be a coherent biology for syndromes as heterogeneous as schizophrenia, it is not surprising that the field has failed to validate distinct molecular targets for the purpose of developing mechanistically novel therapeutics. Although it has taken our field too long to gain this insight, we seem to be getting there. For example, at the 2011 meeting of the American College of Neuropsychopharmacology, the need for change and the need for new strategies were predominant themes.

In summation the excitement in the past two decades about the “Decades of the Brain” are fading to realism. Our human genome is much more complex than we can imagine. Half of our genes are devoted to brain form and function. The interaction between geneotype and phenotype is also more complex that we realize. Thus, we are approaching this science with more skepticism and realism.


Fibiger HC (2012). Psychiatry, the pharmaceutical industry, and the road to better therapeutics. Schizophrenia bulletin, 38 (4), 649-50 PMID: 22837348

Retrieved from: http://brainblogger.com/2012/10/08/the-unfulfilled-promises-of-psychotropics/


Cannabis and the Adolescent Brain

In Brain studies, Fitness/Health, Neuropsychology, Neuroscience on Sunday, 14 October 2012 at 11:23

Cannabis and the Adolescent Brain

By India Bohanna, PhD

For some time, people have known that using cannabis during adolescence increases the risk of developing cognitive impairment and mental illness (e.g. depression, anxiety or schizophrenia) later in life. Importantly however, the mechanisms responsible for this vulnerability are not well understood. A new study, published in Brain, shows that long-term cannabis use that starts during adolescence damages the neural pathways connecting brain regions, and that this may cause the later development of cognitive and emotional problems.

The authors used diffusion tensor imaging (DTI), a MRI technique that measures water diffusion, to examine the microstructure of white matter in 59 heavy cannabis users, who used cannabis at least twice a month for three years or longer, as well as 33 non-users. In the human brain, white matter pathways are formed by bundles of axons, which carry the neural signals, and myelin, which coat the axons and speeds up signal transfer. These white matter pathways are crucial for normal brain function as they enable disparate regions of the brain to communicate, and act together.

When the authors investigated white matter microstructure in the cannabis users, they found damage in the white matter pathways of the hippocampus, crucial for memory, and the corpus callosum, which connects the brain’s two hemispheres. Both pathways are critical for normal brain function. The authors suggest that impaired connectivity due to damage in these pathways may be the cause of the cognitive impairment and vulnerability to schizophrenia, depression and anxiety seen in long-term users.

The authors also show an inverse relationship between the amount of white matter damage and the age of first use. That is, participants who started using cannabis younger had more white matter damage and showed poorer brain connectivity. Adolescence is a critical period in the development of white matter in the brain, when the neural connections we rely on in adulthood are being finally formed. The authors point out that white matter cells have cannabinoid receptors (those susceptible to cannabis) during adolescence, which disappear as the brain matures. This new study demonstrates a mechanism that may help explain how cannabis use in adolescence causes long-term changes in brain function. The cannabis users in the study had significantly higher levels of depression and anxiety compared to the non-users.

This important new study suggests that young people’s brains are at risk of white matter injury due to cannabis, and that cannabis exposure during adolescence may permanently damage white matter development. Future research must address the question; can white matter pathways and connectivity recover when a person quits using cannabis?


Zalesky A, Solowij N, Yücel M, Lubman DI, Takagi M, Harding IH, Lorenzetti V, Wang R, Searle K, Pantelis C, & Seal M (2012). Effect of long-term cannabis use on axonal fibre connectivity. Brain : a journal of neurology, 135 (Pt 7), 2245-55 PMID: 22669080

Retrieved from: http://brainblogger.com/2012/08/18/cannabis-and-the-adolescent-brain/

are we over-medicating?

In ADHD, Anxiety, Brain imaging, Brain studies, Medication, Psychiatry, Psychopharmacology on Wednesday, 3 October 2012 at 05:39

this is one author’s opinion on anxiety and “the little blue pill.”  while anxiety is a VERY REAL and often debilitating condition for some, many wonder if anxiety medications (such as xanax and valium) are too readily prescribed and taken.  in my work as a school psychologist, i am asked constantly if i think adhd is over-diagnosed and children are over-medicated.  my answer is based in my belief that most psychological conditions are brain-based (this is becoming especially evident in light of new ways to examine the brain, i.e. genomic medicine, advanced brain imaging, etc.).  not treating those who have a REAL diagnosis has deleterious effects, but do i think that there are many physicians who will prescribe medications without possibly doing a full evaluation?  yes, i do.  but, i also think there are some VERY savvy parents who know what to say to get their kids medication that they *think* will give them an advantage over others.  while stimulants have a paradoxical effect on those with adhd (meaning they are stimulants but do not act as a stimulant behaviorally, i.e. not hyping kids up, but stimulating parts of the brain that are responsible for attending, focus, etc., thus appearing to calm them down), they also act as true stimulants for those that do not have a valid adhd diagnosis.  there are many stories of all-night study sessions in college and kids who use stimulants to stay awake and keep studying (i have even heard about kids who purchase stimulants just as they would marijuana or other drugs and crush it up and snort it for a cocaine-like effect).  the effect of a stimulant on someone without adhd is much like that of someone on cocaine.  they are ‘stimulated.’  so, while i believe the author has some valid points related to medication, i also believe that people who TRULY have a diagnosis of anxiety, adhd, depression, etc., do more harm than good when they do not take medication.  that is my personal opinion based on the many studies of those with treated issues versus those who do not seek treatment or were not treated until adulthood.  the differences in neuroanatomy and structural changes in the brain show that medication does work IF properly prescribed.  my personal opinion is if you think you are suffering from a brain-based disorder (adhd, anxiety, etc.), do yourself a favor and go to a PSYCHIATRIST.  while pediatricians and general practitioners are good at what they do and are knowledgeable about so many things, you wouldn’t go to an ophthalmologist for a broken leg, so why would you go to a pediatrician for a psychiatric issue?  psychiatrists’ entire business is of the mind and it is their job to keep up with the latest research and medications.  why go to anyone BUT a specialist?  once again, this is nothing more than my PERSONAL opinion.  

Valium’s Contribution to the New Normal


By Robin Marantz Henig

IT wasn’t funny, really, but everybody laughed at the scene in the 1979 film “Starting Over” when Burt Reynolds’s character had a panic attack in the furniture department of Bloomingdale’s (something to do with terror at the prospect of buying a couch). “Does anyone have a Valium?” his brother called out as Burt hyperventilated. The punch line: Every woman in the store reached into her purse and pulled out a little vial of pills.

Nor was it surprising that all those Bloomie’s shoppers could be so helpful, since by that time Valium, which had been introduced in 1963, was the best-selling prescription drug in America, with billions of blue or yellow or white pills, each stamped with a trademark V, sold every year.

Valium was, significantly, one of the first psychoactive drugs to be used on a large scale on people who were basically fine. It has since been surpassed by other drugs, like the popular tranquilizer Xanax. But with the pharmaceutical giant Roche announcing that it will soon close the Nutley, N.J., plant where Valium and its predecessor, Librium, were developed, it’s a good time to remember how revolutionary these “minor tranquilizers” were half a century ago. These were the drugs that gave us a new way to slay our inner demons, medicating our way to a happier life.

How did Roche convince physicians that it was O.K. to offer their patients a bottled form of serenity? How did the physicians persuade their patients? And how did the company’s success in this venture shape our collective attitudes toward normal versus abnormal, stoic versus foolhardy, and the various ways available to cope with the ups and downs of daily life?

Marketing, essentially — which was first put into action with Librium, one of those evocative drug names that pharmaceutical companies invent. Librium was introduced in 1960 and promptly outsold its predecessors, the barbiturates, because it had fewer side effects. (Barbiturates were serious downers, making people sleepy and zombielike, and they were habit-forming; Marilyn Monroe died from an overdose.)

“A Whole New World … of Anxiety” read one of the early Roche ads for Librium, featuring a young woman with a pageboy hairdo holding an armload of books, wearing a short stadium coat and heading off to college. The copy made it sound as though every step in this “whole new world” called out for a tranquilizer. “The new college student may be afflicted by a sense of lost identity in a strange environment … Her newly stimulated intellectual curiosity may make her more sensitive to and apprehensive about unstable national and world conditions.”

The ad lists other sources of “anxiety” in a college student’s life — new friends, new influences, stiff competition for grades and tests of her moral fiber — that could just as easily be seen as growing pains, or as a healthy response to the turbulent world of the 1960s, when this ad appeared in The Journal of the American College Health Association. But Roche wanted doctors to believe that they were problems, not adventures, and that they warranted a prescription for Librium.

The next step was to develop something better — stronger, faster acting, less toxic. The Roche chemist who had originally stumbled upon Librium, Leo Sternbach, went back to the lab and tweaked the compound. Then he tested the drug on humans — in this case, the mothers-in-law of a few Roche executives. The executives thought that the new drug, Valium, rendered their mothers-in-law significantly less annoying.

In retrospect, Librium turned out to be a great first act, teaching Roche how to pitch a psychoactive drug to doctors of healthy patients who just needed a little something to unjangle their nerves. By the time Valium arrived, Roche was poised to dominate the field. In 1974, Americans filled nearly 60 million prescriptions for Valium.

Taking a pill to feel normal, even a pill sanctioned by the medical profession, led to a strange situation: it made people wonder what “normal” really was. What does it mean when people feel more like themselves with the drug than without it? Does the notion of “feeling like themselves” lose its meaning if they need a drug to get them there?

At the same time that Valium became famous for being in everyone’s medicine chest (or in every department store shopper’s purse), it also became famous for ruining lives. Elizabeth Taylor said she was addicted to Valium plus whiskey, Jack Daniel’s in particular. Tammy Faye Bakker said she was addicted to Valium plus nasal spray. Elvis Presley’s personal poison was Valium mixed with an assortment of other prescriptions. And Karen Ann Quinlan, the young woman languishing in a chronic vegetative state while her parents fought all the way to the New Jersey Supreme Court for the right to remove her from life support, originally lapsed into a coma in 1975 from a combination of Valium and gin.

Nearly 50 years after Valium was introduced and aggressively marketed, we’ve learned its lessons well. My generation of aging baby boomers does its brain styling, by and large, with antidepressantsProzac, Wellbutrin, CelexaPaxilZoloft. And for my daughters’ generation, the millennials, the pills of choice tend to be Ritalin and Adderall, for mental focus.

But when Americans are feeling out of sorts, we are still more likely to turn to anti-anxiety drugs than to any other kind. The leading successor to Valium, Xanax, outsells every other psychiatric drug on the market (48.7 million prescriptions last year). And even Valium is still out there, the classic little-black-dress of tranquilizers. In 2011, 14.7 million prescriptions were written for the drug that first made its cultural mark as a Rolling Stones song (“Mother’s Little Helper”) back in 1966.

As Roche closes its New Jersey headquarters, it plans to open a smaller research facility in Manhattan in late 2013, part of a wave that city officials hope will turn New York into a biotech mecca. The company’s transition reminds us of a phenomenon that’s become so common we no longer even think of it as weird: the oxymoronic attainment, through using drugs to make you feel more like yourself, of an artificially induced normal.

Robin Marantz Henig is a contributing writer for The New York Times Magazine and the co-author, with her daughter Samantha Henig, of the forthcoming “Twentysomething: Why Do Young Adults Seem Stuck?”

Retrieved from: http://www.nytimes.com/2012/09/30/sunday-review/valium-and-the-new-normal.html?ref=opinion&_r=0

Your brain on books…

In Brain imaging, Brain studies, Education, Neuroscience on Friday, 21 September 2012 at 04:30

today’s technology has led to SO many amazing breakthroughs and allows for new and more precise understanding of so many things.  possible genetic markers for autism (and a possible vaccine), neurogenesis, new understandings of ADHD and treatment implications, just to name a few i have posted about.  following is an article on reading and our brains.  while fMRI’s have been around a while, it is through such instruments that we are really changing our understanding of the brain and its related functions.  i remember when i first read yvette sheline’s article* on hippocampal volume in 2003 that i realized we were at a turning point in brain research and understanding how the brain works.  from that point on, my interest in all things ‘neuro’ became much stronger.  the following is an article on reading and the brain.  while i can’t conceptualize what i would do if i didn’t have reading as an outlet.  i know, for some, reading is a “necessary evil” and while those people might read all day at work (work-related) are unlikely to read for pleasure.  maybe this research will help to convince people that reading has SO many benefits besides being able to get completely lost in a book.  happy reading, everyone!

*Sheline’s article: http://www.ncbi.nlm.nih.gov/pubmed/12900317 (the one that hooked me)

MRI reveals brain’s response to reading

Posted By Stanford On September 10, 2012 @ 4:13 pm In Science & Technology

STANFORD (US) — Researchers asked people to read Jane Austen in an MRI machine, and say the surprising results suggest reading closely could be “training” for our brains.

Neurobiological experts, radiologists, and humanities scholars are working together to explore the relationship between reading, attention, and distraction—by reading Jane Austen.

Surprising preliminary results reveal a dramatic and unexpected increase in blood flow to regions of the brain beyond those responsible for “executive function,” areas which would normally be associated with paying close attention to a task, such as reading, says Natalie Phillips, the literary scholar leading the project.

During a series of ongoing experiments, functional magnetic resonance images track blood flow in the brains of subjects as they read excerpts of a Jane Austen novel. Experiment participants are first asked to skim a passage leisurely as they might do in a bookstore, and then to read more closely, as they would while studying for an exam.

Phillips says the global increase in blood flow during close reading suggests that “paying attention to literary texts requires the coordination of multiple complex cognitive functions.” Blood flow also increased during pleasure reading, but in different areas of the brain. Phillips suggests that each style of reading may create distinct patterns in the brain that are “far more complex than just work and play.”

The experiment focuses on literary attention, or more specifically, the cognitive dynamics of the different kinds of focus we bring to reading. This experiment grew out of Phillips’ ongoing research about Enlightenment writers who were concerned about issues of attention span, or what they called “wandering attention.”

Phillips, who received her PhD in English literature at Stanford in 2010, is now an assistant professor of English at Michigan State University. She says one of the primary goals of the research is to investigate the value of studying literature.

Beyond producing good writers and thinkers, she is interested in “how this training engages the brain.”

The research is “one of the first fMRI experiments to study how our brains respond to literature,” Phillips says, as well as the first to consider “how cognition is shaped not just by what we read, but how we read it.”

Print overload

Critical reading of humanities-oriented texts are recognized for fostering analytical thought, but if such results hold across subjects, Phillips says it would suggest “it’s not only what we read—but thinking rigorously about it that’s of value, and that literary study provides a truly valuable exercise of people’s brains.”

Though modern life’s cascade of beeps and buzzes certainly prompts a new kind of distraction, Phillips warns against “adopting a kind of historical nostalgia, or assuming those of the 18th century were less distracted than we are today.”

Many Enlightenment writers, Phillips notes, were concerned about how distracted readers were becoming “amidst the print-overload of 18th-century England.”

Rather than seeing the change from the 18th century to today as a historical progression toward increasing distraction, Phillips likes to think of attention in terms of “changing environmental, cultural, and cognitive contexts: what someone’s used to, what they’re trying to pay attention to, where, how, when, for how long, etc.”

Ironically, the project was born out of a moment of distraction. While sitting on a discussion panel (which happened to be one of the first on cognitive approaches to literature), Phillips found herself distracted from the talk by the audience’s varieties of inattention: “One man was chatting to his neighbor; another person was editing their talk; one guy was looking vaguely out the window; a final had fallen asleep.”

The talk inspired Phillips to consider connections between her traditional study of 18th-century literature and a neuroscientific approach to literary analysis.

Phillips was especially intrigued by the concept of cognitive flexibility, which she defines as “the ability to focus deeply on one’s disciplinary specialty, while also having the capacity to pay attention to many things at once,” such as connections between literature, history of mind, philosophy, neuroscience, and so on.

Samantha Holdsworth, a research scientist specializing in MRI techniques, recalls an early conversation about the project when two scientists were trying to communicate with three literary scholars: “We were all interested, but working at the edge of our capacity just to understand even 10 percent of what each other were saying.”

Heightened attention

After working through the challenges of disciplinary lingo, the team devised a truly interdisciplinary experiment. Participants read a full chapter from Mansfield Park, which is projected onto a mirror inside an MRI scanner. Together with a verbal cue, color-coding on the text signals participants to move between two styles of attention: reading for pleasure or reading with a heightened attention to literary form.

The use of the fMRI allows for a dynamic picture of blood flow in the brain, “basically, where neurons are firing, and when,” says Phillips. Eye-tracking compatible with fMRI shows how people’s eyes move as they read. As Phillips explains, the micro-jumps of the eyes “can be aligned with the temporal blood flow to different regions in the brain.”

When participants are done with a chapter, they leave the scanner and write a short literary essay on the sections they analyzed closely. The test subjects, all literary PhD candidates from the Bay Area, were chosen because Phillips felt they could easily alternate between close reading and pleasure reading.

After reviewing early scans, neuroscientist Bob Doherty, director of the Stanford Center for Cognitive and Neurobiological Imaging (CNI), says he was impressed by “how the right patterns of ink on a page can create vivid mental imagery and instill powerful emotions.”

Doherty was also surprised to see how “a simple request to the participants to change their literary attention can have such a big impact on the pattern of activity during reading.”

The researchers expected to see pleasure centers activating for the relaxed reading and hypothesized that close reading, as a form of heightened attention, would create more neural activity than pleasure reading.

If the ongoing analysis continues to support the initial theory, Phillips says, teaching close reading (i.e., attention to literary form) “could serve—quite literally—as a kind of cognitive training, teaching us to modulate our concentration and use new brain regions as we move flexibly between modes of focus.”

With the field of literary neuroscience in its infancy, Phillips says this project is helping to demonstrate the potential that neuroscientific tools have to “give us a bigger, richer picture of how our minds engage with art—or, in our case, of the complex experience we know as literary reading.”

Source: Stanford University

Article printed from Futurity.org: http://www.futurity.org

URL to article: http://www.futurity.org/science-technology/mri-reveals-brain%e2%80%99s-response-to-reading/

For more information on Dr. Sheline and her work: http://wuphysicians.wustl.edu/physician2.aspx?PhysNum=1319http://wuphysicians.wustl.edu/physician2.aspx?PhysNum=1319

Multi-Vitamin Supplements and Brain Function

In Alternative Health, Brain studies, Fitness/Health on Saturday, 15 September 2012 at 08:24

Multivitamin supplements boost brain function, say UK researchers

Taking a multivitamin supplement daily can improve cognitive performance in both children and adults, say UK researchers.

Researchers Create Short-Term Memories In-Vitro

In Brain imaging, Brain studies on Thursday, 13 September 2012 at 07:00

Researchers Create Short-Term Memories In-Vitro


Research in October issue of Nature Neuroscience sheds new light on the mechanics of memory.

Ben W. Strowbridge, PhD, Professor of Neurosciences and Physiology/Biophysics, and Robert A. Hyde, a fourth year MD/PhD student in the neurosciences graduate program at Case Western Reserve University School of Medicine, have discovered how to store diverse forms of artificial short-term memories in isolated brain tissue.

“This is the first time anyone has found a way to store information over seconds about both temporal sequences and stimulus patterns directly in brain tissue,” says Dr. Strowbridge. “This paves the way for future research to identify the specific brain circuits that allow us to form short-term memories.”

Their study, entitled “Mnemonic Representations of Transient Stimuli and Temporal Sequences in Rodent Hippocampus In Vitro,” is slated for publication in the October issue of Nature Neuroscience, and is currently available online.

Memories are often grouped into two categories: declarative memory, the short and long-term storage of facts like names, places and events; and implicit memory, the type of memory used to learn a skill like playing the piano.

In their study, the researchers sought to better understand the mechanisms underlying short-term declarative memories such as remembering a phone number or email address someone has just shared.

Using isolated pieces of rodent brain tissue, the researchers demonstrated that they could form a memory of which one of four input pathways was activated. The neural circuits contained within small isolated sections of the brain region called the hippocampus maintained the memory of stimulated input for more than 10 seconds. The information about which pathway was stimulated was evident by the changes in the ongoing activity of brain cells.

Using isolated pieces of rodent brain tissue, the researchers demonstrated that they could form a memory of which one of four input pathways was activated. The neural circuits contained within small isolated sections of the brain region called the hippocampus maintained the memory of stimulated input for more than 10 seconds. This drawing shows the general layout of the rat hippocampal formation.

“The type of activity we triggered in isolated brain sections was similar to what other researchers have demonstrated in monkeys taught to perform short-term memory tasks,” according to Mr. Hyde. “Both types of memory-related activity changes typically lasted for 5-10 seconds.”

The researchers also demonstrated that they could generate memories for specific contexts, such as whether a particular pathway was activated alone or as part of a sequence of stimuli to different inputs. Changes in ongoing activity of hippocampal neurons accurately distinguished between two temporal sequences, akin to humans recognizing the difference between two different song melodies. The artificial memories Dr. Strowbridge’s group created in the hippocampus continued to recognize each sequence even when the interval between stimuli was changed.

The new research expands upon a previous study, also published in Nature Neuroscience in 2010, in which Dr. Strowbridge’s group found that isolated pieces of the hippocampus could store which one of two inputs was stimulated. That study also found that a relatively rare type of brain cell, originally described in the 1800′s by the famous Spanish anatomist Santiago Ramón y Cajal, but ignored in modern times, played a critical role in the memory effect.

By demonstrating that the same neural circuits also can store information about context, the new study will likely increase the focus on these potential “memory cells” in the hippocampus, called semilunar granule cells, says Dr. Strowbridge.

Understanding normal memory function also lays the groundwork for understanding how neurodegenerative diseases, such as Alzheimer’s or Parkinson’s disease, affect memory and for developing new, more effective treatments for memory impairments associated with aging.

Notes about this memory research:

This study was funded by the National Institutes of Health.

Contact: Jessica Studeny – Case Western Reserve University
Source: Case Western Reserve University School of Medicine
“Mnemonic representations of transient stimuli and temporal sequences in the rodent hippocampus in vitro” by Robert A Hyde and Ben W Strowbridge in Nature Neuroscience online 9 September 2012 doi:10.1038/nn.3208

ADHD in Adults

In ADHD, Anxiety, Brain studies, School Psychology on Thursday, 13 September 2012 at 05:58

Unmasking ADHD in Adults

David W. Goodman, MD


Adult ADHD

During the past decade, awareness has grown that ADHD is not limited to children and adolescents. Rather, ADHD is now recognized as a chronic neuropsychiatric disorder that persists into adulthood in up to 65% of children with ADHD.[1-3] Data from the National Comorbidity Survey Replication (NCSR) estimate that 4.4% of adults in the United States have ADHD, although as many as 75% have never been diagnosed and 90% remain untreated.[4,5] The many similarities in symptoms and impairments seen in ADHD and mood and anxiety disorders likely account for many of the misdiagnoses.[6] In addition, the rate of comorbidity in ADHD with mood and anxiety disorders, sleep disorders, and substance use disorders is high and further complicates accurate diagnosis.[5]

Current criteria for ADHD in the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM-IV-TR) were originally developed and validated for children.[7] Diagnostic criteria require an onset of symptoms before age 7 years; the presence of at least 6 of 9 possible symptoms in 1 or both of the 2 diagnostic clusters of inattentiveness and hyperactivity; and impairment in 2 or more settings (such as home, school, and work).[7] Many similarities exist in the presentations of childhood and adult ADHD; however, adults are more likely to present with symptoms of inattention than hyperactivity.[8] But the presence of childhood symptoms is necessary for a diagnosis of ADHD in an adult.

Clinicians can use several screening tools to help in the ADHD diagnostic process; however, high scores on these tools must be interpreted within a clinical context following a clinical interview. For example, a high score on the ASRS may suggest ADHD[9,10] but may also be the result of acute anxiety, acute depression, or active substance abuse. Patients who take online screeners and self-diagnose ADHD present their symptoms and “diagnosis” to their clinicians in a descriptive rather than a diagnostic context, not understanding how other possible psychiatric disorders may lead to high screening scores. As a result, their self-diagnoses are typically inaccurate.

The clinical interview includes a comprehensive patient history that covers all major psychiatric disorders. The clinician reviews the presenting symptoms in a diagnostic evaluation, inquiring about other possible psychiatric disorders that the patient may not include in the description of symptoms. Through this process, the clinician can rule out primary mood or anxiety disorders (among others), and also ascertain a longitudinal course of symptoms originating during childhood to confirm a diagnosis of ADHD. An accurate account of childhood symptoms of ADHD improves if corroborative historical information can be obtained from an outside informant (for example, a parent). This historical information can be obtained by having a parent complete a childhood ADHD symptom rating scale that can be returned to the PCP. The use of an outside informant also conveys to the patient that third-party information will be used to establish an accurate diagnosis, a disincentive to those who simply seek a prescription for stimulants.


The cognitive and affective symptoms of ADHD can be similar to those of other psychiatric disorders, most notably mood and anxiety disorders. However, specific distinguishing characteristics can assist with the differential diagnosis. In this case, despite reporting current symptoms that might be consistent with ADHD, the notable absence of ADHD symptoms during Ms Jones’s childhood and adolescence precludes a diagnosis of ADHD. A more accurate diagnosis is generalized anxiety disorder (GAD), which is characterized by excessive anxiety and worry that is difficult to control and is associated with at least 3 of the following symptoms: restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and sleep disturbance, which cause clinically significant distress or functional impairments.[7] Significant chronic anxiety exacerbated by an acute, stressful event can produce cognitive symptoms that appear similar to ADHD. Remember: patients use psychological terms descriptively, not diagnostically.

A survey of 400 primary care physicians highlighted the challenges clinicians face when diagnosing ADHD in adults.[11] Approximately two-thirds of the participating respondents referred adults with possible ADHD to specialists for diagnosis and treatment, whereas they felt more competent and confident when diagnosing depression or GAD. Surveys find that only 2% of PCPs refer patients to specialists for the diagnosis and management of depression; for GAD, only 3% refer out.[11,12]

ADHD and Comorbidity

ADHD affects approximately 9 to 10 million adults in the United States (4.4% of the adult population). This makes ADHD in adults the second most prevalent psychiatric disorder after major depressive disorder (MDD), which reportedly affects 6.6% of the US population, and more prevalent than GAD (3%), bipolar disorder (2%), and schizophrenia (1%).[5] Adults with ADHD have a higher percentage of comorbidities than their peers without ADHD.[5] Among the most prevalent psychiatric comorbidities in patients with ADHD are anxiety disorders, mood disorders, and substance use disorders (SUD).[13] Many adults with ADHD present with symptoms of anxiety, MDD, or both. Further, high levels of stress may mimic the symptoms of ADHD.[13] Consequently, the high prevalence rate of ADHD in the adult population makes it essential for clinicians to include ADHD as part of the differential diagnosis in any mental health evaluation or whenever patients present with depression or anxiety.

Data from the NCSR suggest that up to 75% of adults with ADHD were not diagnosed during childhood.[5] Many adults play down a possible diagnosis of ADHD because they do not recall being hyperactive in childhood or because they have not been previously diagnosed with the disorder. Other adults will dismiss the diagnosis because they appear to be functioning well and are successful in their chosen fields, even though they have symptoms such as restlessness, low self-esteem, or poor time-management skills.[14] Exceptionally intelligent individuals or adults who had predominantly inattentive ADHD as children may not have had observable impairments during childhood because disruptive behavior was absent; however, symptoms may surface as demands increase with greater school and work responsibilities.[15] Similarly, clinicians may overlook ADHD among high-functioning patients, not realizing the need to look past a patient’s success to explore whether the patient might have developed strategies to compensate for ADHD-related deficiencies and is working hard to compensate.

PCPs who rely on the accuracy of a psychiatric diagnosis of adult ADHD from mental health clinicians may not serve their patients well. Data from the NCSR indicate that 37% of women and 53% of men later diagnosed with ADHD were currently taking or had been in treatment for other mental disorders or SUDs in the previous year, in contrast to 25% who had been treated for ADHD.[5] From these data, Kessler and colleagues concluded that adult ADHD is often misdiagnosed by mental health providers.[5] Before prescribing medication, the PCP should review the psychiatric presentation and history with the patient to ensure agreement on the diagnosis. Premature prescription of stimulants for ADHD will only cloud the diagnosis, as adults with ADHD, as well as people in general, may report improvements in mood, cognition, and energy when taking stimulants, which does not confirm a diagnosis of ADHD. In addition, undetected psychiatric disorders may worsen in the presence of stimulants prescribed for ADHD.

Strict adherence to the DSM-IV-TR diagnostic criteria might lead to substantial underdiagnosis of ADHD, as these criteria were originally developed for young boys and may not reflect ADHD symptoms in adults.[16] Clinicians may need to examine whether the patient is advancing appropriately in his or her career or has become a workaholic to compensate for disorganization, procrastination, and sloppy errors.[17] Recent research highlights that adults with ADHD often underestimate the degree of ADHD-related impairments.[18] ADHD that persists into adulthood has been associated with many adverse life experiences or outcomes, including divorce, substance abuse, motor vehicle infractions, academic and occupational underachievement, and brushes with the law.[5,16,19-24] Research suggests that although the number of symptoms may decline along the lifespan, the severity of the impairments does not.[25]

Among the numerous medical conditions that may be associated with cognitive symptoms similar to those of ADHD are thyroid disorders, sleep apnea, hypoglycemia, and lead poisoning.[13] The prevalence of psychiatric comorbidity associated with ADHD is high, with 1 large study reporting that 87% of adults with ADHD had at least 1 comorbid psychiatric diagnosis and 56% had at least 2 comorbid psychiatric disorders.[25] Common comorbidities in ADHD include GAD (which occurs in 25% to 43% of the adult population with ADHD), MDD (16% to 31%), bipolar disorder (up to 47%), and SUD (21% to 53%).[26-28]

Differentiating ADHD and Other Psychiatric Disorders

Clinicians often mistake adult ADHD symptoms as manifestations of other psychiatric disorders, especially anxiety, MDD, or bipolar disorder.[29] It is especially important that clinicians attend to the context of the symptoms: when they originated, how long they have persisted, and whether aggravating or alleviating factors exist. Clinicians also need to determine whether the symptoms might be a function of stress or another condition, such as a sleep disorder. Patient misinterpretation of the symptoms may be more prevalent among adults who were not diagnosed with ADHD during childhood, and some adults may be surprised that they did not “outgrow” their childhood ADHD. Other adults may not recall being diagnosed with ADHD during childhood, suggesting that the absence of a self-report of an ADHD diagnosis may not accurately reflect the absence of childhood ADHD.[30] Misdiagnosis and subsequent inappropriate treatment may help to resolve some secondary symptoms (anxiety and minor depression) but will not resolve the core symptoms of inattentiveness, impulsivity, and hyperactivity.

ADHD is historically a disorder of childhood; as such, diagnosis requires evidence of symptoms occurring during childhood. Adults typically present with fewer overt symptoms and different manifestations of hyperactivity, inattention, and impulsivity than children (Table 1).[31] Whereas hyperactive children cannot sit still and are fidgety, adults may feel restless, have difficulty relaxing, and show impatience. Childhood manifestations of inattention include daydreaming, poor reading comprehension, and working slowly; adult manifestations include procrastination, disorganization, forgetfulness, and missing or showing up late for appointments. Making careless mistakes is common among patients of all ages with ADHD. Impulsive symptoms during childhood include blurting out answers, interrupting others, and having temper outbursts; adults will also manifest with temper outbursts and verbal impulsivity, as well as impulsive spending, starting but not necessarily finishing multiple projects, and moving from job to job.[31]

Table 1.

ADHD Symptom Evolution from Childhood to Adulthood

Childhood Adulthood
  Difficulty sustaining attention (meetings, reading, paperwork)
Failure to pay attention to details Makes careless errors
Appears not to listen Easily distracted/forgetful
Lacks follow-through Poor concentration
Cannot organize Difficulty finishing tasks
Loses important items Disorganized/misplaces items
Squirming/fidgeting Inefficiencies at work
Cannot stay seated Internal restlessness
Cannot wait his/her turn Difficulty sitting through meetings
Runs/climbs excessively Works more than one job
Cannot play/work quietly Works long hours
“On the go”/seems “driven by a motor” Self-selects very active jobs
Talks excessively Overwhelmed
Talks excessively
Blurts out answers Impulsive job changes
Cannot wait in line Drives too fast
Intrudes/interrupts others Interrupts others
Easily frustrated

The Question of Early Symptoms

A particularly challenging component in diagnosing adult ADHD is obtaining sufficient retrospective information to confirm the presence of ADHD symptoms during childhood. Patients may not remember having ADHD-related symptoms before age 7 (a diagnostic criterion for pediatric ADHD in the DSM-IV-TR), although they may identify problems in late grade school or early middle school that continued throughout high school. A recent study compared 4 groups of adults: those who met all criteria for childhood-onset ADHD; those who met all criteria except the age-at-onset criterion (late-onset ADHD); those with subthreshold ADHD who did not meet full symptom criteria; and those without ADHD.[32] Substantial similarities existed between the adults who met the age-at-onset criterion and those with late-onset ADHD, leading these and other investigators to conclude that the current age-at-onset criterion of 7 years is too stringent and to suggest extending the criterion to age 12 in the next iteration of the DSM.[32,33]

Many adults who were not diagnosed during childhood have developed compensatory mechanisms enabling them to function, albeit less than optimally. Clinicians could ask to speak with the patient’s parents or other family members who may be able to provide insights into the patient’s childhood symptomatology. Similarly, current family members, a spouse, and friends might report clinically relevant ADHD symptoms that have been observed for a long time. While an adult might recognize restlessness as a possible ADHD symptom and admit to receiving numerous driving citations, others might note that the patient overreacts, has difficulty staying with tasks, is easily frustrated, or has held numerous jobs.

No standard for the screening of adults for ADHD currently exists. Among the tools that clinicians can use to help in the diagnostic process are the 18-item World Health Organization’s (WHO) ASRS, which can be freely downloaded from the Internet[34]; the Conners’ Adult ADHD Rating Scale (CAARS); the Brown Attention Deficit Disorder Scale (BADDS); the Wender Utah Rating Scale; and the Wender-Reimherr Adult Attention Deficit Disorder Scale. A recent factor analysis determined that many of these scales are in strong agreement with one another, suggesting that clinicians can choose whichever scale is the most pragmatic, cost efficient, and least time-consuming to use.[35] Patients who screen positive on these assessments should then undergo a full diagnostic evaluation, including a clinical interview that assesses current and lifetime symptoms, a thorough developmental history, and behavioral assessments to identify any functional impairments and symptoms.[31]

Treatment of ADHD in Adults

As yet, no formal guidelines have been developed for the treatment of adult ADHD in the United States. However, guidelines for the treatment of ADHD in children and adolescents, as well as international guidelines for the treatment of adult ADHD, offer recommendations that can be extrapolated to US adults. Considerable concordance exists among the guidelines established by the Canadian ADHD Resource Alliance (CADDRA),[17] the American Academy of Child and Adolescent Psychiatry (AACAP), the National Institutes of Health (NIH), and the British Association for Psychopharmacology on Childhood ADHD.[36] The National Institute for Health and Clinical Excellence (NICE) guidelines address both childhood and adult ADHD.[37] The European Network Adult ADHD consensus statement on the diagnosis and treatment of adult ADHD notes the substantial negative and far-reaching consequences of non-treatment of ADHD.[38] These guidelines recommend a multimodal approach to the treatment of ADHD in adults, beginning with psychoeducation about ADHD and pharmacotherapy for ADHD and any comorbid disorders. Recognizing that pharmacotherapy is often insufficient to address all the problems associated with adult ADHD, the guidelines recommend various symptom-specific coaching programs and cognitive behavior therapy to teach problem solving, coping, and time management skills.[38] Similar multimodal treatment recommendations have been proposed by CADDRA.[17]

Available pharmacologic treatments include short-acting and long-acting stimulant and nonstimulant medications. Psychostimulants, including amphetamines and methylphenidates, are recommended as first-line therapy for both children and adults across all sets of US and international guidelines. Currently, only long-acting agents have been approved for the treatment of ADHD in adults in the United States. Despite this, research suggests that 46% of adults diagnosed with ADHD are prescribed off-label, short-acting stimulants.[39]

Approximately 95% of children who were diagnosed with ADHD during childhood and treated with stimulants do not persist with their medication into adulthood,[40] perhaps because clinicians and patients continue to believe that ADHD is a disorder of childhood. Stimulant medications have been shown to effectively address many of the symptoms of ADHD, including poor attention span, restlessness, short-term memory, and hyperactivity. Some patients may respond preferentially to either amphetamine or methylphenidate compounds, and a small percentage of patients do not respond to stimulants at all.[41,42] Side effects are dose-dependent and can include insomnia, nausea, loss of appetite and weight loss, irritability, mood changes, and clinically nonsignificant increases in heart rate and blood pressure in the majority of patients.[43,44,45] However, clinical practice dictates monitoring vital signs to detect any clinically significant changes that may need to be addressed. A baseline check of vital signs also allows for the detection of undiagnosed hypertension that would require treatment before consideration of stimulant medication. Treatment should be initiated at a low dose and titrated based on symptom reduction and side effects. The dose response in adults is variable; clinicians should not expect that higher doses are needed because the patient is an adult or overweight.

US Food and Drug Administration (FDA)-approved nonstimulants in the ADHD armamentarium include atomoxetine, extended-release (XR) guanfacine, and extended-release (ER) clonidine. Only atomoxetine is currently approved for use in adults, while guanfacine XR and clonidine ER have been approved for use in children and adolescents up to age 18. Other agents that are used off-label include bupropion, tricyclic antidepressants (especially desipramine), and modafinil. The onset of action for atomoxetine is slower than for stimulants, taking to a few weeks to attain the maximum treatment effect. The lack of an abuse potential with nonstimulants may be particularly attractive for use in patients who have SUDs, are at risk for substance abuse, or are potential diverters or sellers of illicit substances.

Atomoxetine is a selective inhibitor of the presynaptic norepinephrine transporter. It has been associated with slightly increased diastolic blood pressure and heart rate, and patients with milder forms of autonomic impairment should be monitored if given this agent.[46] In addition, atomoxetine is predominantly metabolized by the cytochrome P450 2D6 (CYP2D6) isoenzyme, necessitating caution for patients who take medication that inhibits CYP2D6, including fluoxetine, paroxetine, and bupropion.[13] Guanfacine is a direct agonist of the α-2a subtype of norepinephrine receptors. Guanfacine XR can be used as monotherapy or adjunctive therapy with a long-acting psychostimulant.[47,48] Clonidine ER is an α-2a-adrenergic receptor agonist that is considered a second-line agent in the treatment of ADHD, but it may be particularly useful for patients with ADHD and comorbid Tourette syndrome or other tic disorders. As yet, the α-2a agonists have not been studied sufficiently in adults either as monotherapy or as adjunctive treatment in combination with stimulants. Because of the effects of these agents on blood pressure and pulse, monitoring vital signs is recommended, and caution is needed in adults who are being treated for hypertension with other medications.

Monitoring Effects and Side Effects After Initial Treatment

Routine clinical monitoring is necessary throughout the duration of treatment.[13] It is important to meet with the patient on a more frequent basis after medication has been initiated to review tolerability and efficacy and to adjust the dosage (or the medication) as necessary; this typically requires follow-up every 2 to 3 weeks and availability by phone if the patient encounters problems with the medication or dosage. Patients engaged in psychotherapy or skills training will likely be seen on a more frequent, often weekly or biweekly, basis. Once stabilized on an effective and well-tolerated dosage of medication, patients can be seen every 2 to 3 months to monitor the need for dosage adjustments based on tolerability and residual symptoms. Clinicians should assess ADHD symptoms, medication side effects, medication adherence, and comorbid medical/psychiatric conditions at each visit. Similarly, clinicians should monitor caffeine and nicotine intake, as these will further elevate blood pressure and heart rate for all patients on ADHD pharmacotherapies. Although not a common problem, patients with a low body mass index (BMI) should be monitored for suppressed appetite leading to weight loss. Regular assessment of medication utility as measured by daily functional performance should be part of routine monitoring. In the process, you can discuss the continued benefit of medication with the patient. On occasion, a patient may wish to stop the medication to reassess its benefit, and the physician should provide support and oversight in this process. A follow-up reassessment when the patient is off the medication can clarify the re-emergence of ADHD symptoms and impact on daily productivity.

One means for monitoring symptom reduction is through the periodic use of symptom checklists, such as the patient-rated 18-item ASRS. The ASRS is an easy and preferred tool to use because it is standardized, validated, nonproprietary, and readily available on the Internet. It can be administered at baseline and then intermittently, especially with changes to medication dosage, to complement the clinical interview. Patients and their clinicians can get a sense of ADHD symptom improvement with treatment or an increase in symptoms if treatment is suspended or stopped. Patients may forget their ratings of baseline symptoms and find the change in symptom ratings helpful to verify treatment benefit. Although symptom reduction is desirable, the true measure of treatment benefit is the improvement in daily function, such as the ability to initiate and complete more tasks, sustain attention, be less distractible in conversations and meetings, finish tasks on time, reduce careless oversights and errors, and have better, more patient social interactions.

Stimulants, Nonstimulants, and Cardiovascular Risk in Adults

Stimulants are associated with mild elevations in both blood pressure and pulse. It is recommended that patients receiving stimulants have blood pressure and heart rate checked at baseline and regularly throughout treatment.[49] A retrospective database analysis in the United Kingdom found no additional risk of sudden death associated with either stimulants or atomoxetine in children and adolescents 2 to 21 years of age with ADHD.[50] Another retrospective study of adults with new ADHD treatments found that preexisting cardiovascular conditions appeared more likely to reduce prescribing of stimulant treatment in younger vs older patients but did not appear to influence initiation of atomoxetine therapy.[51] In this cohort of 8752 patients, 41% with 1 or more preexisting cardiovascular conditions were prescribed stimulants.[51] Small studies have demonstrated that adults being treated for primary essential hypertension can be safely treated with mixed amphetamine salts[52,53] and methylphenidate.[54] However, stimulant medications for ADHD should not be initiated until the patient is normotensive with a stable antihypertensive medication dose.

In 2008, in response to evidence supporting concerns that the use of stimulants for ADHD could augment the risk of serious cardiovascular events by increasing heart rate and blood pressure, the American Heart Association (AHA) recommended an electrocardiogram (ECG) before initiating treatment in children.[55] This recommendation contradicted recommendations by the AACAP and the American Academy of Pediatrics (AAP), which found that sudden cardiac death in persons taking stimulants was a rare event that could not be prevented or predicted by routine screening with ECG.[56] The AAP recommends an ECG only in those patients with the following risk factors: previously detected cardiac disease, palpitations, syncope, or seizures; a family history of sudden death in children or young adults; hypertrophic cardiomyopathy; or long QT syndrome.[56] Two recent large studies found no significant additional risk of sudden death, myocardial infarction, or stroke in children, young adults, or middle-age adults who were receiving stimulants or atomoxetine.[45,57]

Clinical trials of ADHD medications demonstrate short-term efficacy and safety; however, the majority of patients require chronic long-term treatment.[58-60] Recent studies have demonstrated the safety and efficacy of stimulants, atomoxetine, and guanfacine XR over 24-month treatment periods in children and adolescents.[61] Significant differences between stimulants regarding efficacy or risk of cardiac or cerebrovascular events are not apparent.[62] If clinicians observe any cardiovascular changes, they should determine whether these changes are directly related to the ADHD medication or might instead be related to cardiovascular risks and changes associated with normal aging — for example, weight gain as a cause of hypertension. Nevertheless, long-term studies addressing adverse events are warranted.[59]

Approaches to Improve Executive Function in Adults With ADHD

ADHD can be associated with executive function impairments that can compromise occupational functioning.[63] Executive function is broadly defined as the ability to organize, sequence, prioritize, and hold information in your memory as you consider multiple factors (working memory). Executive function can be defined behaviorally (symptoms observed by patient or others) or by specific neuropsychological measures. Most ADHD symptom checklists enumerate executive function symptoms because they are part of the ADHD symptom criteria. By this definition, all patients with ADHD have executive dysfunction. Executive function may improve with ADHD medication such that inattention, distractibility, and sustained attention improve. In this case, executive dysfunction may be an epiphenomenon of inattention, distractibility, and restlessness. Adults with ADHD may notice improvements in many of their symptoms of impulsivity, inattention, and restlessness but may still struggle with difficulties in organization, developing timelines, planning, and making and initiating decisions.

If the definition of executive function is based on abnormalities that appear on specific neuropsychological tests, then approximately one-third of ADHD patients have executive dysfunction, not 100% as the behavioral definition demands.[64] The clinical relevance of these distinctions is that patients with ADHD may have improved attention and less distractibility and restlessness but still be disorganized. If the clinician believes the disorganization is a residual ADHD symptom, the clinician may respond by increasing the dose of ADHD medication, only to find no further benefit but more side effects. These residual executive dysfunction symptoms tend not to improve with escalating medication dosing.

Results from 2 large trials indicate that adults with ADHD who experienced improvements in executive function with stimulant treatment also experienced improvements in health-related quality of life, particularly in the domains of performance and function.[65] However, a clinical trial of adults with ADHD found that the presence of executive function deficits, as assessed by standardized neuropsychological testing, did not affect clinical response to treatment with osmotic controlled-release oral delivery system (OROS) methylphenidate, and that measures of executive function were not affected by treatment response.[66] The need to better define executive function deficits so that an accurate assessment can be determined is critical; the means to minimize such impairments can be challenging.

Some patients might benefit from adjunctive therapy to address executive function deficits. Research in children and adolescents suggests that the concurrent use of stimulant and nonstimulant therapies can afford significantly greater improvements in ADHD symptoms than stimulant monotherapy, although some combinations have been associated with an additive adverse effect burden and higher cost.[67;48]

Many clinicians recommend cognitive behavior therapy (CBT) or other forms of psychotherapy once the patient has been stabilized on pharmacotherapy. CBT and other interventions can help the patient address organization skills and self-efficacy that have evolved over many years of insufficient treatment for ADHD; it can help patients develop effective compensatory strategies and improve other functional impairments typically associated with ADHD.[68,69] CBT may also help the subset of patients who choose not to use medications (or for whom medications are not appropriate or intolerable), as well as the large proportion of patients who have comorbid conditions.[70] Research suggests that adding CBT may enhance the response to and benefits of pharmacologic treatments.[68]

Metacognitive therapy uses principles and methods of CBT to teach time management, organization, and planning skills, and to address depressive and anxious thoughts that undermine effective self-management. Solanto and colleagues[71] compared a 12-week course of group metacognitive therapy (N = 41) with supportive therapy (including nonspecific group support and validation, psychoeducation, and therapist attention; N = 38) in adults with ADHD. They found that metacognitive therapy provided significantly more benefit in adults with ADHD “with respect to inattention symptoms that reflect the specific functions of time management, organization, and planning.” These benefits were seen in patients who were receiving medication treatment as well as those who were not.

When appropriate, patients may also benefit from couples or family counseling or both, and life skills training or coaching. A review of studies of group and individual psychosocial treatments for adult ADHD found that various psychosocial therapies, including skills-training and psychoeducation, improved motivation and reduced residual symptoms in adults with ADHD.[72]

ADHD and Substance Use Disorders

Up to 75% of adults with ADHD have had at least one comorbid condition,[13] and 40% of adults with ADHD present with a concurrent comorbidity.[73] The high rate of comorbid psychiatric conditions — particularly anxiety disorders, mood disorders, and SUDs — can influence both diagnosis and treatment of ADHD as well as the other condition(s). A significant number of adults with ADHD have a comorbid mood disorder, and a significant proportion of adults with mood disorders have comorbid ADHD.[74] As many as 50% of adult patients with ADHD have had comorbid SUDs.[23] Consequently, clinicians should maintain a high index of suspicion for ADHD among patients with any mental health concern because of its high prevalence in these subpopulations.[75,13]

Evidence suggests that ADHD is a significant risk factor for the development of both SUDs and cigarette smoking.[76] A recent meta-analysis and meta-regression analysis suggests that nearly 1 in 4 patients with SUD met DSM criteria for comorbid ADHD,[77] and 10% to 30% of adults with ADHD have SUD.[78] Alcohol dependence is associated with higher ADHD prevalence than cocaine dependence.[77] Substance use, including cigarette smoking, begins at an earlier age among adults with ADHD,[79] and SUDs are generally more severe in patients with comorbid ADHD.[16] Moreover, SUD may manifest with self-control, attention, and behavioral symptoms similar to those seen in ADHD. The prognosis for patients with ADHD and SUD worsens with additional comorbidities. Adolescents with ADHD and comorbid major depression generally have more severe substance use at baseline and throughout treatment compared with nondepressed adolescents with ADHD and SUD.[80]

Concerns that children treated for ADHD with stimulants are at elevated risk for developing SUD have not been supported by the research. A naturalistic, controlled, 10-year follow-up study of 112 boys and men over 10 years and found no statistically significant associations between stimulant treatment and alcohol, drug, or nicotine use disorders.[81] The investigators concluded that the risk for subsequent SUD is neither increased nor decreased in individuals treated with stimulants for ADHD during childhood and adolescence.

ADHD Comorbidity

It is estimated that only 25% of adult ADHD cases are uncomplicated.[26] In addition to SUD, ADHD has a high comorbidity with mood and anxiety disorders. Data from the NCSR indicate that 9.4% of adults with MDD have ADHD, as do 22.6% of adults with dysthymia.[5] The lifetime prevalence of anxiety disorders among adult patients with ADHD is 40% to 60%.[23] ADHD has been identified in 21.2% of adults with bipolar disorder,[5] and the presence of ADHD may increase the risk of developing bipolar disorder.[17] Many patients do not have just 1 comorbid diagnosis; diagnosing patients with SUD and comorbid psychiatric disorders can be particularly challenging because of the high rate of symptom overlap.

The numerous similarities in clinical presentation among these psychiatric disorders can interfere with accurate diagnosis. For example, symptoms of both ADHD and depression may include trouble sleeping, eating, and concentrating; patients with MDD, ADHD, or GAD may be restless and fidgety. It is important to obtain a comprehensive evaluation for child and adult symptoms, including the temporal relationship between the various comorbid disorders.[82] A primary complaint of a consistent negative mood for 3 months is more suggestive of MDD than ADHD, whereas a report of persistent poor concentration and lack of motivation dating from childhood is more consistent with ADHD. Poor concentration and anhedonia following a depressive episode suggests MDD; poor concentration, depression, organizational problems, and impulsivity that are long-standing suggest ADHD.[17] The clinical presentation of MDD is not affected by comorbid ADHD.[23] Clinicians need to distinguish between a lack of motivation suggestive of ADHD, dysregulated mood and irritability that might indicate ADHD with comorbid mood disorder, and significantly low affect symptomatic of depression.[17] The psychotic symptoms present in bipolar disorder are not likely to be misdiagnosed as ADHD; patients with ADHD do not report a cyclic pattern to their symptoms.[28] Primary care physicians who suspect bipolar disorder, or a manic or hypomanic episode, may want to refer the patient to a specialist, particularly if the patient is diagnosed with comorbid ADHD.

What to Manage First?

Identifying the primary disorder can be particularly challenging in adults with ADHD, as many comorbidities have an onset in mid-to-late-adolescence and these individuals have had many years of dealing with their disorders. In patients with active substance abuse, experts recommend that SUD be considered the primary diagnosis and treated first, regardless of age; once the SUD is under control, clinicians can then reassess the patient to determine whether the presenting symptoms were caused by the SUD, comorbid ADHD, or a mood disorder.[17,38] This strategy is based on controlled studies suggesting that treatment for ADHD in patients with comorbid active SUDs has little effect on either ADHD symptoms or substance use.[83] Adults with SUD who require treatment for ADHD cannot be treated with stimulants until they are in recovery treatment, as stimulants are contraindicated for patients who are actively using addictive substances. However, in adults with comorbid SUD, ADHD can be treated with FDA-approved nonstimulants such as atomoxetine or off-label bupropion, tricyclic antidepressants, or modafinil.[84] Stimulants, preferably long-acting formulations, can be used once patients are in stable substance use remission.

In adults, severe psychiatric mood or anxiety disorders are treated before treating ADHD, whereas ADHD is typically treated prior to initiating treatment for other psychiatric disorders of mild to moderate severity. In some cases, treating ADHD will help resolve the mild or moderate symptoms of the other psychiatric disorders. Clinicians must perform an adequate screen in adult patients with ADHD suspected of comorbid depression to rule out bipolarity. It is recommended that patients with comorbid bipolar disorder and ADHD be treated with mood stabilizers or atypical antipsychotics before initiating treatment with stimulants, which can destabilize bipolar symptoms.[85] Patients with comorbid ADHD and MDD can be treated with a stimulant and an antidepressant, particularly selective serotonin reuptake inhibitors (SSRIs).[74] Stimulants can be administered with serotonin-norepinephrine reuptake inhibitors (SNRIs), but this combination needs to be closely monitored for sympathomimetic side effects.[13] However, when atomoxetine is co-administered with SSRIs, one should be mindful of potential kinetic interactions through the cytochrome P450 enzyme system.

ADHD Treatment for Patients in Stable Recovery

Guidelines support and encourage treatment of ADHD in patients with SUD.[2,17,37,38] Indeed, optimal treatment for ADHD may improve adherence to treatment for SUD. Pharmacotherapy choices for adult patients in stable recovery can follow usual adult recommendations. Stimulants are more effective than nonstimulants for adult ADHD[86]; however, stimulants may be diverted or abused. These risks are lower for long-acting stimulants approved for adult ADHD (OROS methylphenidate, dexmethylphenidate XR, mixed amphetamine salts, and lisdexamfetamine) than for the short-acting agents.[83] At this time, atomoxetine is the only nonstimulant treatment approved for adult ADHD. The nonstimulant α-2 receptor agonists guanfacine XR and clonidine ER have not been studied in adults; their use is currently off-label in this population.


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  86. Faraone SV, Glatt SJ. A comparison of the efficacy of medications for adult attention-deficit/hyperactivity disorder using meta-analysis of effect sizes. J Clin Psychiatry. 2010;71:754-763.

Taking Charge of Adult ADHD-R. Barkley

In ADHD, Brain studies, School Psychology on Wednesday, 12 September 2012 at 06:38

Here is some general information regarding ADHD in adults.  For an incredibly informative and helpful read, please look to Russell Barkley’s book “Taking Charge of Adult ADHD.”  I highly recommend it for anyone who wants to know more about ADHD, has been diagnosed with ADHD (child or adult), or treats those with ADHD.


What the research shows about the causes of ADHD: Studies of twins and families have made it abundantly clear that genetic factors are the major causes of ADHD. If a child has ADHD, nearly one out of three siblings will also have ADHD. A study done at UCLA examined 256 parents of children with ADHD and found that 55% of these families had at least one parent affected by the disorder. An estimated 75–80% of variation in the severity of ADHD traits is the result of genetic factors, and some studies place this figure at over 90%—higher than the genetic contribution to personality traits, intelligence, and other mental disorders such as anxiety and depression and nearly the same as the genetic contribution to individual differences in height. Several recent studies have scanned the entire human genome searching for genes that carry the risk of ADHD and have found at least 20 to 25 sites on chromosomes to be associated with ADHD. It is therefore likely that ADHD arises from a combination of multiple risk genes, with each contributing a small likelihood of risk for the disorder. The more risk genes you inherit, the greater the number and severity of ADHD symptoms, and so the greater the probability you will be impaired by and diagnosed with the disorder. A very small number of cases are caused by early-development (often prenatal) neurological injury, such as alcohol and tobacco exposure during pregnancy, premature delivery, especially with minor brain hemorrhaging, early lead poisoning, stroke, and frank brain trauma, to name just a few. The frontal lobes, basal ganglia, cerebellum, and anterior cingulate cortex are 3–5% smaller in people with ADHD than in others of the same age and substantially less active. Studies show that the brains of those with ADHD react to events more slowly than the brains of those without ADHD. People with ADHD have less blood flow to the right frontal region of the brain than those who don’t have ADHD, and severity of symptoms increases the more blood flow is reduced.

What the research says about popular myths regarding the causes of ADHD: Available evidence suggests that sugar plays no role in the disorder and that fewer than 1 in 20 preschool children with ADHD may have their symptoms worsened by additives and preservatives. No compelling evidence exists to support the claim that ADHD results from watching too much TV or playing too many video games as a child, other than that people growing up with ADHD may be more likely to watch television or play video games. Little evidence has emerged that child-rearing practices can cause ADHD. There is no question that families with children having ADHD show more conflict and stress than other families. But researchers found that this was largely due to the impact of the child’s ADHD in disrupting family functioning and also to the likelihood that the parent also had ADHD.

PREPARE BY KNOWING WHAT TO EXPECT AND WHAT TO TAKE ALONG Here are the typical elements in a diagnostic evaluation:  Collection of rating scales and referral information before or during the evaluation  An interview with you  A review of previous records that may document your impairments  Psychological testing to rule out general cognitive delay or learning disabilities  Interviews with others who know you well to corroborate your reports  A general medical examination when medication might be part of your treatment or coexisting medical conditions need to be evaluated (if your physician hasn’t already done this) What you can take along to facilitate these steps:  Any records you have or can collect in advance from schools you attended and physicians and mental health professionals you’ve seen, any driving and criminal records, and any other documentation of problems that could be related to ADHD or another disorder  The names of a few people who know you well and whom you trust to speak honestly and objectively with the evaluators  Results of a medical exam if you’ve already had one from your physician  A list of family members with mental disorders you know about  A description of impairments during childhood and adolescence, as well as more recent ones

Here’s how the anti-ADHD medications work neurogenetically: Brain imaging, EEGs, and a variety of other testing methods have shown that the brains of those with ADHD are different from those of others in several important ways: Certain regions of the brain are different structurally, mainly being smaller than in those without ADHD: the right prefrontal region, associated with attention and inhibition; the striatal region, associated with pursuing pleasurable or rewarding behavior; the anterior cingulate cortex, which helps you govern or self-regulate your emotional reactions; and the cerebellum, associated with the timing and timeliness of your actions, among other executive functions. People with ADHD have less electrical activity in the brain, particularly in these regions, meaning they don’t react to stimulation in these regions as much as others. Children and adolescents with ADHD also have less metabolic activity in the frontal regions. The brains of those with ADHD seem to be deficient in or show excessive reuptake of norepinephrine and dopamine. Other neurochemicals may also be involved. Scientists believe the structural abnormalities in the ADHD brain underlie the development of the disorder: this is the genetic legacy that causes ADHD to appear in the descendants of those who have ADHD. We don’t know how to restore a typical structure to these brains. We do, however, know how to correct the neurochemical imbalance found in those with ADHD, at least temporarily: medication. When the neurotransmitters dopamine and norepinephrine are not available in the same measure as they are in typical adults, the messages these chemicals are supposed to send don’t get through as they should. Without the help of these neurotransmitters, the brain does not respond to stimulation (any input, like an event or an idea or an emotion) the way it should. Impulse control doesn’t kick in when it should. Memories of the past and visions of the future aren’t triggered to keep you mentally on track. And even when they are, they cannot be sustained for very long, leading you to forget what it is you were planning on doing. The motor-control brakes don’t keep you from fidgeting with restlessness. This is why ADHD medications work (though some operate on other neurochemicals). By causing nerve cells to express more of these neurochemicals, or by keeping the nerve cells from pulling them back in once they’ve been released, they increase communication between nerve cells in regions of the brain linked to ADHD. The two basic categories of drugs approved by the U.S. Food and Drug Administration for use with adults who have ADHD—stimulants and a few nonstimulants—boost your mind’s ability to respond to whatever is going on in your day.


Barkley, Russell A. (2011-04-04). Taking Charge of Adult ADHD.  Guilford Press. Kindle Edition.

Neurogenesis and Depression/Stress

In Brain studies, Neurogenesis on Monday, 10 September 2012 at 14:27


Impaired adult neurogenesis leads to depression – is it realistic?


Jason Snyder | 08/31/2012

About a year ago we published a paper linking adult neurogenesis to depression. A causal sort of ‘linking’, right? I mean, we found that, when adult neurogenesis was eliminated, mice had elevated glucocorticoids in response to stress and showed depressive-like behaviours1. So doesn’t this mean that impaired adult neurogenesis could lead to depression in humans, in the real world?

Well, it could…and we did end our paper with the following:

Because the production of new granule neurons is itself strongly regulated by stress and glucocorticoids, this system forms a loop through which stress, by inhibiting adult neurogenesis, could lead to enhanced responsiveness to future stress. This type of programming could be adaptive, predisposing animals to behave in ways best suited to the severity of their particular environments. However, maladaptive progression of such a feed-forward loop could potentially lead to increased stress responsiveness and depressive behaviours that persist even in the absence of stressful events.

We had to end it somehow – I was just happy that after 3 years of work we were DONE2! But our final speculation makes it clear that, while this chapter may be done, the story is not. And this fact was rightly pointed out in a recent commentary by Lucassen et al. in Molecular Psychiatry3, where they continue the discussion and bring up some good points. Here is a loose elaboration on some of the outstanding issues they bring up.

Is a feed-forward cascade plausible? In other words, is it possible that stress reduces neurogenesis, which leads to a hyperactive HPA response, which further reduces neurogenesis, thereby additionally increasing the stress response etc etc, eventually damaging the brain and leading to depression? As Lucassen et al point out, stress typically reduces neurogenesis by only ~30% which is much smaller than the 100% reduction seen in our transgenic mice. Could a 30% reduction be enough to initiate this vicious cycle? What if it was chronic? People have looked in the past and not observed HPA alterations after smaller (but also equally large) reductions in neurogenesis, so the answer might appear to be negative. But there are many important differences between studies, including when stress hormones were measured (e.g. baseline or after stress) as well as factors such as life history, genetic makeup, and stressor controllability, as is suggested in the commentary. Of course, in reality, chronic stress has multiple effects throughout the hippocampus (and brain) and so the development of depression is certainly due to additive effects (this is both their sentiment and mine). And so perhaps in the real world a more modest reduction in neurogenesis does have the potential to tip the scales towards depression, if it is coupled with other (which?) pathologies.

How could so few adult-born neurons regulate the HPA axis? Depending on my mood, my thoughts on this question fluctuate quite a bit. Half of the time I think “This is ridiculous” and the other half of the time I look at the evidence and think “Heck yeah. Maybe4.” (see our recent review for more detailed arguments on the heck yeah side of things). In our study we reduced neurogenesis for up to 12 weeks, preventing about 50,000 cells from being added or 10% of the total population. More important than sheer numbers, however, is the ever-increasing evidence that adult-born neurons are different from mature neurons – more plastic, more excitable, uniquely neuromodulated. Some of the most intriguing evidence comes from one of the authors themselves who has shown that even 4 month old neurons (but potentially older?) undergo extensive structural modification following learning whereas perinatal-born cells do not. We have estimated that ~40% of the total granule cell population is added in adulthood in the rat and so my point is that in the real world we have to consider that there are probably cumulative effects of adult neurogenesis over years, and even decades in humans. And so the population of adult-born cells, and its functionality, may not be so small in the end.

Do new neurons sense detect stress through glucocorticoids? One common assumption is that glucocorticoid receptors are necessary for inhibition of the HPA axis…but must that always be the case? By 1-2 weeks of age the majority of adult-born neurons do express MRs and GRs and therefore certainly could directly detect glucocorticoid levels and initiate a shutting down of the HPA axis. But perhaps new neurons process stressful information that is relayed through glutamatergic pathways. In this scenario new neurons might not be required for sensing glucocorticoids and initiating negative feedback. Instead, after being stressed, they could be required for biasing the animal away from the negative experience (akin to perceiving a change in context, similar Opendak & Gould’s proposal for reconciling stress and memory hypotheses of new neuron function) which might reduce CNS drive on the HPA axis. This opens the door to the possibility that the HPA and behavioural roles of adult neurogenesis are somewhat dissociable, in which case a role for new neurons in the development of depression is not (only) through the feedforward cascade hypothesis but through direct effects on behaviour. This might also help explain the inconsistent links between stress hormones, hippocampal volume, and depression that plague the stress-depression literature.

So, we showed that adult-born neurons are required (in mice) for normal stress responses and emotional behaviour. Our final speculation was, well, just that – a leap towards the next big question. Maybe realistic, maybe not. Maybe a component of the real picture. In any case, the route has been mapped.


Lucassen PJ, Fitzsimons CP, Korosi A, Joels M, Belzung C, & Abrous DN (2012). Stressing new neurons into depression? Molecular psychiatry PMID: 22547116

Snyder JS, Soumier A, Brewer M, Pickel J, & Cameron HA (2011). Adult hippocampal neurogenesis buffers stress responses and depressive behaviour. Nature, 476 (7361), 458-61 PMID: 21814201


1You thought this footnote was going to be some comment on human depression vs. depressive-like behaviour in animal models but instead I just wanted to mention that, now that I’ve moved back to Canada, I feel compelled to use ‘behaviour’ instead of ‘behavior’ and it feels silly because the same people read this stuff no matter which country I’m in when I write it.

2Is there an emoticon for dusting the dirt off your hands, blowing smoke away from the tip of a revolver, or enjoying a refreshing beverage after chopping a bunch of wood or giving birth? Insert it here.

3One of the authors having actually commented on this blog (!), and who is 1st author on what looks to be a very interesting paper that is related to this whole discussion.

4I may be a pessimist. Realist? A guy with a healthy amount of skepticism?

5The photo? It’s a depression.

Neurogenesis…never ceases to amaze me.

In Brain imaging, Brain studies, Neurogenesis on Sunday, 9 September 2012 at 08:17

We have come very far from the faulty belief that the birth of new neurons only occurred in developing organisms.  Now, it is a fairly known phenomenon.  One we probably would have eschewed years ago.

Neurons, neurons…how they do grow!

I like this blog about neurogenesis and hope you do as well!




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