What goes wrong in the brain when someone can't spell

By studying stroke victims who have lost the ability to spell, researchers have pinpointed the parts of the brain that control how we write words.

"When something goes wrong with spelling, it's not one thing that always happens—different things can happen and they come from different breakdowns in the brain's machinery," said lead author Brenda Rapp, a professor in the Department of Cognitive Sciences. "Depending on what part breaks, you'll have different symptoms."In the latest issue of the journal Brain, Johns Hopkins University neuroscientists link basic spelling difficulties for the first time with damage to seemingly unrelated regions of the brain, shedding new light on the mechanics of language and memory.

Rapp's team studied 15 years' worth of cases in which 33 people were left with spelling impairments after suffering strokes. Some of the people had long-term memory difficulties, others working-memory issues.

With long-term memory difficulties, people can't remember how to spell words they once knew and tend to make educated guesses. They could probably correctly guess a predictably spelled word like "camp," but with a more unpredictable spelling like "sauce," they might try "soss." In severe cases, people trying to spell "lion" might offer things like "lonp," "lint" and even "tiger." With working memory issues, people know how to spell words but they have trouble choosing the correct letters or assembling the letters in the correct order—"lion" might be "liot," "lin," "lino," or "liont."

The team used computer mapping to chart the brain lesions of each individual and found that in the long-term memory cases, damage appeared on two areas of the left hemisphere, one towards the front of the brain and the other at the lower part of the brain towards the back. In working memory cases, the lesions were primarily also in the left hemisphere but in a very different area in the upper part of the brain towards the back.

"I was surprised to see how distant and distinct the brain regions are that support these two subcomponents of the writing process, especially two subcomponents that are so closely inter-related during spelling that some have argued that they shouldn't be thought of as separate functions," Rapp said. "You might have thought that they would be closer together and harder to tease apart."

Though science knows quite a bit about how the brain handles reading, these findings offer some of the first clear evidence of how it spells, an understanding that could lead to improved behavioral treatments after brain damage and more effective ways to teach spelling.

Inflammation attacks brain's reward center

A new study by Neil Harrison and colleagues published in Biological Psychiatry suggests that a brain reward center, the striatum, may be directly affected by inflammation and that striatal change is related to the emergence of illness behaviors.   

Inflammation increases the risk for depression.

More specifically, inflammation induces behavioral changes similar to depression that are often associated with illness, including fatigue, difficulty concentrating, lack of motivation, and reduced experience of pleasure.  

The authors recruited 23 patients with hepatitis C who were beginning treatment with interferon-alpha (INF-α). This treatment provokes an immediate inflammatory response, confirmed by measuring cytokines in the blood.  

Four hours after INF-α administration, a specialized type of imaging, called magnetization transfer imaging, was performed that showed evidence of microstructural changes in the striatum when compared to scans conducted prior to INF-α administration. This suggests that the striatum is highly sensitive to IFN-α.  

IFN-α also induced fatigue and depression in the patients, particularly over weeks 4 through 12 of treatment. Interestingly, the early striatal structural change predicted the later emergence of fatigue, but not depression, in the study participants.  

Changes in the striatum were heterogeneous with some changes associated with the risk for fatigue, while other changes seemed to be protective against developing fatigue.  

"Inflammation-related fatigue and depression are big clinical problems," said Dr. John Krystal, Editor of Biological Psychiatry. "This study highlights that the brain regions central to reward and motivation are directly altered by inflammation in ways that that appear to predispose or protect against developing fatigue but not depression. The heterogeneous striatal response may suggest that fatigue and mood are supported by different microcircuits within the striatum."  

"These findings are important as they show that a relatively simple MRI technique can be used to measure effects of inflammation on the brain," Harrison commented. "Inflammation is increasingly implicated in the cause of common mental illnesses, particularly depression. This technique could be a powerful way to identify patients who are most sensitive to effects of inflammation on the brain. It could also be used to monitor response to novel anti-inflammatory therapies that are now being tested in depression."

Top 15 Neuroscience Jokes

We know neuroscientists are a fun group, so it didn’t surprise us that there are so many great jokes out there. Here’s a collection of our favorites. Take some notes and be prepared to share with your colleagues!

What’s your favorite neuroscience joke? If you don’t see it below, we encourage you to include it in a comment!

1. What is a sleeping brain’s favorite musical group (rock band)? REM.
2. What does a brain do when it sees a friend across the street? It gives a brain wave.
3. What did the neuron say to the glia cell? “Thanks for the support!”
4. What do neurons use to talk to each other? A cellular phone. 
5. What did the stimulus do to the neuron after they got married? Carried it over the threshold.
6. If some of Fred Flintstone’s neurotransmitters could talk, what would they say? “GABA-daba-doo!”
7. How did the mother know her son would become a neuroanatomist? He was always staining things.
8. What did the angry brain say to the nociceptor? “You’re a real pain.”
9. Why does the spinal cord belong in the brass section of an orchestra? Because it has dorsal and ventral horns.
10. What did the hippocampus say during its retirement speech? “Thanks for the memories.”
11. What do you call a skull without 1 billion neurons? A no-brainer.
12. What did parietal say to frontal? “I lobe you.”
13. What happens when a neurotransmitter falls in love with a receptor? You get a binding relationship. 
14. What do you call a group of brains who form a singing group? A glia club.
15. What does a neuroscientist order at a bar? A spiked drink. 

Brain study suggests consciousness a matter of optimal degree of connectedness in neural network

Loss of cortical integration and changes in the dynamics of electrophysiological brain signals characterize the transition from wakefulness towards unconsciousness. In this study, we arrive at a basic model explaining these observations based on the theory of phase transitions in complex systems. We studied the link between spatial and temporal correlations of large-scale brain activity recorded with functional magnetic resonance imaging during wakefulness, propofol-induced sedation and loss of consciousness and during the subsequent recovery. We observed that during unconsciousness activity in frontothalamic regions exhibited a reduction of long-range temporal correlations and a departure of functional connectivity from anatomical constraints. A model of a system exhibiting a phase transition reproduced our findings, as well as the diminished sensitivity of the cortex to external perturbations during unconsciousness. This framework unifies different observations about brain activity during unconsciousness and predicts that the principles we identified are universal and independent from its causes.

 

A team of European researchers has found evidence that suggests that human consciousness is a state where the neural network that makes up the brain operates at an optimal degree of connectedness. In their paper published in Journal of the Royal Society Interface, the team describes their study of the human brain using volunteers undergoing fMRI scans while succumbing to the effects of an anesthetic that caused them to lose consciousness, and what was revealed in reviewing the scan data.

Human beings, when awake, exist in a state of consciousness that is uniquely difficult to define. Scientists try by agreeing that it is the ability to have subjective experiences and to enjoy a first-person perspective on the "reality" of the world. But that does not explain the voice that is our own self, nor the varying degrees of consciousness, such as the differences between being asleep, versus partially awake, versus being completely unconscious. In this new effort, the researchers sought to learn more about the state that exists in the mind when consciousness occurs by enlisting the assistance of 12 volunteers who agreed to be made unconscious by the drug propofol, normally used to put people under during surgical procedures (and notably, also the drug that led to the death of singer Michael Jackson) while undergoing fMRI scans.

Scientists (and surgeons) believe that propofol causes people to become completely unconscious, which by definition would mean to become incapable of processing thoughts. The brain should not be able to process pain signals, for example, thus making surgery a pain free experience. To gain a better perspective on the various states of consciousness, the team watched blood flow changes in the brains of the volunteers as they moved from a conscious state, to unconsciousness and then back to consciousness.

In studying the scans, the researchers found that when the volunteers were conscious, there was what they describe as "a flurry of ever-changing activity," with a lot of activity between the various neural networks. In contrast, they found that while unconscious, the brains of the volunteers were engaged in far less interconnectivity and were less variable over time.

These findings, the team suggests, show that consciousness in the brain is merely, in a physical sense, a state where there is an optimal level of neural network connectedness.

Asthma vs. COPD, similar symptoms—different causes and treatment

Coughing, wheezing and shortness of breath are symptoms asthma sufferers are used to. They are also the symptoms of chronic obstructive pulmonary disease (COPD). For sufferers, as well as physicians, it can be difficult to tell the difference between the two conditions.
According to a presentation at the American College of Allergy, Asthma and Immunology (ACAAI) Annual Scientific Meeting, as many as 50 percent of older adults with obstructive airway disease have overlapping characteristics of asthma and COPD. And this percentage increases as people get older.
"Based on symptoms alone, it can be difficult to diagnose COPD vs. asthma. The pathway to a diagnosis of COPD or asthma - smoking vs. a long-term persistence of asthma - can be quite different," said allergist William Busse, MD, ACAAI fellow and presenter. "In every patient, but in older patients in particular, we need to take a thorough history and perform a physical examination, as well as measurements of lung functions. In patients with COPD and asthma, the changes in lung function may be severe, and it is not often readily apparent, which is the predominant, underlying condition - asthma or COPD. Treatment will differ depending on diagnosis."
Lung function changes in asthma are due to airway inflammation, and treatment is directed at reducing inflammation with corticosteroids - largely, inhaled corticosteroids. But the changes in lung function associated with COPD are caused by cigarette smoking and, except with an exacerbation, are not particularly responsive to corticosteroids.
"The primary treatment in COPD is bronchodilators, including long-acting beta agonists. They help relax muscles around the airways in the lungs, allowing air to flow more freely," said allergist Michael Foggs, MD, ACAAI president. "They should not be given alone to people with asthma. In COPD, but not asthma, inhaled corticosteroids have been associated with an increased risk for pneumonia and in some cases, features of both asthma and COPD exist. For these patients a combination of inhaled corticosteroids and long-acting beta agonists is usually best."
Some treatments for COPD and asthma are similar. Bronchodilators are used for both conditions. Other treatments tend to be more condition-specific. People with asthma are encouraged to avoid their personal triggers, like keeping pets out of the home or avoiding the outdoors when allergen concentrations are high. While people with COPD are also encouraged to avoid triggers, the emphasis in this condition is to stop smoking. Similarly, if a patient has
asthma , smoking makes the underlying disease worse and reduces the response to inhaled corticosteroids .
Allergists who treat these conditions recognize that each patient, and their symptoms, must be treated according to their unique set of circumstances. People need to tell their allergists all their symptoms and complete medical history in order to receive the correct diagnosis and appropriately tailored therapy.

Severe asthma patients less responsive to treatment

People with severe asthma, who are often described as 'steroid-dependent', are actually less likely to respond to the treatment they depend on, when compared to people with mild asthma.
The study, presented at the European Respiratory Society (ERS) Annual Congress in Barcelona today (9 September 2013), represents the first analysis of a cohort of patients from an unparalleled research project that will collect over 3 million samples from 300 children and 700 adults with severe and non- severe asthma , and without asthma.
Although asthma is common, it is not widely known that there are different types of the condition. Experts don't yet understand why some people suffer a more severe form of the disease than others.
The EU-funded U-BIOPRED project is looking at how severe asthma differs from one person to another in the hope of categorising the disease into sub-groups. The aim is for researchers to develop more personalised medicine, which treats the specific disease in each specific individual.
The results of this initial study have described common characteristics found among children and adults with severe asthma. The key findings include:
In adults
55% of adults with severe asthma took regular oral corticosteroids and yet showed greater airway obstruction than the mild/moderate cohort.
Patients with severe asthma still experienced exacerbations and severe symptoms despite taking high doses of the corticosteroids. In children
The level of airway obstruction in severe and mild/moderate asthma was similar.
The severe asthma group had higher FeNO levels (fraction exhaled nitric oxide), which is a measurement used to diagnose asthma.
David Gibeon, lead author of this study from Imperial College, London, said: "We would like to understand why people with more severe asthma are less responsive to the effects of corticosteroids. Our parallel work on the ways in which patients with asthma respond to corticosteroid treatment, which is a commonly-used treatment for asthma, show that asthmatics may become less responsive to this treatment in many different molecular ways. This initial analysis will provide an overview of the groups which exist within asthma, which will help us develop a more personalised approach to treating the individual patient with asthma."
A second study from the U-BIOPRED project was also presented at the meeting. This investigated the use of an electronic nose platform to analyse breath samples of asthma patients. The aim was to classify patients based on their exhaled molecular patterns rather than on traditional clinical characteristics. The study included breath samples from 57 patients and was able to find common patterns within four sub-groups of severe asthma patients. The findings represent a further step towards a biological classification of severe asthma and the development of more specific treatments for different groups of
asthma patients.
Peter Sterk, project lead for U-BIOPRED, said: "The findings of both these studies take us one step closer to understanding more about severe asthma . We know that people with this condition suffer from repeated exacerbations of symptoms and do not respond as well to treatment, but we don't know why this is the case. In order for us to help improve the lives of these people, we need to make a full biological and clinical "fingerprint" of each patient, by embarking on a huge analysis of data including a wide-range of samples from CT scans, to sputum samples, analysis of a person's genetics and results from bronchoscopies. The U-BIOPRED project is doing that and we are confident that it will take us one step closer to developing personalised treatment for this condition."

Do asthma and COPD truly exist?

Obstruction of the lumen of a bronchiole by mucoid exudate, goblet cell metaplasia, and epithelial basement membrane thickening in a person with asthma.
Defining a patient's symptoms using the historical diagnostic labels of asthma and chronic obstructive pulmonary disease (COPD) is an outdated approach to understanding an individual's condition, according to experts writing in the
European Respiratory Journal today (Feb. 1, 2016).
In a perspective article, Professor Alvar Agusti and colleagues call for a new approach to patient management, which moves away from categorising patients using the broad disease terms of asthma and COPD and towards a more personalised approach to management that identifies 'treatable traits' in each patient.
Hospitalisation rates for COPD are continuing to increase and a majority of asthma patients live with significant symptoms, impairing their quality of life. While the labels of asthma and COPD are valuable for patients who display stereotypical symptoms, there are a growing number of patients who do not fit this category, including patients with adult-onset asthma, smoking asthmatics, or patients with the so-called asthma-COPD overlap syndrome.
In the past 30 years, new technologies have developed, providing clinicians with a range of tools to allow them to observe a patient and define that patient's condition. Previously, understanding a patient's condition relied on analysis of symptoms and signs, such as lung function measurements and airway hyper-responsiveness, but now clinicians can access information about a range of other underlying complex biological traits, including cellular and molecular traits. This could include measures such as CT scanning, cellular and molecular markers taken from blood samples, sputum and exhaled air and microbiome anaylsis.
Professor Agusti commented: "We propose a label-free precision medicine approach based on treatable traits that categorise the clinical and biological complexity of airway disease. The approach we are suggesting would radicalise healthcare and have significant implications for the organisation of a healthcare system. By recognising the clinical and biological complexity of a disease, we can use causal mechanistic disease pathways to adopt a more precise approach, which is hopefully more effective at managing patients with these conditions."
In an accompanying editorial, Professor Peter Sterk, from the University of Amsterdam, supports the call for a move away from diagnostic labels. Professor Sterk commented: "We are living in an era where we have new biological knowledge and new targets for therapy but we largely continue to guide patient management with diagnostic labels. It is the right time for healthcare professionals to take bold steps and move aware from historical diagnoses that are impeding modern medicine."