Lindsey Kay, MD – Brain Blogger http://brainblogger.com Health and Science Blog Covering Brain Topics Wed, 30 May 2018 15:00:03 +0000 en-US hourly 1 https://wordpress.org/?v=4.9.6 Using Infrared Light to Diagnosis Alzheimer’s http://brainblogger.com/2008/06/17/using-infrared-light-to-diagnosis-alzheimers/ http://brainblogger.com/2008/06/17/using-infrared-light-to-diagnosis-alzheimers/#comments Tue, 17 Jun 2008 13:08:02 +0000 http://brainblogger.com/?p=842 Neuroscience and Neurology CategoryThe definitive diagnosis of Alzheimer’s disease requires microscopic examination of brain tissue, something that cannot be performed safely in a living patient. Instead, physicians use a constellation of symptoms and patterns of progression, combined with exclusion of all other causes of dementia, to diagnosis patients with the disease. But there are many alternative causes of memory loss in the elderly that must be excluded in order to make the diagnosis of Alzheimer’s. Many of these have signs and symptoms that overlap, making it difficult to determine the correct diagnosis.

Because each of these disorders is treated differently, with some responding well to specific therapy, it is imperative to determine the true underlying cause of a patient’s symptoms.

lBrain cellNear-infrared optical spectroscopy may provide some help in clarifying this problem. This type of light is nonionizing and travels safely through the brain tissue with no adverse effects. The light is scattered by the physical components of the brain, and the brains of Alzheimer’s patients scatters this light differently, allowing for a noninvasive and simple diagnosis.

Currently, the diagnostic finding in Alzheimer’s disease is the presence of amyloid plaques and neurofibrillary tangles, which are only visible under the microscope. The amyloid plaques accumulate as the disease progresses, and this plaque accumulation affects the way near-infrared light scatters when it hits the brain. Optical spectroscopy detects the pattern of light scatter in living patients without the need for biopsy or invasive procedure.

Researchers used this technique recently to accurately predict the presence or absence of Alzheimer’s associated amyloid plaques in brain tissue. The technique is currently being studied in living patients to determine its viability as a diagnostic and prognostic tool.

In addition to allowing for accurate differentiation from other causes of dementia, near-infrared optical spectroscopy may also be used to detect the disease at an earlier state, before symptoms are apparent, and allow for early initiation of therapy. It could also prove useful as a measurement of response to treatment and as a method of following Alzheimer’s patients over time.

Reference

Hanlon, E.B., Perelman, L.T., Vitkin, E.I., Greco, F.A., McKee, A.C., Kowall, N.W. (2008). Scattering differentiates Alzheimer disease in vitro. Optics Letters, 33(6), 624. DOI: 10.1364/OL.33.000624

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Interactive Effects of Genetics on Depression http://brainblogger.com/2008/06/04/interactive-effects-of-genetics-on-depression/ http://brainblogger.com/2008/06/04/interactive-effects-of-genetics-on-depression/#comments Thu, 05 Jun 2008 03:54:22 +0000 http://brainblogger.com/?p=834 Psychiatry and Psychology CategoryIt is well known that depression results from the combination of many different factors. Environmental effects, such as stressful life events, are a trigger in many patients for the development of major depressive disorder (MDD) and the milder disorder, dysthymia. It is also true that the same major stressors will not produce depressive symptoms in some, pointing to underlying risk factors that make some more susceptible to depression than others. Researchers have attempted to identify a single gene that can be linked to MDD, and while familial clustering of depressive disorders is a common finding, single-gene inheritance patterns are not seen. Instead, patterns suggested that several genes are involved in depression, and a recent research study demonstrated the interactive effects of these genes on the disease.

DepressionSLC6A4 is one allele for the serotonin transporter protein, and individuals who inherit this gene are at a 4-times greater risk of developing depression following major life stressors. It clearly plays a role in depression susceptibility, but inheritance mapping does not demonstrate a clear, one-to-one ratio of this gene and the presence of depression. Other factors are clearly required. A second gene, BDNF, is also linked to mood disorders. Several different alleles for this protein exist, and patients who inherit a specific combination of the BDNF allele in combination with the SLC6A4 allele are at a significantly increased risk of depression.

The interaction of these two genes helps to explain why scientists have failed to find a clear genetic link in major depression. Instead of depending upon a single mutated gene, depression results from a multifactorial combination of several genes and environmental factors. Thus, depression cannot be predicted by single gene mutations, but increased susceptibility to MDD may one day be detectable by molecular testing for a combination of genes.

The effects of the SLC6A4 allele are thought to occur during brain development, affecting the way negative environmental events are interpreted. This sets the stage for an exaggerated negative response to life stressors. The protein produced by the BDNF gene may affect the way the serotonin receptor interacts with the cell, extracellular proteins or both.

Further elucidation of genes that play a role in mood disorders stand to have an important impact on mental health treatment. By detecting specific alleles associated with depression, molecular therapeutics can be developed that directly target the affected protein with minimal side effects. Genetic testing of at-risk individuals may allow for early detection and prevention of major depression. The ability to clearly identify and treat patients at a high risk for major depression will allow physicians to intervene before the disease reaches it’s full-blown form, instead diagnosing patients at an early stage and providing pharmacological and psychological treatment to prevent progression.

Reference

Pezawas, L., Meyer-Lindenberg, A., Goldman, A.L., Verchinski, B.A., Chen, G., Kolachana, B.S., Egan, M.F., Mattay, V.S., Hariri, A.R., Weinberger, D.R. (2008). Evidence of biologic epistasis between BDNF and SLC6A4 and implications for depression. Molecular Psychiatry DOI: 10.1038/mp.2008.32

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Are You Depressed Because You’re Introverted? http://brainblogger.com/2008/05/02/are-you-depressed-because-your-introverted/ http://brainblogger.com/2008/05/02/are-you-depressed-because-your-introverted/#comments Fri, 02 May 2008 16:48:33 +0000 http://brainblogger.com/?p=841 Psychiatry_Psychology.jpgA study published in Psychological Science evaluated the link between happiness and personality traits in 973 twins. The authors found that happiness was heritable, and that it showed genetic linkage to certain personality traits. Those who were extroverted, open, agreeable and conscientious were more likely to be happy. Moreover, twins who exhibited similar personality traits had similar levels of happiness in a seemingly genetic pattern.

TwinsThe authors concluded that these results mean happiness could be the result of these specific personality traits, and that depression was brought about by the opposing traits of introversion, disagreeability and neuroticism. While this is a potentially correct conclusion, it seems that the opposite could also be true — depression is an inheritable trait, which leads to certain personality traits that occur in response to this depressed mood.

Many studies have linked certain personality traits to depression. But whether the underlying cause is these traits or depression itself remains to be determined. Alternatively, it may be that both personality traits and depressive tendencies are genetically inherited, but they are inherited together in a predictable pattern, i.e. genes for depressive mood and introversion travel together.

Anyone who has been depressed can vouch for the fact that, when things get bad, you do not want to socialize, you do not feel agreeable or open, and you are not very conscientious about yourself or those around you. So it seems plausible that these traits are as much a product of the depression as they are its underlying cause.

The truth probably lies somewhere in between. Personality traits are not always inherited, and environmental factors clearly also play a role in the development of personality development. Environmental factors are also important in the development of depression — but we still cannot explain why some individuals become depressed but others do not in response to the same stressful event. Underlying genetic susceptibility to depression and other mood disorders clearly exists, and likely interacts with life events and personal habits in a complex fashion to ultimately determine our personality and our mood. But the idea that our personality traits are genetically determined and are the major determinate of mood disorders is still just a theory.

Reference

Weiss, A., Bates, T.C., Luciano, M. (2008). Happiness Is a Personal(ity) Thing: The Genetics of Personality and Well-Being in a Representative Sample. Psychological Science, 19(3), 205-210. DOI: 10.1111/j.1467-9280.2008.02068.x

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A Genetic Susceptibility to PTSD? http://brainblogger.com/2008/04/16/a-genetic-susceptibility-to-ptsd/ http://brainblogger.com/2008/04/16/a-genetic-susceptibility-to-ptsd/#comments Wed, 16 Apr 2008 14:59:13 +0000 http://brainblogger.com/?p=840 BioPsychoSocial_Health2.jpgPost-traumatic stress disorder (PTSD) has been in the news a lot lately, primarily due to the prevalence of PTSD in Iraq war veterans. PTSD can occur following any severely stressful event, and recent research has shown that some individuals are genetically “at-risk” for its development.

A study of adult victims of childhood trauma compared the occurrence of PTSD and genetic variations in the FKBP5 gene, which is related to stress response. Not surprisingly, the study found that both abusive and nonabusive childhood traumatic events were linked to the development of PTSD. In addition, four specific variations of the FKBP5 gene significantly increased the risk of PTSD in child abuse victims. This effect was still present after controlling for depression severity, age, sex, and the occurrence of other kinds of trauma.

StressedThese genetic variants did not increase the risk of PTSD in those who experienced childhood trauma other than abuse. The FKBP5 gene encodes a protein that modulates the glucocorticoid receptor. Glucocorticoids, such as cortisol, are one of the body’s basic stress hormones, released in response to a variety of physical and psychological stressors. Variants of the gene produce proteins with more or less activity, which in theory would affect the ability of the glucocorticoid receptor to bind and transmit intracellular signals from circulating glucocorticoids.

The physical effects of cortisol excess are easy to detect — high blood sugar, weight gain, hypertension, and dementia all occur with extremely high levels of cortisol that result from exogenous administration or tumor production of the hormone. Its effects on mental function at lower levels seen with psychological stress are harder to pinpoint. Cortisol levels are frequently abnormal in patients with mood disorders, suggesting that it does affect, or is affected by, one’s mental state.

Identification of genetic variants that place individuals at increased risk of PTSD is still a long way from clinical utility. However, with further research, genetic testing may be used to identify people who need close follow-up after traumatic events, allowing for early detection and implementation of therapy.

Reference

Binder, E.B. et al. (2008). Association of FKBP5 Polymorphisms and Childhood Abuse With Risk of Posttraumatic Stress Disorder Symptoms in Adults. JAMA, 299(11), 1291-1305.

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Inflammatory Markers Altered in Depression and Suicide http://brainblogger.com/2008/04/12/inflammatory-markers-altered-in-depression-suicide/ http://brainblogger.com/2008/04/12/inflammatory-markers-altered-in-depression-suicide/#respond Sat, 12 Apr 2008 14:25:15 +0000 http://brainblogger.com/?p=831 BioPsychoSocial_Health2.jpgInflammation is a hot topic in medical research, with studies showing links to heart disease, dementia and longevity. Depression is a relatively new addition to the list of inflammation-associated diseases, with two recent publications demonstrating altered levels of inflammatory molecules in the blood of patients with major depressive disorder (MDD). Both studies evaluated the levels of cytokines in patient’s blood.

Cytokines are proteins produced by a variety of different cell types, most commonly cells of the immune system. They can circulate in the blood stream or stay localized in certain tissues, and serve as communication signals between cells. Both pro- and anti-inflammatory cytokines are recognized and the effects of different cytokine molecules are wide-ranging.

DepressionIn the first study, depressed patients who did not respond to pharmacological treatment with escitalopram (Lexapro) had increased levels of tumor necrosis factor-alpha (TNF-alpha). TNF-alpha is a potent cytokine with a variety of cellular activities, including effects on cell death and reproduction, systemic inflammation and control of viral replication. TNF-alpha has proinflammatory effects throughout the body. When release during acute inflammation, it causes fever, loss of appetite, activation of immune cells and release of cortisol, a major stress hormone.

A second study compared levels of cytokines produced in the laboratory by blood cells from non-suicidal and suicidal MDD patients and normal controls. Non-suicidal MDD patients had increased levels of interleukin-6 (IL-6), another cytokine associated with acute inflammation and fever. Levels of IL-6 correlated directly with depression severity. Suicidal MDD patients did not have increased levels of IL-6, but instead showed markedly decreased levels of interleukin-2 (IL-2). IL-2 is another proinflammatory cytokine that acts primarily by increasing the activity of the cells of the immune system, in order to fight off infection.

SynapseWhat the increased levels of inflammatory cytokines actually means in depressed patients is uncertain. Prior to these two reports, numerous other investigators have reported aberrant levels of inflammatory cytokines in patients with MDD. The immune system is affected by stress hormones, which are often elevated with depression. It is also possible that these cytokines possess as yet undetermined functions, in addition to their role in inflammation, that directly links them to brain function and the development of depression.

The fact that cytokine levels differed not only from normal controls, but also between suicidal and non-suicidal patients and between responders and nonresponders to pharmacological therapy, further confuses the issue. The relationship is far from clear. However, it is possible that future research will provide more substantial evidence as to the serum cytokine profile in MDD and allow physicians to prescribe directed therapy, based on predicted response to specific medications or risk of suicidal behavior.

References

Eller, T. et al. (2008). Pro-inflammatory cytokines and treatment response to escitalopram in major depressive disorder. Progress in Neuro-psychopharmacology and Biological Psychiatry, 32(2), 445-450.

Kim, Y. et al. (2008). Differences in cytokines between non-suicidal patients and suicidal patients in major depression. Progress in Neuro-psychopharmacology and Biological Psychiatry, 32(2), 356-361.

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Multiple Sclerosis: Nature, Nurture, or Something Else? http://brainblogger.com/2008/04/09/multiple-sclerosis-nature-nurture-or-something-else/ http://brainblogger.com/2008/04/09/multiple-sclerosis-nature-nurture-or-something-else/#comments Wed, 09 Apr 2008 13:11:41 +0000 http://brainblogger.com/2008/04/09/multiple-sclerosis-nature-nurture-or-something-else/ Neuroscience_Neurology.jpgMultiple sclerosis (MS) is a poorly understood disease that affects patients at an early age and, usually, lasts a lifetime. Factors that predispose to the development of MS include genetics, geographic location, sex and birth month, suggesting an interesting nature-nurture interaction in this disease process.

The increased rate of MS at high latitudes has been demonstrated in many studies, with those living in the Northern United States and Canada at a higher risk than those closer to the equator. This geographical influence is most commonly linked to the decreased (UV) radiation in these locations. UV light is a requirement for the production of vitamin D, and it is this effect that is most commonly thought to increase the risk of MS. In addition to affecting bone strength, vitamin D interacts with over 1,000 intracellular pathways, most of which are not well understood. Vitamin D deficiency is documented in patients living at higher latitudes, where MS is more prevalent. Conversely, individuals who work outdoors and have increased sun exposure show a decreased prevalence of MS. Interestingly, the effect of latitude on MS risk is most prominent in infancy in childhood — meaning that moving to an equatorial climate later in life is of limited benefit.

SunHowever, a direct link to early childhood vitamin D deficiency and development of MS is lacking, and there are other factors that may cause the same geographical effects. In North America, people of Scandinavian descent are concentrated in the Northern and Western areas, which are the exact locations with the highest MS rates. This suggests the possibility that genetics, in addition to environment, play an important role. Some studies have found South Asian immigrants to Northern climates to have no increased risk of MS, while others find they, or their offspring, to have increased rates of the disease. British migrants to Africa have lower rates than their counterparts who remain in the UK. Clearly there is some interplay between genetic and environmental factors.

There is seasonal variation in the development of MS, based on birth month. Infants born in May have the highest risk, while those born in November have the lowest. This phenomenon may also be explained by exposure to UV light. Women who are pregnant during the winter, and giving birth in late spring, have decrease sunlight exposure compared to those who are pregnant during summer months, suggesting beneficial effects of UV exposure in utero (womb).

Inheritable factors are also present — monozygotic (identical) twins show a higher concordance rate of the disease than non-twin siblings and unrelated persons. In addition to genetic and geographic factors, certain viruses, smoking and female sex are also associated with increased risk of MS.

Clearly we are far from understanding this disease. MS has a variety of seemingly independent factors associated with its development. In addition to the usual suspects — genetics, sex and poor health habits such as smoking — MS is also linked to what appear to be unrelated and uncontrollable factors such as birth place and birth month. The true link underlying all of these factors is currently unknown, but when it is ultimately identified may provide key insights into the pathogenesis and potential treatment pathways of this poorly understood disease.

Reference

EBERS, G. (2008). Environmental factors and multiple sclerosis. The Lancet Neurology, 7(3), 268-277. DOI: 10.1016/S1474-4422(08)70042-5

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Runner’s High Revealed http://brainblogger.com/2008/04/07/runners-high-revealed/ http://brainblogger.com/2008/04/07/runners-high-revealed/#comments Mon, 07 Apr 2008 12:18:16 +0000 http://brainblogger.com/?p=832 Neuroscience_Neurology2.jpgMost long distance runners have experienced the “runner’s high” — a feeling of enhanced mood and relaxation following a strenuous run. Its presence is unmistakable, but also hard to explain, and even harder to scientifically prove. Recently, researchers used high-tech brain imaging to demonstrate changes in brain activity that correlate with this phenomenon. Perhaps more importantly, this runner’s high is also linked to decreased pain perception, providing a potential therapeutic mechanism for sufferers of chronic pain.

German researchers used positron emission tomography (PET) to detect brain activity before and after a 2 hour run. Endorphins are the proposed molecules that increase after a long run, and their actions are primarily on the opiate receptors within the brain. In the study, radioactive opiate receptor agonist were injected and imaged with PET. After a long run, participants brains’ showed decreased binding of the radioactive molecule, demonstrating that their opiate receptors were occupied by an endogenous substance. The level of radioactivity within the brain was markedly decreased from that imaged before running.

RunnerThe brain regions involved in this running-induced endorphin binding included the limbic and prefrontal regions, both involved in emotional processing. Participants reported increased euphoria and happiness, with euphoria levels correlating directly with the activity in these brain regions following exercise.

Opioid receptors in the brain are targets of potent painkillers and elicit drugs, such as morphine, codeine and heroine. These drugs markedly reduce the perception of pain, and increased doses produce euphoria. Because this same effect, albeit to a lesser degree, has now been detected with strenuous exercise, researchers may be able to apply exercise as a harmless and non-addictive painkiller.

Many patients with chronic pain become resistant to the effects of prescription pain medicine, and they also run the risk of addiction and dependence. By triggering the release of natural endorphins, long distance running may allow chronic pain patients to find some relief without the attendant risks of addictive medications.

Reference

Boecker, H., Sprenger, T., Spilker, M.E., Henriksen, G., Koppenhoefer, M., Wagner, K.J., Valet, M., Berthele, A., Tolle, T.R. (2008). The Runner’s High: Opioidergic Mechanisms in the Human Brain. Cerebral Cortex. DOI: 10.1093/cercor/bhn013

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Stroke Recovery Improves with Music http://brainblogger.com/2008/04/05/stroke-recovery-improves-with-music/ http://brainblogger.com/2008/04/05/stroke-recovery-improves-with-music/#comments Sat, 05 Apr 2008 14:07:04 +0000 http://brainblogger.com/?p=830 BioPsychoSocial_Health2.jpgStroke victims face a long and difficult road to recovery, and many of them suffer from irreparable residual effects. Researchers around the globe are searching for treatment options that improve recovery in stroke patients, but to date no magic bullet has arrived. Currently, patients are treated with a multimodal approach, including physical therapy, occupational therapy and counseling as needed.

One simple thing that may aid in the recovery of mental function following stroke is listening to music. According to a recent study, stroke victims who listened to music for 1 to 2 hours daily showed significant improvement in certain mental functions than those that did not.

When compared to patients who listed to audio books or nothing at all, patients who listened to music had significantly better performance on tasks of attention and verbal memory. Patients in the music group also reported lower levels of depression.

Previous studies have proven that healthy individuals learn more effectively when listening to music they enjoy. Studies also showed music to be beneficial in patients with dementia, schizophrenia, autism, dyslexia and depression.

The reason for this widespread beneficial effect of music on cognition is a mystery. Some have hypothesized that improvements in mental function are due to the mood-enhancing and stress-lowering effects of music. Others point to the complexity of neural circuits that are activated when listening to music. Music requires activity of emotional, cognitive and memory centers in both brain hemispheres. Stimulation of divergent neural networks may have beneficial effects on these pathways by as yet unknown mechanisms.

The great thing about music is that is cheap and easily accessible. In the most recent study, stroke patients were asked to listen to music of their choosing for 1 to 2 hours a day. Almost any patient will be able to participate in this simple plan.

Reference

Sarkamo, T., Tervaniemi, M., Laitinen, S., Forsblom, A., Soinila, S., Mikkonen, M., Autti, T., Silvennoinen, H.M., Erkkila, J., Laine, M., Peretz, I., Hietanen, M. (2008). Music listening enhances cognitive recovery and mood after middle cerebral artery stroke. Brain, 131(3), 866-876. DOI: 10.1093/brain/awn013

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New Treatment Option for Difficult Diseases: Chronic Fatigue Syndrome and Fibromyalgia http://brainblogger.com/2008/03/31/new-treatment-option-for-difficult-diseases/ http://brainblogger.com/2008/03/31/new-treatment-option-for-difficult-diseases/#comments Mon, 31 Mar 2008 15:35:52 +0000 http://brainblogger.com/?p=843 Neuroscience_Neurology2.jpgChronic fatigue syndrome and fibromyalgia are two diagnosis that remain difficult discern, both to patients and physicians. Both produce nonspecific symptoms of fatigue and pain, with no clear underlying cause. They are a diagnosis of exclusion, given when all other possibilities have been ruled out.

Many people believe that chronic fatigue and fibromyalgia result from an underlying psychiatric illness, based on the associated of anxiety and depression. Still others think an underlying autoimmune disorder or viral infection may be to blame.

A recent report published by a leading expert in the treatment of chronic fatigue syndrome states that an underlying endocrine disorder may be partly to blame. Based on a literature review of more than 50 published studies, it was determined that the majority of patients with these disorders have a dysfunctional hypothalamic-pituitary-adrenal (HPA) system. The HPA system is a complex pathway involving hormones released from the brain that promote the production of cortisol by the adrenal glands. Cortisol has a huge range of effects on a variety of body systems, including metabolism, inflammation and mental function.

The review supported the theory that problems with the hypothalamic or pituitary gland, both located in the brain, result in decreased production of cortisol by the adrenal glands. More importantly, treatment with a low dose oral cortisol medication resulted in improvement in the majority of patients. A further study found 94% of patients to show improvement by their fourth office visit, with the majority reporting a doubling in their energy level and sense of well-being.

There is currently no good treatment for chronic fatigue syndrome or fibromyalgia. A variety of approaches, including pain medication, anti-anxiety medication and counseling may be attempted. Still, the majority of patients are left with significant fatigue and pain that prevent normal daily activities. Administration of low-dose oral cortisol is advocated by some to be a low risk and potentially useful tool in the treatment of these complex and poorly understood conditions.

Reference

Holtorf, K. (2008). Diagnosis and Treatment of Hypothalamic-Pituitary-Adrenal (HPA) Axis Dysfunction in Patients with Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM). Journal of Chronic Fatigue Syndrome, 14(3), 59-88. DOI: 10.1300/J092v14n03_06

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The Science of Premenstrual Syndrome (PMS) http://brainblogger.com/2008/03/29/the-science-of-premenstrual-syndrome/ http://brainblogger.com/2008/03/29/the-science-of-premenstrual-syndrome/#comments Sat, 29 Mar 2008 13:25:46 +0000 http://brainblogger.com/2008/03/29/the-science-of-premenstrual-syndrome/ Neuroscience_Neurology.jpgWomen take a lot of criticism for premenstrual syndrome, being accused by male friends and partners of irritability and moodiness. Now, women may have a good explanation for their behavior.

During the 2 weeks before their period, women experience a gradual surge of progesterone secretion. Progesterone is produced by an ovulated egg within the ovaries, and is released into the bloodstream. Is has effects throughout the body, most recognizably in preparing the lining of the uterus for implantation of a fertilized egg.

Progesterone is metabolized into several different compounds. Two of these metabolites, allopregnenolone and pregnenolone, are capable of crossing the blood-brain barrier and affecting neural function. Previous research showed these two molecules to increase the activity of the neurotransmitter GABA, which has effects throughout the cerebral cortex. Animal studies demonstrated increased anxiety with administration of progesterone, suggesting that it affects parts of the brain related to anxiety and mood.

In order to investigate the effect of progesterone in humans, researchers recruited females and monitored brain activity following progesterone administration. The women were given progesterone during the follicular phase of their menstrual cycle, the phase just before a physiological increase in progesterone occurs each month. The dose increased their serum progesterone and allopregnenolone levels to the normal values seen during premenstrual and early pregnancy periods. Functional magnetic imaging (fMRI) of the participants brains found increased brain activity localized to the amygdala, a small region deep within the brain that is responsible for emotions and emotional memory. This new data provides a link between the physiological progesterone surge seen just before menstruation and mood changes that occur at this same time. This information may be applicable to providing treatment for women who suffer from severe PMS — or least providing a biological explanation for women’s seemingly irrational behavior!

Reference

van Wingen, G.A., van Broekhoven, F., Verkes, R.J., Petersson, K.M., Backstrom, T., Buitelaar, J.K., Fernandez, G. (2008). Progesterone selectively increases amygdala reactivity in women. Molecular Psychiatry, 13(3), 325-333. DOI: 10.1038/sj.mp.4002030

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The Increasing Influence of Biopsychosocial Medicine http://brainblogger.com/2008/03/22/the-increasing-influence-of-biopsychosocial-medicine/ http://brainblogger.com/2008/03/22/the-increasing-influence-of-biopsychosocial-medicine/#comments Sat, 22 Mar 2008 14:34:05 +0000 http://brainblogger.com/2008/03/22/the-increasing-influence-of-biopsychosocial-medicine/ BioPsychoSocial_Health.jpgThe biopsychosocial model of health and disease was originally a fringe idea, and is still criticized by some. But its popularity is growing as more healthcare professionals and patients recognize the link between emotional health and physical disease. A recent literature search on Medline, the U.S. government database of medical literature, found 1,973 articles relating to the biopsychosocial model, with 433 published within the last three years alone.

The variety of medical conditions to which the biopsychosocial model has been applied is staggering. Among the recently published articles are the usual entities — depression, anxiety, chronic pain, sexual dysfunction, fatigue. But biopsychosocial medicine is beginning to take hold in far-reaching areas, including spina bifida, asthma and cancer.

As a recent graduate of a U.S. medical training institution, I can vouch for the emphasis now placed on psychological factors related to physical health. Unlike 50 years ago, physicians-in-training are becoming more attuned to the effect of stress, fatigue and mental states on the ability of the body to heal itself. Science is, in many ways, backing up the premise of the biopsychosocial models. Reports of stress affecting the immune system and the gastrointestinal tract are now frequent findings in medical literature.

The reductionist model of medicine is still the basis of understanding the pathophysiology of disease and development of treatment for most medical problems, but this is not in direct contrast to the ideas of the biopsychosocial theory. Proponents of the theory point to the effects of poor mental health on wound healing and rates of infection, and molecular biology supports this idea by demonstrating aberrant activity in the immune system of stressed animals and humans. The two are not mutually exclusive, but instead complimentary. Biopsychosocial ideas provide the link between depression and pain, and biological sciences demonstrate exactly how this link functions.

Future generations of doctors will likely continue to be trained in a system that places heavy emphasis on biological research and molecular mechanisms of disease, but the biopsychosocial model will grow in its influence as it is recognized as a true factor in health and disease. There is no need to choose one over the other — both reductionist and biopsychosocial thinking can be mutually supportive in the proper practice and growth of human medicine.

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Irritable Bowel Syndrome and the Brain Revisited http://brainblogger.com/2008/03/18/ibs-and-the-brain-part-ii/ http://brainblogger.com/2008/03/18/ibs-and-the-brain-part-ii/#comments Tue, 18 Mar 2008 15:43:14 +0000 http://brainblogger.com/2008/03/18/ibs-and-the-brain-part-ii/ BioPsychoSocial_Health2.jpgA few weeks ago, I wrote about irritable bowel syndrome (IBS) and the abnormal brain activity seen on magnetic resonance imaging (MRI) in a recent clinical trial. These findings supported the theory that patients with IBS have an altered sensation of abdominal pain and respond more strongly and more emotionally to pain than unaffected patients.

Now, researcher at the the University of Buffalo, State University of New York have shown that the powers of the mind can be harnessed to effectively reduce the symptoms of pain, bloating and altered bowel function.

Cognitive behavioral therapy proved effective for IBS patients in a recent trial, whether it was administered by a certified therapist or by at-home techniques. Cognitive behavioral therapy (CBT) focuses on replacing negative beliefs and behaviors with positive ones. Self-administered techniques were included because many patients do not have access to CBT-trained therapists who treat IBS. These at-home techniques included relaxation and problem-solving exercises.

Other studies have found hypnotherapy to be beneficial in the majority of IBS patients.

These findings further support the interconnected nature of the gut and the mind, and the alterations in this relationship that result in IBS. It is well known that IBS symptoms are worsened by stress or negative emotions and improved with relaxation. CBT and hypnotherapy both exploit the power of the mind to control peripheral sensations — like abdominal pain and bloating — and allow patients to better control their reactions to these events.

Current medications available to IBS patients include painkillers, laxatives and anti-diarrhea agents. Unfortunately, these medicines only treat the symptoms and do not address the underlying cause. And for many patients, medications provide little or no relief at all. This is probably because the real problem does not lie in the digestive tract, but in the brain, where processing of sensations from the gut takes place.

By directly targeting the brain, CBT and hypnotherapy may prove more effective for many patients who do not respond to traditional medical therapy. These psychological therapies may allow the brain to ignore or correct the abnormal processing of gut sensation that leads to pain and discomfort.

References

Berman, S.M., Naliboff, B.D., Suyenobu, B., Labus, J.S., Stains, J., Ohning, G., Kilpatrick, L., Bueller, J.A., Ruby, K., Jarcho, J., Mayer, E.A. (2008). Reduced Brainstem Inhibition during Anticipated Pelvic Visceral Pain Correlates with Enhanced Brain Response to the Visceral Stimulus in Women with Irritable Bowel Syndrome. Journal of Neuroscience, 28(2), 349-359. DOI: 10.1523/JNEUROSCI.2500-07.2008

Naliboff, B.D., Frese, M.P., Rapgay, L. (2007). Mind/Body Psychological Treatments for Irritable Bowel Syndrome. Evidence-based Complementary and Alternative Medicine, 5(1), 41-50. DOI: 10.1093/ecam/nem046

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Chronic Pain and the Brain http://brainblogger.com/2008/03/16/chronic-pain-and-the-brain/ http://brainblogger.com/2008/03/16/chronic-pain-and-the-brain/#comments Sun, 16 Mar 2008 14:22:26 +0000 http://brainblogger.com/2008/03/16/chronic-pain-and-the-brain/ Neuroscience_Neurology2.jpgThe brains of chronic pain patients fail to maintain the state of “activity equilibrium” seen in healthy patients. New research has demonstrated that a key emotional control center in the frontal lobe remains active constantly in chronic pain, while in pain-free patients it shuts down in order for other areas of the brain to function adequately.

Researchers compared functional magnetic resonance imaging (fMRI) brain scans of chronic pain patients to healthy controls. The healthy patients showed decreased function of a specific area in the frontal cortex while performing simple tasks. The chronic pain patients, however, performed the task equally well but with constant activity in this frontal lobe emotional center.

It is normal for the brain to shut off one area while another is being used. This allows nutrients and oxygen to be efficiently delivered to the part of the brain whose activity is most important, and allows neurons to rest from their normal excitatory state. When areas of the brain become constitutively active, as seen in the brains of chronic pain patients in this study, the abnormal activity may produce a variety of unwanted effects. Overactive cells may “steal” energy that would otherwise supply different parts of the brain; they may also alter their connections with other neurons or may “burn out” and die from over-excitation.

Chronic pain patients frequently suffer from a variety of concomitant health problems, including depression, anxiety and insomnia. This research may help us to understand the underlying factors that allow chronic pain to produce these symptoms. It may be that hyperactivity of this emotional center in the frontal cortex results in altered emotional response to a variety of normal life occurrences.

Understanding the effects of chronic pain on brain function will hopefully aid in the treatment of the emotional and psychological symptoms that many patients experience, and may provide insight into the underlying mechanisms of the pain and its consequences.

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Videophilia Takes Over http://brainblogger.com/2008/03/13/videophilia-takes-over/ http://brainblogger.com/2008/03/13/videophilia-takes-over/#respond Thu, 13 Mar 2008 19:48:30 +0000 http://brainblogger.com/2008/03/13/videophilia-takes-over/ The benefits of spending time outdoors are numerous — fresh air, sunshine, relaxation. Who wouldn’t want that? Apparently, many Americans don’t. Researchers at the University of Illinois in Chicago tracked outdoor activities over several decades, and found a sharp decline among US citizens. Rates of fishing, hiking, hunting, backpacking and national and state park visits were followed over time and showed decreased use by about 1% per year, for an average of 18% to 25% total decrease.

What’s to blame? Videophilia. The term was coined to refer to the rapid rise in television, video game and computer activity that has occurred in recent years. This is no surprise, as the Internet has exploded not only as a business tool but also as a social networking, shopping and entertainment hub. Instead of taking the family on a drive through Yellowstone, why not just relax at home, let the kids play video games and catch up on your favorite blog?

It’s easy to understand why Americans are choosing to spend their free time at home. We are busier than ever, and unlike a few decades ago, our homes a full of entertainment. Between TiVo, Netflix, video games and the Internet, you could easily spend all day lying on the couch without getting bored. But aren’t we missing out on something important?

Being outdoors is almost synonymous with being active, something that videophilia can’t claim. The mental benefits of nature are equally important, providing a sense of serenity that you’re not going to get from ESPN or the latest violent video game. Everyone could benefit from the physical and emotional boost that inevitably occurs when you spend time outside.

When I was growing up, my family took a vacation almost every year. We visited Yellowstone, the Blue Ridge Mountains, the Rocky Mountains, just to name a few. I have vivid memories of spending time in the wilderness, even if it was just for a day, fishing or boating with my family. I can’t imagine what it would be like to think back on my childhood with fond thoughts of Facebook.

I don’t doubt that people enjoy their videophilia, but it would be healthy for us as individuals and as a nation if we managed to not only enjoy the technological advances available to us today, but also the simpler pleasures of a walk through the woods.

Reference

Pergams, O.R., Zaradic, P.A. (2008). Evidence for a fundamental and pervasive shift away from nature-based recreation. Proceedings of the National Academy of Sciences, 105(7), 2295-2300. DOI: 10.1073/pnas.0709893105

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Are Insurance Copayments Unethical? http://brainblogger.com/2008/03/04/are-insurance-copayments-unethical/ http://brainblogger.com/2008/03/04/are-insurance-copayments-unethical/#respond Tue, 04 Mar 2008 16:11:44 +0000 http://brainblogger.com/2008/03/04/are-insurance-copayments-unethical/ Opinion.jpgMammograms are recommended for all women over the age of 45 as a breast cancer screening tool. Some insurance and Medicare plans provide full coverage for these tests because they are deemed necessary and beneficial. Other plans apply co-pays to mammograms, and other similar medical interventions, despite the prevalent medical opinion that they are both necessary and beneficial to the health of the patient.

A large-scale study published in the New England Journal of Medicine found that patients who are required to pay $10 or more for a mammogram are significantly less likely to have the examination on a biannual basis when compared to individuals whose insurance plans provided complete coverage. This discrepancy was highest among lower income and less educated individuals, but was present across the board, including educated and financially stable patients.

Many writers and reporters have commented that co-payments for such important medical studies as mammograms are unethical, because they deter patients from having the exam regularly. I have no problem with providing free mammograms for women who legitimately cannot afford their co-pay. However, if someone who has the financial capability to pay $10 for a mammogram chooses not to do so, it is not the fault of the insurance company or the healthcare system, but of the patient.

Patients are responsible for eating healthy, exercising, getting enough sleep, and a myriad of other factors that doctors and insurers cannot control. They are also responsible for having good judgment. If you can afford the co-payment, but you just don’t like it, that is no excuse for failing to access medical care.

Healthcare providers bear the very important responsibility of educating patients about the importance of preventive measures such as annual mammography. Insurers have the task of making healthcare affordable and accessible. No one is responsible for making it free.

Reference

Trivedi, A.N., Rakowski, W., Ayanian, J.Z. (2008). Effect of Cost Sharing on Screening Mammography in Medicare Health Plans. New England Journal of Medicine, 358(4), 375-383. DOI: 10.1056/NEJMsa070929

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