Neuroscience & Neurology – Brain Blogger http://brainblogger.com Health and Science Blog Covering Brain Topics Sat, 30 Dec 2017 16:30:10 +0000 en-US hourly 1 https://wordpress.org/?v=4.9.1 Social Media Anxiety Disorders: What’s Going on in the Brain? http://brainblogger.com/2017/12/27/social-media-anxiety-disorders-whats-going-on-in-the-brain/ http://brainblogger.com/2017/12/27/social-media-anxiety-disorders-whats-going-on-in-the-brain/#respond Wed, 27 Dec 2017 16:30:07 +0000 http://brainblogger.com/?p=23207 Too much of anything can be dangerous, and social media is no exception. Today many of us spend more time on internet-enabled devices than even sleeping. Due to this overindulgence in social media and the internet, we may become socially reclusive rather than inclusive. This, in turn, may lead to various physical and mental health problems.

Nowadays, around two billion residents of our planet are online. Hundreds of millions of emails and social messages are exchanged each day. Perhaps, this online over-engagement is becoming more of a problem. The amount of time we spend online and on social media is increasing each year. It is estimated that most people spend more than two hours each day on social media in the US.

Although social media anxiety and addiction are still not recognized as individual disorders, most investigations support the view that mental issues related to internet overuse are on the rise. Moreover, it seems to be a particularly big problem in younger people. Most individuals nowadays have their first exposure to the internet while in school. Overuse of the internet may lead to problems with concentration, sleep deprivation, failure to exercise, anxiety, and even depression. Although studying the prevalence of internet addiction or social media addiction is challenging, it could be affecting as many as 10% of people in certain sections of society.

Is social media engagement a disorder?

Is social media engagement itself a disorder? Perhaps the answer is both yes and no. It is no secret that some people get too submerged in the internet and social media. They feel bad if they do not get likes or see negative comments on their posts, and may even get depressed. Many others, however, think that social media is helpful in overcoming loneliness and depression, having a positive effect on self-esteem. The supporters of social media are saying that the compulsion to go online is not associated with the kind of harm done by substance abuse.

Most scientific review studies have provided mixed results, with only one thing certain: not all users gets depressed or feel anxiety with social media, but some do. For mental disorders related to internet abuse, as with any other psychological issues, there have to be predisposing factors like genetics, personality, lifestyle, other diseases, or a recent history of trauma.

Risk factors and identification of social media disorder

With all of the contradicting findings, there is still no doubt that social media disorder exists, and some people are at higher risk of developing it than others. Some individuals are more prone to get dependent on the internet, cultivate impulsive behavior, and are inclined towards risky internet use, as well as being more susceptible to social and emotional impairment, and even physical harm.

In recent years, some tools and measures have been developed to qualify and quantify the disorders related to social media and internet overuse. One of the scales that can be used to measure social media disorder assesses several items over the period of one year—preoccupation, tolerance, withdrawal, persistence, displacement (neglecting other hobbies), problems (arguments on social media), deception, escape, and conflict.

Social media addiction and neural changes

Some anatomical brain structures are well known to be associated with mood, emotion, and learning. Hence in one investigation, specific attention was given to the structures involved in the limbic system and reward pathway.

In the study, 20 subjects known to be addicted to social media were examined for any morphological changes in the brain, with the help of MRI. The study identified changes characteristic of impulsive behavior, with a bilateral decrease in grey matter in the amygdala without any changes in the nucleus accumbens. In contrast to other types of addiction, the anterior and mid-cingulate cortex was not found to be impaired in social media addiction, indicating that the inhibitor function of these structures is well-preserved in this condition. The study demonstrated both similarities and differences between the structural changes in the brain in social media addiction and in addiction related to substance abuse or gambling.

Other health aspects

Social media is a powerful tool that affects multiple facets of life. It has an additive effect on our already increasing sedentary lifestyle. Hence it is not stretch of the imagination that is is related to increased risk of obesity, insulin resistance, cardiovascular ailments, and other non-communicable diseases.

People who use social media too often are also more prone to bullying. They may get involved in risky behavior more frequently. In some people, social media addiction may also lead to disturbed sleep patterns. Moreover, adolescents are considered to be at higher risk of developing an addiction to social media.

Management of social media or internet addiction

Treatment of social media addiction-related pathologies depends on the nature of the problem. Although there is a lack of trials and evidence for treatment of social media-related mental issues, treatment is often a combination of pharmacological drugs and cognitive-behavioral therapy (CBT)—the kind of treatment that has already shown efficacy in other types of addictions, anxiety, and depression.

Although at present there are very few clinical studies on the topic, one can surmise that social media-related addiction, anxiety, depression, and other mental issues are going to become more common. It would be unwise to think that of social media disorder as merely a habit, we should keep in mind the related structural changes in the brain, imparting serious problems for an affected person.

References

ACOG (2016, February). Concerns Regarding Social Media and Health Issues in Adolescents and Young Adults – ACOG.  Access here.

Cash, H., Rae, C. D., Steel, A. H., & Winkler, A. (2012). Internet Addiction: A Brief Summary of Research and Practice. Current Psychiatry Reviews, 8(4), 292–298. https://doi.org/10.2174/157340012803520513

He, Q., Turel, O., & Bechara, A. (2017). Brain anatomy alterations associated with Social Networking Site (SNS) addiction. Scientific Reports, 7, 45064. https://doi.org/10.1038/srep45064

Li, W., O’Brien, J. E., Snyder, S. M., & Howard, M. O. (2015). Characteristics of Internet Addiction/Pathological Internet Use in U.S. University Students: A Qualitative-Method Investigation. PLoS ONE, 10(2). https://doi.org/10.1371/journal.pone.0117372

Moreno, M. A., Jelenchick, L. A., & Christakis, D. A. (2013). Problematic internet use among older adolescents: A conceptual framework. Computers in Human Behavior, 29(4), 1879–1887. https://doi.org/10.1016/j.chb.2013.01.053

Seabrook, E. M., Kern, M. L., & Rickard, N. S. (2016). Social Networking Sites, Depression, and Anxiety: A Systematic Review. JMIR Mental Health, 3(4). https://doi.org/10.2196/mental.5842

Spada, M. M. (2014). An overview of problematic Internet use. Addictive Behaviors, 39(1), 3–6. https://doi.org/10.1016/j.addbeh.2013.09.007

Statista (2017). Global time spent on social media daily 2017. Access here.

van den Eijnden, R. J. J. M., Lemmens, J. S., & Valkenburg, P. M. (2016). The Social Media Disorder Scale. Computers in Human Behavior, 61(Supplement C), 478–487. https://doi.org/10.1016/j.chb.2016.03.038

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The Dangers of Antidepressants http://brainblogger.com/2017/12/22/the-dangers-of-antidepressants/ http://brainblogger.com/2017/12/22/the-dangers-of-antidepressants/#respond Fri, 22 Dec 2017 16:25:46 +0000 http://brainblogger.com/?p=23202 A fortunate knock of luck is always welcomed by scientists and researchers, yet any treatment modalities should be novel by design rather than by serendipity. Antidepressants were discovered by chance in the 1950s, and it seems that they suffer from specific deficiencies when it comes to their clinical effectiveness and safety profile. It is something that very few in the medical field negate, although the degree of disagreement may vary.

Depression—a poorly understood disorder

Depression is a heterogeneous disorder that may be characterized by a group of common symptoms, but the underlying cause may vary from person to person. Despite considerable research about the structural and neurochemical changes caused in the brain of a person suffering from depression, there is no specific brain-based test for the condition. Two of the most widely accepted diagnostic systems, ICD-10 and DSM-IV, have similar but not identical criteria. This means that they have a different threshold for various depression symptoms.

Some of the universally accepted symptoms of depression are depressed mood, fatigue, loss of interest, worthlessness, recurrent thoughts of suicide, insomnia, and alternation in appetite.

The rise of antidepressants

Both the US- and European-based statistics show a sharp increase in the prescription of antidepressants since the 1990s. Although statistics also indicate that no more than 8% of the population suffers from depression, 13% are taking antidepressants. Moreover, these drugs are much more commonly used in people above 60 years of age, with almost one-fourth of them taking antidepressants and many older adults using them for more than a decade.

Such a rise in the use of antidepressants is also explained by the fact that these drugs are given not only to treat depression. They have become a kind of all-purpose drugs that are considered useful to treat various mood disorders, painful conditions, inflammatory bowel syndrome, anxiety, panic disorders, and many more.

How antidepressants work?

Antidepressants are drugs belonging to various groups. Almost all of them work by changing the level of monoamine neurotransmitters in the brain. There are some additional effects too, as not all drugs capable of altering monoaminergic functioning may work as antidepressants.

Antidepressants change the presynaptic and postsynaptic concentration of dopamine, serotonin, and norepinephrine in the neurons, with most modern antidepressants targeting serotonin and to some extent norepinephrine. Dopamine, serotonin, and norepinephrine are vital neurotransmitters, playing an essential role in the limbic system and reward system. The drugs help to reset these systems, consequently contributing to the regain of mood and emotional balance.

Antidepressants have been shown to increase the activation of the prefrontal cortex but decrease the activation of the hippocampus, parahippocampal region, amygdala, ventral anterior cingulate cortex, and orbitofrontal cortex. These areas of the brain play an important role in shaping mood and emotions and are part of limbic and reward systems.

Apart from modifying the transmission of monoaminergic neuromediators, antidepressant drugs also have a complex effect on various receptors and the hypothalamic–pituitary–adrenal (HPA) axis. The impact of some of the novel antidepressants on different serotonin receptors (e.g., 5-hydroxytryptamine receptors) has been well-studied.

Some of the most commonly used antidepressants these days are tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), and selective serotonin noradrenaline reuptake inhibitors (SSNRIs).

What are the safety issues?

When we talk about drug safety, it is not just about the adverse effect but also about the clinical efficacy. Too many side effects and little clinical effectiveness as compared to placebo could put the utility of any drug therapy under doubt.

When it comes to side effects, anticholinergic side effects like dryness of mouth, blurring of vision, and dizziness are common with most antidepressants. Most of them may also alter appetite and sexual function, and cause an upset stomach, joint and muscular pains, problems with drug interactions, irritability, mood changes, movement disorders and the risk of falling in the elderly, and much more. Moreover, these side effects continue to persist when the drugs are used long term.

The development of tolerance and withdrawal symptoms are widespread. Discontinuation syndrome can be really bad in many cases.

Perhaps the most worrisome of all the adverse effects is the higher occurrence of suicide and violence in those on antidepressants. Although there are many studies with contradicting conclusions, the majority seem to show that suicide and violence are much higher in those taking antidepressants. Moreover, abnormal behavior is equally common with the newer SSRIs and SSNRIs.

There is an abundance of literature mentioning the risk of suicide in depression. However, the efficacy of antidepressants in the prevention of depression-related suicide remains inconclusive.

Clinical studies have demonstrated that the newer non-tricyclic antidepressants are not any better in their safety profile in the elderly population.

Finally, a considerable number of studies seems to put doubt on the effectiveness of antidepressants. Some medical specialists believe that antidepressants do not help at all, and many studies support their view. Thus in one of the studies published in the JAMA, it was concluded that the therapeutic benefit with antidepressants may actually be non-existent or minimal for mild to moderate depression, with more substantial benefits in severe cases of depression.

Conclusion

Although the diversity of depression is well-recognized, almost all the drugs made to treat depression inhibit reuptake of one or another monoamine neuromediator, and very little has changed in our approach towards treatment since the advent of the first antidepressant drug. In order to overcome the dangers and limitations of therapy with antidepressants, there is an urgent need to create antidepressants that have a novel mechanism of action and better tolerance.  More caution should be exercised by medical professionals when prescribing anti-depressants, as the ability to promote positive effects in many patients is questionable.

References

Bet, P. M., Hugtenburg, J. G., Penninx, B. W. J. H., & Hoogendijk, W. J. G. (2013). Side effects of antidepressants during long-term use in a naturalistic setting. European Neuropsychopharmacology, 23(11), 1443–1451. https://doi.org/10.1016/j.euroneuro.2013.05.001

Bielefeldt, A. Ø., Danborg, P. B., & Gøtzsche, P. C. (2016). Precursors to suicidality and violence on antidepressants: systematic review of trials in adult healthy volunteers. Journal of the Royal Society of Medicine, 109(10), 381–392. https://doi.org/10.1177/0141076816666805

Delaveau, P., Jabourian, M., Lemogne, C., Guionnet, S., Bergouignan, L., & Fossati, P. (2011). Brain effects of antidepressants in major depression: A meta-analysis of emotional processing studies. Journal of Affective Disorders, 130(1), 66–74. https://doi.org/10.1016/j.jad.2010.09.032

Fournier, J. C., DeRubeis, R. J., Hollon, S. D., Dimidjian, S., Amsterdam, J. D., Shelton, R. C., & Fawcett, J. (2010). Antidepressant Drug Effects and Depression Severity: A Patient-Level Meta-analysis. JAMA, 303(1), 47. https://doi.org/10.1001/jama.2009.1943

Hollinghurst, S., Kessler, D., Peters, T. J., & Gunnell, D. (2005). Opportunity cost of antidepressant prescribing in England: analysis of routine data. BMJ, 330(7498), 999–1000. https://doi.org/10.1136/bmj.38377.715799.F7

Köhler, S., Cierpinsky, K., Kronenberg, G., & Adli, M. (2016). The serotonergic system in the neurobiology of depression: Relevance for novel antidepressants. Journal of Psychopharmacology, 30(1), 13–22. https://doi.org/10.1177/0269881115609072

Mahar, I., Bambico, F. R., Mechawar, N., & Nobrega, J. N. (2014). Stress, serotonin, and hippocampal neurogenesis in relation to depression and antidepressant effects. Neuroscience & Biobehavioral Reviews, 38(Supplement C), 173–192. https://doi.org/10.1016/j.neubiorev.2013.11.009

National Collaborating Centre for Mental Health (UK). (2010). THE CLASSIFICATION OF DEPRESSION AND DEPRESSION RATING SCALES/QUESTIONNAIRES. British Psychological Society. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK63740/

Pratt, L. A., Brody, D. J., & Gu, Q. (2017). Antidepressant Use Among Persons Aged 12 and Over: United States, 2011–2014. https://www.cdc.gov/nchs/products/databriefs/db283.htm

Image via HASTYWORDS/Pixabay.

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The Neurological Basis of Anxiety http://brainblogger.com/2017/12/20/neurological-basis-of-anxiety/ http://brainblogger.com/2017/12/20/neurological-basis-of-anxiety/#respond Wed, 20 Dec 2017 16:20:43 +0000 http://brainblogger.com/?p=23150 A person suffering from an anxiety disorder experiences neurology-based changes in mood and bodily functions that are discussed in more detail in this article.

As with anxiety, various personality traits and emotional responses are by-products of the interaction between our genetic coding and environmental influences. Our genes make us more receptive to some specific stimuli and play a role in developing the resilience to some other stimuli. Our brain is a plastic organ. Thus, the role of environmental factors in its development and casting cannot be negated.

Fear and stress are normal defensive reactions to threats that help our body to deal with challenges more efficiently. Anxiety is different from fear in that it is a set of emotional and somatic reactions to a future threat that may or may not be realistic. To some extent, having anxiety is a normal human reaction. However,  if it continues for a prolonged period, it may have an adverse effect on our daily life and health.

In the state of anxiety, worrying about the future makes it difficult to concentrate and leads to irritability. Somatic symptoms like palpation, sweating, and gastrointestinal changes are also common in this state. Anxiety is considered as a disorder if such symptoms persist over a period of six or more months.

Anxiety disorders are most prevalent among people with psychiatric disorders, affecting around 10% of the population at any given time. Nonetheless, only a small number of those suffering from anxiety disorders seek treatment. This can be partially explained by the difficulties in identifying the condition. General anxiety disorder, panic disorder, specific phobias, and social anxiety are some of the most common types of anxiety disorders.

What makes a person vulnerable to anxiety disorders?

The hereditary nature of various forms of anxiety disorders has been established through clinical and observational studies. Multiple studies have demonstrated that a person is at 3–5 times greater risk of developing anxiety disorders if such a condition is found among first-degree relatives. The importance of familial clustering in anxiety has been demonstrated by a number of twin studies. Other internal factors like certain personality traits also make a person more vulnerable to developing anxiety disorders.

Apart from internal factors, environmental factors may also make some people more anxious. These factors include exposure to stressful condition, drug or alcohol use, parenting style, and stressful life events.

Neuroanatomy of stress and anxiety

Higher cognitive centers in our brain are located in the prefrontal cortex. They are involved in thinking, planning, and social behavior. From an evolutionary perspective, the prefrontal cortex is the “newer” part of the brain that helps us to keep our emotional responses in check.

Most of the emotion processing takes place in more ancient parts of the cortex. These anatomical brain structures are collectively called the “limbic system”. One fundamental structure in the limbic system is the hippocampus that plays a vital role in the stress response and regulation of the hypothalamic–pituitary–adrenal (HPA) axis. Both hippocampal growth and neurogenesis play an essential role in the development of resiliency towards stress and anxiety.

But perhaps the most crucial part of the limbic system that plays a central role in the regulation of emotions is the amygdala. The amygdala is central to the formation of fear and anxiety-related memory and has been shown to be hyperactive in anxiety disorders. It is well connected with other brain structures like the hippocampus, thalamus, and hypothalamus.

Apart from anatomical changes, it is essential to understand that brain functionality or communication between various brain centers and networks takes place through neurotransmitters. In the case of emotional responses, gamma-aminobutyric acid (GABA) is known to have an inhibitory effect on emotions, while glutamate has an excitatory effect. The roles of serotonin, dopamine, and norepinephrine are also well documented in the pathogenesis of various emotional states. Other neurotransmitters that may play a role in the pathogenesis of anxiety disorders are cholecystokinin (CCK), galanin (Gal), neuropeptide Y (NPY), oxytocin (OT), vasopressin (AVP), and corticotrophin-releasing factor.

Neuroanatomical changes in stress

Most anxiety disorder cases develop in childhood, where the long-term and repetitive experience of anxiety leads to changes in specific brain structures that can be observed using neuroimaging. fMRI studies on generalized anxiety disorder (GAD) have shown a higher level of activity in the ventrolateral prefrontal cortex. Furthermore, a significant level of activity is seen in the amygdala, especially when a person is told to focus on his or her stress, as well changes in the cingular cortex and insular cortex.

During adolescence, there is an acceleration in the physical growth, along with changes in behavior, cognition, and emotional control. The development of the body during this period may result in permanent changes in various brain areas that can be implicated in the development of psychiatric disorders in adult life.

During adolescence, it might be easier to remodel various brain structures with the help of cognitive behavioral therapy or other modalities than in adults. Meanwhile, in adults, various therapeutic agents can be used to alter the biochemical structure of the brain.

For patients with anxiety disorders, selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) are often prescribed as the first line treatment. Other drugs that can be used to treat various anxiety disorders include monoamine oxidase inhibitors, tricyclic antidepressants, and benzodiazepines.

Despite the immense progress in our understanding of neuroanatomy and neuroendocrinology, not all cases of anxiety can currently be treated. However, the latest research on the subject has improved the selection of drugs available for various anxiety disorders. For instance, benzodiazepines are known to be more efficient in the treatment of panic disorders than GAD.

As neuroimaging technologies continue to evolve, a better understanding of the neurobiology of anxiety is bound to influence the way we treat anxiety and other related disorders.

References

Andrews, G., Stewart, G., Allen, R., & Henderson, A. S. (1990). The genetics of six neurotic disorders: a twin study. Journal of Affective Disorders, 19(1), 23–29. doi:10.1016/0165-0327(90)90005-S

Bandelow, B., & Michaelis, S. (2015). Epidemiology of anxiety disorders in the 21st century. Dialogues in Clinical Neuroscience, 17(3), 327–335. PMCID: PMC4610617

Bystritsky, A., Khalsa, S. S., Cameron, M. E., & Schiffman, J. (2013). Current diagnosis and treatment of anxiety disorders. Pharmacy and Therapeutics, 38(1), 30–57. PMCID: PMC3628173

Martin, E. I., Ressler, K. J., Binder, E., & Nemeroff, C. B. (2009). The neurobiology of anxiety disorders: brain imaging, genetics, and psychoneuroendocrinology. The Psychiatric Clinics of North America, 32(3), 549–575. doi:10.1016/j.psc.2009.05.004

Miguel-Hidalgo, J. J. (2013). Brain structural and functional changes in adolescents with psychiatric disorders. International Journal of Adolescent Medicine and Health, 25(3), 245–256. doi:10.1515/ijamh-2013-0058

Morris-Rosendahl, D. J. (2002). Are there anxious genes? Dialogues in Clinical Neuroscience, 4(3), 251–260. PMCID: PMC3181683

Ravindran, L. N., & Stein, M. B. (2010). The pharmacologic treatment of anxiety disorders: a review of progress. The Journal of Clinical Psychiatry, 71(7), 839–854. doi:10.4088/JCP.10r06218blu

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Gambling Addiction: Is it as Bad as Cocaine? http://brainblogger.com/2017/12/15/gambling-addiction-is-it-as-bad-as-cocaine/ http://brainblogger.com/2017/12/15/gambling-addiction-is-it-as-bad-as-cocaine/#respond Fri, 15 Dec 2017 16:20:36 +0000 http://brainblogger.com/?p=23209 Is gambling an addictive pathology that causes changes in the brain and requires treatment? Or is it merely a compulsive behaviour? This question has long kept the medical world confused.

Traditionally, it was thought that addiction could happen only when a person is dependent on some physically existing substance. However, now this traditional way of thinking is changing. The brain seems to have a weakness of getting trapped by either a substance or experience that brings a reward, be it drugs, sex, eating, or gambling. Like addiction to substances, addiction to gambling can affect a person of any background, education level, and level of income. Many celebrities are known to be overindulging in gambling. The list includes Tiger Woods, Ben Affleck, and Pamela Anderson, to name just a few.

Once researchers agreed that pathological gambling exists, the question as to whether it is more like drug addiction or similar to other obsessive-compulsive disorders remained unanswered. Modern research seems to support the idea of higher similarity with substance addiction than with obsessive-compulsive disorder. However, it is entirely possible that pathological gambling is a heterogeneous disorder and thus shares the components of both conditions. Hence, in some people it may be more like an obsessive-compulsion, while in others it is similar to substance dependence.

Functional MRI studies seem to support the view that gambling addiction is more like a substance-abuse disorder. Therefore, in the Diagnostic and Statistical Manual of Mental Disorders (5th edition; DSM-5) is has been classified as a behavioral addiction. It does not necessarily mean that other types of this disorder do not exist, as this condition is still not fully understood from a medical point of view.

Why should gambling be considered an addiction?

Perhaps due to the absence of any physical substance, addition to experiences like gambling is more challenging to recognize until considerable harm is done. A large number of people addicted to gambling fail to accept this fact. Yet, it is no secret that gambling addiction can ruin life as effectively as substance addiction.

The person involved in gambling gets ‘high’ and finds it difficult to control or limit gambling, which is also characteristic of drugs addiction. Moreover, there are negative emotions similar to withdrawal syndrome when a person is deprived of the gambling activity. And finally, even the medications used to treat substance addiction have shown to be efficient in the management of gambling disorder.

Neural changes in gambling addiction

Any addiction is caused by the combination of several factors such as genetic causes, environmental issues, and social influences and problems.

Mesolimbic and mesocortical dopaminergic pathways are central to motivation, desire, and perception of pleasure. Dysregulation in the mesolimbic pathway (often referred to as reward pathway) is known to play a vital role in the development of addiction.

Research on pathological gambling is still ongoing; this phenomenon is still not fully understood from a neurobiological point of view. It is clear that in pathological gambling multiple neurotransmitter systems (including dopamine, serotonin, norepinephrine, opioid, and glutamate) and various brain regions are implicated (including the amygdala, nucleus accumbens, prefrontal cortex, and insula).

Addiction to gambling is the result of a pathological importance being attached to the activity. High level gambling and substance addicts give excessive motivational significance to the addictive activity. Glutamatergic projections from the prefrontal cortex to the accumbens is thought to be the neural pathway involved in provoking gambling seeking behavior. This anatomical path is found to play a role in most forms of behavior dysregulation and addiction. The prefrontal accumbens pathway is vital to providing motivational or reward salience and goal-directed behavior.

A few years ago, fMRI was used to compare the brain activity of people occasionally involved in gambling against those known to be suffering from pathological gambling. The scans demonstrated a significant difference in blood-oxygen-level dependent (BOLD) signals between the two groups in the superior temporal regions, inferior frontal, and thalamic region. Those pathologically addicted to gambling showed a distinct frontoparietal activation pattern triggered by gambling-related cues, which is known to play a role in the addiction memory network.

Treatment of pathological gambling

Though the prevalence of pathological gambling is much higher than many psychiatric disorders like schizophrenia, there is a lack of studies and trials aimed at finding the appropriate treatment for this problem. Still, there is a small number of studies that seem to favor the effectiveness of pharmacological treatment.

Drugs that have shown the ability to modulate dopaminergic transmission in the mesolimbic pathways, like opioid-receptor antagonists (e.g., naltrexone) have demonstrated effectiveness in trials. Antidepressants and mood stabilizers are the groups of drugs that may prove to be effective in overcoming gambling addiction.

Various clinical investigations have also examined the effectiveness of non-pharmacological treatments. It has been demonstrated that cognitive-behavioural therapy (CBT) could be one such option. Some studies have also investigated the usefulness of video conferencing for ongoing supervision, and the use of congruence couple therapy and therapies that have a holistic approach to the problem.

To sum up, the latest neurobiology studies confirm that gambling addiction is similar to substance addictions. It may also have serious implications for the person involved, yet little is known regarding how to effectively treat this problem.

References

Blanco, C., Moreyra, P., Nunes, E. V., Sáiz-Ruiz, J., & Ibáñez, A. (2001). Pathological gambling: addiction or compulsion? Seminars in Clinical Neuropsychiatry, 6(3), 167–176. doi:10.1053/scnp.2001.22921

Grant, J. E., & Kim, S. W. (2006). Medication Management of Pathological Gambling. Minnesota Medicine, 89(9), 44–48.

Holden, C. (2001). “Behavioral” Addictions: Do They Exist? Science, 294(5544), 980–982. doi:10.1126/science.294.5544.980

Kalivas, P. W., & Volkow, N. D. (2005). The Neural Basis of Addiction: A Pathology of Motivation and Choice. American Journal of Psychiatry, 162(8), 1403–1413. doi:10.1176/appi.ajp.162.8.1403

Leung, K. S., & Cottler, L. B. (2009). Treatment of pathological gambling. Current Opinion in Psychiatry, 22(1).  doi:10.1097/YCO.0b013e32831575d9

Miedl, S. F., Fehr, T., Meyer, G., & Herrmann, M. (2010). Neurobiological correlates of problem gambling in a quasi-realistic blackjack scenario as revealed by fMRI. Psychiatry Research: Neuroimaging, 181(3), 165–173. doi:10.1016/j.pscychresns.2009.11.008

Potenza, M. N. (2013). Neurobiology of gambling behaviors. Current Opinion in Neurobiology, 23(4), 660–667. doi:10.1016/j.conb.2013.03.004

Potenza, M. N. (2014). The neural bases of cognitive processes in gambling disorder. Trends in Cognitive Sciences, 18(8), 429–438. doi:10.1016/j.tics.2014.03.007

Urban, N. B. L., & Martinez, D. (2012). Neurobiology of Addiction:Insight from Neurochemical Imaging. Psychiatric Clinics, 35(2), 521–541. doi:10.1016/j.psc.2012.03.011
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The Neuroscience Behind the Placebo Effect http://brainblogger.com/2017/12/07/the-neuroscience-behind-the-placebo-effect/ http://brainblogger.com/2017/12/07/the-neuroscience-behind-the-placebo-effect/#respond Thu, 07 Dec 2017 16:30:51 +0000 http://brainblogger.com/?p=23200 As a child, did you ever feel better after your mother kissed your bumped knee? How do you think that worked? The power of suggestion—or the placebo effect—is a powerful psychological phenomenon that affects every aspect of our lives, dictating our preferences for food, drink, medication, social activities, and more.

Pioneering experiments describing the use of sham drugs date back to the late 18th century. A version of John Quincy’s Lexicon Medicum published in 1811 defines the placebo as ‘an epithet given to any medicine adapted more to please than to benefit the patient’. However, physicians of the past tended to use forms of treatment that they assumed were ineffective, as opposed to the modern day usage of inert substances.

A wide variety of conditions have been proven to be amenable to placebos, including depression, sleep disorders, Parkinson’s disease, and pain2. The placebo effect has been shown to impart tangible changes on the immune system similar to those who received real medication, where patients given syrup had increased white blood cell counts. Remarkably, patients with Parkinson’s disease stopped experiencing tremors and muscle stiffness after taking inert sugar pills. The success of mirror therapy in relieving phantom pain in amputees can be thought of as another example of the power of suggestion.

How our minds are fooled is not fully understood. The placebo effect may be an evolutionary adaptation that allows the brain to make quick decisions and assumptions about the environment. Consider this: if we had to analyse every single stimulus that our environment threws at us, we’d go mad in no time.

Scientists have identified that the psychological mechanisms of the placebo effect lie in both conscious expectations and learning. Although learning and expectations are not mutually exclusive, they are heavily dependent on each other.

To explain, when we expect a drug to reduce pain levels, our brains release endogenous endorphins that in turn are responsible for alleviating pain. On the other hand, the learning process involves integrating environmental and social cues in order to generate an internal expectation and subsequent placebo response. Experiencing repeated patterns of learning conditions (as in classical conditioning – think Pavlov’s dogs), causes a person to respond in a way that has spill-over-effects effects that influence unconscious physiological processes.

Multiple studies have singled out the ventromedial prefrontal cortex (vmPFC) as a main player in mediating the placebo effect. Other areas of significant importance are the dorsolateral PFC, lateral orbitofrontal cortex, periaqueductal grey area, rostroventral medulla, and nucleus accumbens-ventral striatum.

In short, the complex underlying neuronal circuits involve the higher functioning areas of the brain (frontal cortices) and the seat of unconscious processes such as breathing, the brainstem. Interestingly, rsearch reports that the placebo effect is absent in those with Alzheimer’s disease (due to degeneration of the frontal cortex) and in patients subjected to external suppression of frontal cortex function via transcranial magnetic stimulation.

The endogenous opioid system and its role in placebo-induced analgesia is perhaps the best studied neurotransmitter system involved in the placebo effect. Naloxone, an opioid receptor antagonist, has been found to nullify the effects of placebo pain-killers. Other systems that have been implicated include the cannabinoid system.

These neuroanatomical and neurobiological findings likely have much room for growth and refinement considering that different placebo responses have been found to invoke different parts of the placebo circuit.

Given the complicated psychological mechanisms behind the placebo, it comes as no surprise that various factors are able to modulate its strength. Social context has a real impact on the placebo effect, as it fosters preconceived notions regarding treatment. For example, several trials showed that similar benefits were experienced by both groups of patients who underwent either traditional or sham Chinese acupuncture (the latter involving superficial needling at non-acupuncture points). The physician attitude and appearance of competency, as well as the cost, branding, shape, size, color, and taste of the pills were able to affect the perceived treatment efficacy.

It is common beleif that one must be unaware of the placebo in order for the placebo effect to work. Not so, argue a group of researchers from the University of Basel (Switzerland) and Harvard Medical School. They demonstrated that participants who were told that they were getting placebos and who received detailed explanations of the placebo effect experienced significant relief from heat-induced pain compared to those that were not told that they were given bogus drugs.

These surprising results underscore the formidable effects of the placebo effect and how much more there is still left to learn. Furthermore, this study opens doors to more ethically designed placebo-controlled studies. Withholding potentially beneficial treatment from patients in placebo-controlled trials is considered inherently unethical. However, with this study, it appears that full disclosure may not be that different to the traditional practices of keeping placebo patient groups in the dark.

In order to manipulate the placebo effect for clinical benefit, the notion of placebo responders and non-placebo responders was investigated. Are some people more amenable to the power of suggestion than others? If so, is it due to unchangeable genetic makeup or individual personality? Other questions that come to mind regard the persistency of the placebo effect. For how long does it last and does it transfer to other types of placebos? To illustrate, will a person responding to placebo painkillers for pain relief also respond to placebo antidepressants for improved moods?

In conclusion, we know that the placebo is a strong weapon in the clinician’s armamentarium. Despite that, the unpredictable variability of its effects obligates future research that enables us to get a better understanding of exactly when and for how long the placebo effect will work.

References

de craen A, Kaptchuk T, Tijssen J et al. Placebos and placebo effects in medicine: historical overview. J R Soc Med. 1999;92:511-515. PMCID: PMC1297390

Price DD, Finniss DG, Benedetti F. A comprehensive review of the placebo effect: recent advances and current thought. Annu. Rev. Psychol. 2008. 59:565–90. doi:10.1146/annurev.psych.59.113006.095941

Colloca L, Miller FG. How placebo responses are formed: a learning perspective. Philosophical Transactions of the Royal Society B: Biological Sciences. 2011;366(1572):1859-1869. doi:10.1098/rstb.2010.0398.

Geuter S, Koban L, Wager TD. The cognitive neuroscience of placebo effects: concepts, predictions and physiology. Annu. Rev. Neurosci. 2017. 40:167–88. doi:10.1146/annurev-neuro-072116-031132.

Wager TD, Atlas LY. The neuroscience of placebo effects: connecting context, learning and health. Nat Rev Neurosci. 2015 Jul;16(7):403-18. doi:10.1038/nrn3976.

Miller FG, Colloca L, Kaptchuk TJ. The placebo effect: illness and interpersonal healing. Perspectives in biology and medicine. 2009;52(4):518. doi:10.1353/pbm.0.0115.

Buckalew LW, Coffield KE. An investigation of drug expectancy as a function of capsule color and size and preparation form. J Clin Psychopharmacol. 1982 Aug;2(4):245-8. PMID: 7119132

Howe LC, Goyer, J. P., & Crum, A. J. Harnessing the placebo effect: Exploring the influence of physician characteristics on placebo response. Health Psychology. 2017;36(11):1074-82. doi:10.1037/hea0000499.

Locher C, Frey Nascimento A, Kirsch I et al. Is the rationale more important than deception? A randomized controlled trial of open-label placebo analgesia. Pain. 2017 Dec;158(12):2320-2328. doi:10.1097/j.pain.0000000000001012.

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God in the Brain: the Science of Neurotheology http://brainblogger.com/2017/11/19/god-in-the-brain-the-science-of-neurotheology/ http://brainblogger.com/2017/11/19/god-in-the-brain-the-science-of-neurotheology/#respond Sun, 19 Nov 2017 16:30:20 +0000 http://brainblogger.com/?p=23114 We are the only species on the planet known to practice religion. This feature is universal among humans: there is no nation on Earth that does not practice one or another form of spiritual belief.

The question is what makes our brain different so that we practice spirituality? Does religion serve any purpose to our species in terms of benefiting survival and progress? These questions are very philosophical. Many thinkers believe that religiosity is what distinguishes Homo sapiens from the rest of the animal kingdom and brought our species to dominate this planet. On the other hand, a large numbers of thinkers believe that religion impedes progress and keeps our society in a barbaric state. There is no doubt that religion played a very important role in early human history: providing the first explanations for the existence of the world around us. The need for such explanation highlights an important step in the development of the brain and cognitive processes.

Behavioral traits might become strengthened by evolution if they bring survival benefits. Researchers think that altruism, for instance, is this kind of behavioral trait: it might be disadvantageous for a particular individual at a particular instance, but it brings advantages to the species in general. Altruistic behavior is promoted by the majority of the world’s religions. Therefore, religious practices might have provided evolutionary advantages for early humans in terms of survival too.

Some people are so deeply religious that the system of beliefs they practice shapes their whole life. It would be reasonable to assume that something interesting should be going on in their brain. It is also quite likely that these brain processes are different from the processes in the brains of unbelievers. This is what the new science of neurotheology is aiming to study. Neurotheology investigates the neural correlates of religious and spiritual beliefs. Such studies may help to uncover why some people are more inclined towards spirituality, while others remain deeply skeptical about the whole idea of God’s existence.

There are already some interesting findings from the field of neuroscience that can help to open the window into the spiritual brain.

First, there is no single part of the brain which is “responsible” for an individual’s relationship with their God/s. Like any emotionally intense human experience, religious experiences involves multiple parts and systems of the brain. Several experiments with the use of brain scanners confirm this point of view. In one study, Carmelite nuns were asked to remember their most intense mystical experience while neuroimaging of their brain was conducted. The loci of activation in this experiment were observed in the right medial orbitofrontal cortex, right middle temporal cortex, right inferior and superior parietal lobules, right caudate, left medial prefrontal cortex, left anterior cingulate cortex, left inferior parietal lobule, left insula, left caudate, and left brainstem.

Similarly, an fMRI study on religious Mormon subjects found areas of activation in the nucleus accumbens, ventromedial prefrontal cortex, and frontal attentional regions. The nucleus accumbens is the brain area associated with reward. It is also involved in emotional responses to  love, sex, drugs, and music. One recent study also identified a number of changes in regional cortical volumes that are associated with several components of religiosity, such as an intimate relationship with God and fear of God.

It appears likely that life-changing religious experiences may be linked to changes in brain structure. For instance, one study demonstrated that the brains of older adults who reported such experiences feature a degree of hippocampal atrophy. Hippocampal atrophy is an important factor in the development of depression, dementia, and Alzheimer’s disease. It remains unclear exactly how structural changes in the brain and the level of religiosity relate to each other.

It is well known that some drugs simulate spiritual experiences. For instance, psilosybin, the active ingredient in “magic mushrooms”, stimulates temporal lobes and mimics religious experiences. This implies that spirituality is rooted in neuronal physiology. It is no wonder that psychoactive compounds are often used in ritualistic and shamanistic practices around the world.

All studies that involve brain imaging of people in specific states suffer from one major limitation: it is hard to be sure that people are actually in that particular state at the time of measurement. For instance, if we measure the brain activity when a subject is supposed to solve a mathematical task, we can’t be 100% sure that his or her mind is not wondering around instead of focusing on the task. The same applies to the measurement of any spiritual state. Therefore, the patterns of brain activation obtained through brain imaging should not be viewed as ultimate proof of any theory.

Various religious practices have the potential to influence our health, in both positive and negative directions. It was noted that religious people, in general, have a lower risk of anxiety and depression. This, in turn, is linked to a stronger immune system. On the other hand, people engaged in religious struggles might experience the opposite effects. Research into the brain’s response to religious practices might help to develop further our understanding of the connection between health and spirituality.

References

Beauregard M and Paquette V (2006) Neural correlates of a mystical experience in Carmelite nuns. Neuroscience Letters 405(3):186-90. DOI: 10.1016/j.neulet.2006.06.060

Ferguson MA et al. (2016) Reward, salience, and attentional networks are activated by religious experience in devout Mormons. Social Neuroscience: 1–13. doi:10.1080/17470919.2016.1257437.

Griffiths RR et al. (2006) Psilocybin can occasion mystical-type experiences having substantial and sustained personal meaning and spiritual significance. Psychopharmacology. 187 (3): 268–83; discussion 284–92. doi:10.1007/s00213-006-0457-5.

Griffiths RR et al. (2008) Mystical-type experiences occasioned by psilocybin mediate the attribution of personal meaning and spiritual significance 14 months later. Journal of psychopharmacology. 22 (6): 621–32. doi:10.1177/0269881108094300.

Kapogiannis D et al. (2009) Neuroanatomical Variability of Religiosity. PLoS ONE4(9): e7180. https://doi.org/10.1371/journal.pone.0007180

Kapogiannis D et al. (2009). Cognitive and neural foundations of religious belief. Proceedings of the National Academy of Sciences of the United States of America, 106(12), 4876–4881. http://doi.org/10.1073/pnas.0811717106

Owen AD et al. (2011) Religious factors and hippocampal atrophy in late life. PLoS ONE. 6 (3): e17006. doi:10.1371/journal.pone.0017006.

Sayadmansour A (2014) Neurotheology: The relationship between brain and religion. Iranian Journal of Neurology, 13(1), 52–55.

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Criminal Brain: Fact or Fiction? http://brainblogger.com/2017/11/16/criminal-brain-fact-or-fiction/ http://brainblogger.com/2017/11/16/criminal-brain-fact-or-fiction/#respond Thu, 16 Nov 2017 16:30:54 +0000 http://brainblogger.com/?p=23105 When we are confronted with the acts of excessive and unprovoked violence, we can’t help but wonder what is wrong with individuals committing such crimes. Think of serial killers: what motivates them? Both researchers and society, in general, have wanted to know how to explain the extreme brutality observed in some people. In most cases, they have no mental disorders that could explain their behavior. Even without going to the extremes, most of us did at some point in life come across people whose level of aggressiveness seemed beyond any reasonable explanation. Think of a hooligan looking for any excuse to pick a fight and beat someone up. Or a young boy torturing a defenseless animal with a smile on his face. Multiple theories were invented to this end, ranging from religious explanations (satanic possession) to scientific and psychological theories that involve a variety of mental disorders or problems with brain development.

The idea that excessive aggressiveness and criminal tendency might be heritable traits gained popularity with the publication of Dr. Cesare Lombroso’s book “Criminal Man” in 1878. In the book, Lombroso introduced the concept of the “born criminal”. He also developed the field of criminal anthropology that studied specific anatomical differences between normal and criminal individuals. Lombroso’s theory contributed to the science of eugenics that played a crucial role in the Nazi ideology of selective breeding of a superior race and the policy of exterminating the Untermenschen.

Although Lombroso was eventually proven wrong, the concept that criminal behavior might be linked with genes survived. Evidence that criminal and violent behaviors run in some families was a particularly strong argument to investigate the issue further. These investigations produced rather interesting discoveries.

The question to what degree the predisposition for crime might be genetically determined was first answered by a twin study performed in Denmark. Twins are ideal subjects for genetic research: identical twins have exactly the same sets of genes, while non-identical twins are as similar to each other as usual brothers and sisters. However, both identical and non-identical twins, if brought up together, can be considered as having the same upbringing. The study compared the rate of crime offenses among the identical twins with this rate in non-identical twins. It turned out that a Danish man with an identical twin who has a criminal record is 50% more likely to be an offender himself, as compared with the average Danish man. In non-identical twins, the chances of both of them having the criminal records are 15-30% higher than the average for the population. The findings definitely point to a degree of genetic predisposition. In addition, another study performed in Sweden has shown that when the identical twins were brought up separately, the chances of developing a criminal career were higher among children from parents with criminal records, even when the children were brought up in law-abiding adopted families.

Twin studies can detect correlations but certainly can’t help in finding out which genes are behind these correlations. The study performed in the Netherlands provided important information on the possible identity of such genes. Researchers have studied genetic defects in one particular family with 14 males spanning 4 generations that displayed an unusually high level of aggression and criminal offenses. The subjects in question had very low IQ (around 85) and were prone to impulsive behavior and physical and sexual violence. The researchers found a specific hereditary defect in the family: the gene for monoamine oxidase A (MAOA) was mutated. Mutation prevented the enzyme from working properly. This is important as this enzyme is responsible for breaking down neurotransmitters, including serotonin, dopamine, and noradrenaline. A lack of MAOA activity leads to the rising of neurotransmitter levels in the brain and they, in turn, cause the over-excitation of neurons. The gene for MAOA is located on the X chromosome, and this explains why high levels of aggression were observed only in males. Meanwhile, females have a second X chromosome with the non-mutated functional version of the gene.

An important question, which sparked fierce ethical debate, is to what extent criminal behavior might indeed be genetically programmed. This is a classic discussion of nature vs nurture. To what extent do our genes make us who we are? We easily accept the fact that some people are born smarter or physically stronger than the rest of us. We know that genes are involved in making these individuals who they are. Genes responsible for stronger muscles or better brain connections allow these people to excel where others may struggle. Nonetheless, the idea that some of us are born with a predisposition for a higher level of aggression or reduced empathy appears very unpalatable to many people. However, this idea makes perfect biological sense. We evolved as hunter-gatherers, and at this stage of our evolutionary history, aggressiveness was crucially important for survival. Genetically, we didn’t change since the Stone Age. And this aggressiveness still plays an important role in our society, from competition in the workplace to multiple armed conflicts around the world. Aggression levels, like many other human behavioral traits, can be genetically determined to a degree. This means that there is variability: in some people, the level of aggressiveness is very low, while in others it can be quite high.

Aggressiveness still doesn’t equal crime: although violent crime requires a perpetrator to be aggressive, the two things are not the same. Social factors still play a key role when it comes to the expression of aggressive behavior. It works the same way with other genetic attributes. A born athlete will never reach his Olympic dream and could turn into a couch potato if they don’t train. Most scientists, even the very successful ones, are not born geniuses: they simply worked and studied hard. Similarly, people with a predisposition for higher levels of aggression are at higher risk of becoming criminals when they are exposed to the social factors that lead them in that direction.

References

Baum ML (2013) The Monoamine Oxidase A (MAOA) Genetic Predisposition to Impulsive Violence: Is It Relevant to Criminal Trials? Neuroethics 6, 287-306. doi: 10.1007/s12152-011-9108-6.

Brunner HG; Nelen MR; van Zandvoort P; Abeling NGGM; van Gennip AH; Wolters EC; Kuiper MA; Ropers HH; van Oost BA (1993) X-linked borderline mental retardation with prominent behavioral disturbance: phenotype, genetic localization, and evidence for disturbed monoamine metabolism. Am. J. Hum. Genet. 52 (6): 1032–9. PMID 8503438.

Buades-Rotger, M., & Gallardo-Pujol, D. (2014). The role of the monoamine oxidase A gene in moderating the response to adversity and associated antisocial behavior: a review. Psychology Research and Behavior Management, 7, 185–200. doi: 10.2147/PRBM.S40458

Christiansen KO. Seriousness of criminality and concordance among Danish twins. In: Hood R, editor. Crime, Criminology and Public Policy. The Free Press; New York: 1974. pp. 63–77.

Farrington DP, Gundry G, West DJ (1975) The familial transmission of criminality. Med Sci Law 15(3):177-86. doi: 10.1177/002580247501500306

Hunter P (2010) The psycho gene. EMBO Rep. 11 (9): 667–9. doi: 10.1038/embor.2010.122.

Kendler, K. S., Lönn, S. L., Morris, N. A., Sundquist, J., Långström, N., & Sundquist, K. (2014). A Swedish national adoption study of criminality. Psychological Medicine, 44(9), 1913–1925. doi: 10.1017/S0033291713002638.
McDermott R et al. (2009) Monoamine oxidase A gene (MAOA) predicts behavioral aggression following provocation. Proc Natl Acad Sci USA 106, 2118–2123. doi: 10.1073/pnas.0808376106.

Taylor S (2013) Criminal Minds: The Infuence of the Monoamine Oxidase AGenotype and Environmental Stressors on Aggressive Behaviour. Burgmann Journal II, 71-77. link here

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The Puzzle of Multiple Personality Disorder http://brainblogger.com/2017/11/14/the-puzzle-of-multiple-personality-disorder/ http://brainblogger.com/2017/11/14/the-puzzle-of-multiple-personality-disorder/#respond Tue, 14 Nov 2017 16:30:21 +0000 http://brainblogger.com/?p=23056 Dissociative identity disorder (DID, commonly referred to as multiple personality disorder) is well known to the general public through multiple movies and books. However, the disease remains poorly understood and rather mysterious for the medical specialists. The definition of this disorder implies that a patient has at least two distinctive and relatively long-lasting identities (sometimes called “alters”) that manifest themselves in a person’s behavior. Their presence is accompanied by memory impairments that cannot be explained by usual forgetfulness.

However, there are no clear clinical criteria to help in the diagnostics. There is a whole range of dissociative disorders that range from daydreaming and lapses in attention to serious pathologies. The diagnostics rely on descriptive data rather than something measurable. This leads to lots of confusion, controversies, and inconsistencies.

Historically, the incidence of multiple personality disorder varied wildly. For a long time, the condition was considered among the rarest psychological disorders, with less than 100 cases described before 1944. The incidence of DID rose sharply in the 1970s–1980s, reaching 20,000 by the end of the century. In addition, this growth was accompanied by the increase in the number of alters reported in patients, from just one to 13–16 by the 1980s. These changes in the statistics might have been caused by increasing recognition of the disease symptoms among practitioners, but also led to the growing skepticism in the research community about the very existence of this distinct condition.

The variability on the geographic distribution of this condition is substantial too: the disorder is diagnosed in the US much more frequently than anywhere else. The overwhelming majority of publications on this condition originate from North America, making some researchers believe that DID is a purely American disease confined to this continent. This further adds to the skepticism of many health practitioners: there are no reasons to believe that qualified specialists capable of recognizing this condition are vastly underrepresented in other developed countries.

There is little clarity regarding what causes the disorder. The iatrogenic hypothesis suggests that DID can be a result of psychotherapeutic treatment, while the traumatogenic hypothesis states that the disease develops as a result of severe trauma, usually in childhood. Some researchers believe that most cases of DID are pseudogenic, i.e., simulated. There is an opinion that many patients want to believe that they have the disorder, to explain the inconsistencies in their own behavior.

The incidence of DID is 5–9 times higher in females compared to males. Again, there is no agreement among specialists regarding what causes such a big gender difference.

The potential reasons for the sharp increase in the incidence of DID were examined in the scientific literature. Although there are many possible explanations for this phenomenon, the iatrogenic explanation appears to be the most substantiated. The unusually large number of diagnosis in the 1980s were clustered around a small number of practitioners, many of whom used hypnosis as a therapeutic tool. It is quite possible that under the influence of hypnosis the patients with a higher level of suggestibility may start to believe that they are suffering from split personality disorder, and behave accordingly. The level of hypnotisability of people with the diagnosis of DID is known to be the highest among any clinical population.

The rise of the DID diagnosis numbers also correlated with the growing number of split personality cases in the criminal court cases. The defense on the basis of DID was rarely successful, as it was often assumed that the defenders simply pretend to have the disorder to avoid taking responsibility for their crimes.

An opinion exists that the manifestations of DID are simply the consequences of other disorders such as bipolar disorder, schizophrenia, and borderline personality disorder. Many patients diagnosed with DID have previous history of these and other psychiatric conditions. Another theory suggests that the manifestations of DID are the consequences of trauma. There is plenty of clinical cases in support of this theory, but not so much statistical data.

Nonetheless, it is well proven that people with DID are at higher risk of depression and suicide. The patients often suffer from post-traumatic stress disorder, substance abuse, anxiety and eating disorders. Such statistics are not uncommon in other psychiatric conditions, though.

Importantly, there is a shortage of proper neurological studies of this disorder. Nobody knows what exactly causes it and what kind of changes take place in the brains of patients diagnosed with this disease. The brain imaging data from patients with DID do not reveal any specific diagnostic patterns. Several studies demonstrated that the changes in personality state in the DID patients are associated with certain changes in the blood flow in the brain. There are also differences in the brain blood flow patterns between patients with DID and healthy control subjects. It remains uncertain if these differences can be used in the diagnostics.

The question of how real the majority of DID cases are is yet to be fully answered. In general, researchers agree that there are cases with very pronounced and obvious manifestations that would be rather hard to explain without invoking the concept of DID. However, when it comes to less severe cases, the diagnostic remains really problematic. This creates a problem for patients, as not knowing the specific diagnosis means the lack of clarity with treating the problem. Also, there is no consensus regarding how to treat the split personality disorder. Various psychotherapeutic and hypnotherapeutic techniques are currently used, but their efficacy remains unknown due to the absence of controlled randomised clinical trials. Clearly, there is a lot of room for further research in this field.

References

Maldonado, JR; Spiegel D (2008) Dissociative disorders — Dissociative identity disorder (Multiple personality disorder). In Hales RE; Yudofsky SC; Gabbard GO; with foreword by Alan F. Schatzberg. The American Psychiatric Publishing textbook of psychiatry (5th ed.). Washington, DC: American Psychiatric Pub.

Reinders AA (2008) Cross-examining dissociative identity disorder: Neuroimaging and etiology on trial. Neurocase. 14 (1): 44–53. doi:10.1080/13554790801992768.

Paris J (1996) Review-Essay: Dissociative Symptoms, Dissociative Disorders, and Cultural Psychiatry. Transcult Psychiatry. 33 (1): 55–68. doi:10.1177/136346159603300104.

Kihlstrom JF (2005) Dissociative disorders. Annual Review of Clinical Psychology. 1 (1): 227–53. doi:10.1146/annurev.clinpsy.1.102803.143925.

Atchison M, McFarlane AC (1994) A review of dissociation and dissociative disorders. The Australian and New Zealand Journal of Psychiatry. 28 (4): 591–9. doi:10.3109/00048679409080782.

Piper A, Merskey H (2004) The persistence of folly: A critical examination of dissociative identity disorder. Part I. The excesses of an improbable concept. Canadian Journal of Psychiatry. 49 (9): 592–600. PMID 15503730.

Spiegel D, Loewenstein RJ, Lewis-Fernández R, Sar V, Simeon D, Vermetten E, Cardeña E, Dell PF (2011) Dissociative disorders in DSM-5. Depression and Anxiety. 28 (9): 824–852. doi:10.1002/da.20874.

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Antidepressants During Pregnancy Dangerous for the Child? http://brainblogger.com/2017/10/25/antidepressants-during-pregnancy-dangerous-for-the-child/ http://brainblogger.com/2017/10/25/antidepressants-during-pregnancy-dangerous-for-the-child/#respond Wed, 25 Oct 2017 15:00:25 +0000 http://brainblogger.com/?p=23013 Depression is sometimes described as a disease of modernity, as sharp changes in lifestyle during the last century or so have given rise to many chronic disorders including or linked to depression. Depression is a state of low mood: the person affected tends to lose interest in previously enjoyable activities. In severe cases, self-harm is also possible. Fortunately, there are many options available today to help treat this condition.

Research studies and statistics show that although pregnant women are less prone to major depression, they are more inclined to minor depressive episodes. The prevalence of depression can be anywhere between 8–16% among pregnant women. There are also higher chances that diagnosis of depression is overlooked in pregnant women.

The treatment of depression is quite challenging in pregnancy, as medical specialists have to weigh the benefits of treatment against the risks for the mother and the health of her unborn baby. Furthermore, the health professional has to take into consideration the risks and benefits of any such therapy to the long-term health of the child. New research seems to indicate that treatment of pregnant women with antidepressant drugs may increase the risk of autism, disturbances in motor function, and mental health problem in children. Some of these issues may become clear later in the life, thus studying this subject remains a challenge for researchers.

Why treat depression in pregnancy?

There is a widespread misconception that depression is not as threatening as other medical illnesses. Thus, treating depression is viewed as a matter of choice or even a luxury. Moreover, many patients that are on antidepressant drugs before pregnancy are in the remissive stage. Therefore, their doctors may think of discontinuing the therapy.

However, if a pregnant woman that is vulnerable to depression is not provided with antidepressant therapy, there is a higher risk of preterm birth, low birth weight, substance abuse in pregnancy (e.g., smoking and drinking alcohol), and a significantly higher risk of postpartum depression.

Research has shown that if antidepressants are discontinued for the period of the pregnancy, the relapse rate of major depression is as high as 60–70%. This can have severe consequences for the patient, family, and child. In addition, children born to mothers with untreated depression have higher levels of cortisol, which may have adverse impacts on their health.

Risks of antidepressants

As already mentioned, the use of antidepressants in pregnancy is a complicated issue due to possible dangers. Below are some of the common problems associated with the use of antidepressants during pregnancy.

Persistent pulmonary hypertension

This is a failure of lungs blood vessels to dilate in a child post-birth. Thus, a new-born may have breathing difficulties, a deficit of oxygen in the blood, leading to intubation. In many cases, outcomes may be fatal. This condition is also found to be related to maternal smoking, diabetes, and sepsis. Though the risk of persistent pulmonary hypertension in new-born increases up to six times with the use of antidepressants, at the same time there is a consensus among the medical community that non-use of antidepressants may be even more harmful.

Withdrawal symptoms

This is also called “poor neonatal adaptation.” These symptoms are common when a mother has been exposed to antidepressants during the third trimester of pregnancy. Some of the symptoms characteristic of this syndrome include difficulties in breathing, unstable body temperature, hypo- or hypertonia, irritability, constant crying, and seizures. Therefore, some specialists recommend tapering the dose of antidepressants in the third trimester.

Motor development

By motor development, we mean child’s ability to move around and handle the environment. There are clinical studies that indicate that the use of antidepressants during pregnancy may slow the motor development. A child may start walking later than other kids, or may have other problems related to movements.

Autism spectrum disorders

This is a neurodevelopmental disorder of children. Studies seem to show the modest increase in the risk of autism if a mother is exposed to antidepressants during the first trimester.  However, no link has been found if such treatment has been given before the pregnancy, nor much relationship has been demonstrated if the therapy was initiated in a later phase of pregnancy. Thus, researchers caution that decision of prescribing antidepressants should be taken on a case by case basis by analysing the risks and potential benefits for maternal and child health.

Psychiatric disorders

In one of the large-scale studies, scientists analysed the data of almost one million births, and they found that the use of antidepressants in pregnancy was related to higher risk of developing psychiatric disorders later in life. Nonetheless, at the same time, researchers cautioned against jumping to the quick conclusions because it is a well-known fact that mental disorders have relation to genetics. It means that women prescribed antidepressants during the pregnancy have higher chances of passing to children the genes that may result in psychiatric diseases later in life.

Although antidepressants may increase the risk of specific disorders in the new-born babies or may even have a negative impact later in the life, it does not mean that antidepressants should not be taken during the pregnancy. It is essential that women should not feel guilty about taking such drugs. The medical specialists must be aware of the risks and weigh them against the benefits before they prescribe antidepressants to pregnant women.

References

Casper, R.C., Fleisher, B.E., Lee-Ancajas, J.C., Gilles, A., Gaylor, E., DeBattista, A., Hoyme, H.E., 2003. Follow-up of children of depressed mothers exposed or not exposed to antidepressant drugs during pregnancy. J. Pediatr. 142, 402–408. doi:10.1067/mpd.2003.139

Croen, L.A., Grether, J.K., Yoshida, C.K., Odouli, R., Hendrick, V., 2011. Antidepressant Use During Pregnancy and Childhood Autism Spectrum Disorders. Arch. Gen. Psychiatry 68, 1104–1112. doi:10.1001/archgenpsychiatry.2011.73

Ko, J.Y., Farr, S.L., Dietz, P.M., Robbins, C.L., 2012. Depression and Treatment Among U.S. Pregnant and Nonpregnant Women of Reproductive Age, 2005–2009. J. Womens Health 2002 21, 830–836. doi:10.1089/jwh.2011.3466

Payne, J.L., Meltzer-Brody, S., 2009. Antidepressant Use During Pregnancy: Current Controversies and Treatment Strategies. Clin. Obstet. Gynecol. 52, 469–482. doi:10.1097/GRF.0b013e3181b52e20

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One Ring to Rule Them All: Cure-all Drug for Neurodegenerative Conditions Possible http://brainblogger.com/2017/10/23/one-ring-to-rule-them-all-single-drug-for-several-neurodegenerative-conditions-looks-possible/ http://brainblogger.com/2017/10/23/one-ring-to-rule-them-all-single-drug-for-several-neurodegenerative-conditions-looks-possible/#respond Mon, 23 Oct 2017 15:00:36 +0000 http://brainblogger.com/?p=22946 The secret to finding a single drug treatment for neurodegenerative conditions may lie in unfolding the mystery of misfolded proteins. Most of the non-infectious neurodegenerative diseases (like Alzheimer’s and Parkinson’s) are characterized by progressive death of neurons due to the accumulation of misfolded proteins in brain cells.

To understand the pathogenesis of these diseases we have to first understand proteins.  They are essential for building our body structures and functional regulation. Thus, there are thousands of different proteins with various functions. These proteins are made up of only 20 amino acids. These 20 amino acids are like the alphabet in a language, they can create thousands or millions of proteins when used in different combinations. A single misplaced letter in a word results in a spelling error. Similarly, a misplaced amino acid can create the wrong kind of protein. Misplaced words can create a grammatically wrong and incomprehensible sentence. In a similar fashion, misfolded proteins have no structural or functional value.

Another important concept that has to be understood is how prions are involved. From school books, we know that infections are caused by microorganisms like bacteria, fungi, and viruses. All of them have genetic material in the form of nucleic acids (as DNA or RNA, or both), that is essential for the reproduction or multiplication of these microorganisms. But prions, unlike microorganisms, are just protein chains that are infectious. These proteins, after entering the living organism, cause misfolding of proteinaceous infectious particles (PrPs). PrPs are found in all of us, our brain and neurons are especially rich in them. Their role, however, is still poorly understood.

Misfolded PrPs cause encephalopathies. These misfolded proteins are also thought to cause a chain reaction resulting in the misfolding of other proteins. These misfolded proteins propagate further like an infectious microorganism. What causes this chain reaction and propagation is still unclear. These chains of proteins are called prions. They cause Creutzfeldt-Jakob disease (CJD) in humans and bovine spongiform encephalopathy (BSE) in cattle. Prions have a long incubation period, it takes a long time for the disease to appear and progress.

In many neurodegenerative diseases like Alzheimer’s and Parkinson’s, misfolded proteins get progressively accumulated in brain cells, leading to the death of neurons. There is growing evidence that the prion-like process of seeding and templated protein corruption are behind the progression of these diseases.

PrP (healthy prion) is commonly found in our brain cells. However, when a defective prion protein is somehow introduced into the cells, it causes misfolding of newly forming PrP. This process is progressive and propagated like an infectious disease to the other cells. Thus, one of the potential treatment approaches is to block the propagation of this prion-like protein.

Accumulation of these prion-like misfolded, mutant proteins is toxic for cells. The prolonged toxic stress produced in brain cells induces specific death pathways. Understanding how these toxic proteins cause stress for neurons and why the cells die could also help to find new treatment strategies.

With increasing evidence that prion-like mechanisms are behind the progression and propagation of most neurodegenerative disorders, scientists have started looking for methods to stop this propagation. One such method is the use of specific immunotherapy, where researchers are trying to develop vaccines that can cure these disorders, or at least stop disease progression.

Larger proteins in our body contain hundreds or thousands of amino acids in various combinations. These large proteins are folded into specific structures. If a protein is misfolded, it loses its specific structure too. It also loses its properties and becomes toxic for cells. One therapeutic approach aims to develop a vaccine that can activate our immune system (B and T cells) against these defective misfolded proteins so that they are destroyed in a timely manner.

To achieve this aim, scientist have tried two methods. One of them is to create a vaccine that works against very short chains of misfolded proteins called monomers. They exist while these proteins are being assembled. Another approach is to target the fully formed misfolded protein fibrils. However, both of these methods have so far failed to produce the intended results.

Recently, researchers are exploring a new strategy for the development of immunotherapy against these diseases. This strategy targets so-called “oligomers”. The oligomers are molecular intermediates that exist in the process of assembling the prion fibrils. They are not very small like monomers (initial building blocks of prions) and are also not fully formed prion fibrils.

Smaller monomers lack the antigenic properties (associated with protein structures called beta-sheets) of misfolded proteins that are needed for an immune response. Meanwhile, fully formed fibrils are too big to propagate through cell walls. Thus, it is quite possible that these oligomers play a critical role in the disease propagation processes. A vaccine or immunotherapy targeting these oligomers could be more effective in initiating an immune response against the misfolded pathological prions than their smaller or larger counterparts. Moreover, these intermediate oligomers are common to most neurodegenerative disorders, unlike fully formed fibrils that are specific to each disease.

Although this new approach has shown some success in animal models, there are several challenges to using such immunotherapy in humans. In humans, it is not easy to initiate the immune response because of “self-tolerance.” The misfolded proteins are very similar to normal proteins (normal PrPs). Even if this immune tolerance can be overcome, there is a risk of initiating the wrong kind of immune response against normal proteins. This may lead to sterile encephalopathy or another kind of damage. Further, the blood-brain barrier also poses a challenge: it is important that antibodies created by a vaccine are able to reach a good concentration in the brain.

Despite these challenges, the idea of having just a single approach to treat all (or at least most) types of neurodegeneration is clearly exciting. These diseases have lots in common in terms of the molecular mechanisms involved, and it is quite likely that immunotherapy targeting all of them can be developed.

References

Frost, B., Diamond, M.I., 2010. Prion-like Mechanisms in Neurodegenerative Diseases. Nat. Rev. Neurosci. 11, 155–159. doi:10.1038/nrn2786

Goedert, M., Clavaguera, F., Tolnay, M., 2010. The propagation of prion-like protein inclusions in neurodegenerative diseases. Trends Neurosci. 33, 317–325. doi:10.1016/j.tins.2010.04.003

Marciniuk, K., Taschuk, R., Napper, S., 2013. Evidence for Prion-Like Mechanisms in Several Neurodegenerative Diseases: Potential Implications for Immunotherapy. J. Immunol. Res. doi:10.1155/2013/473706

Rao, R.V., Bredesen, D.E., 2004. Misfolded proteins, endoplasmic reticulum stress and neurodegeneration. Curr. Opin. Cell Biol. 16, 653–662. doi:10.1016/j.ceb.2004.09.012

Walker, L.C., Diamond, M.I., Duff, K.E., Hyman, B.T., 2013. Mechanisms of Protein Seeding in Neurodegenerative Diseases. JAMA Neurol. 70, 304–310. doi:10.1001/jamaneurol.2013.1453

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Electrical Brain Stimulation in Treatment of Neurodegenerative Diseases http://brainblogger.com/2017/10/16/electrical-brain-stimulation-in-treatment-of-neurodegenerative-diseases/ http://brainblogger.com/2017/10/16/electrical-brain-stimulation-in-treatment-of-neurodegenerative-diseases/#respond Mon, 16 Oct 2017 15:30:51 +0000 http://brainblogger.com/?p=22944 The early Egyptians and Romans recognized the numbing effect of the electric properties of catfish. In fact, Romans were the first to cultivate electric fishes for pain relieving effect. But since then, not much has changed in the development of electricity based medical treatments. Things only started to change two millennia later with the discovery of electricity and a better understanding of neurophysiology.

Electroconvulsive therapy was born in the middle of the 19th century. In the early days, it was primarily used to treat neuropsychiatric disorders. In the mid-19th century, direct electric current was used for electroconvulsive therapy. By the end of 19th-century, the alternate current was discovered, and its use along with the use of magnetic fields became the subject of experiments not only investigating neuropsychiatric conditions but also other diseases like epilepsy and chronic severe headaches.

Electroconvulsive therapy is still used in the treatment of severe neuropsychiatric conditions like schizophrenia or depression, where suicidal tendencies do not respond to pharmacological agents. Unlike in the old days, now this is a non-invasive treatment usually performed under general anesthesia. The therapy non-selectively resets various centers in the brain and thus has wide-ranging side effects like loss of memory, headaches, and muscle aches.

Considering the widespread side effects of electroconvulsive therapy, the need for more selective stimulation of particular brain centers specific for a particular disease was obvious. The improvements in understanding of brain physiology and surgical techniques gave rise to “deep brain stimulation” (DBS). This is an invasive method where electrodes are surgically placed inside the specific part of the brain that are connected to a small electrical device that generates the stimulation.

At present, DBS has been shown to be effective in the treatment of Parkinson’s disease, epilepsy, obsessive compulsive disorder, and dystonia. It is being studied for applications in treating depression, drug addiction, and other neurodegenerative disorders such as dementia. As the method is invasive and involves the surgical implantation of electrodes inside the brain, it is reserved for cases that fail to respond to pharmacological therapy.

Deep brain stimulation in Parkinson’s disease

Dopamine is a chemical messenger in the brain that plays an important role in physical movement. In Parkinson’s disease, there is a progressive loss of dopamine-producing neurons resulting in motor deficiencies. Thus, the first line therapy for this disease is to give dopamine replacement therapy by prescribing a drug called levodopa.

The problem is, one-third of cases of Parkinson’s disease progress quickly and stop responding to the therapy with levodopa or other pharmacological agents, thus necessitating a treatment like DBS.

For the best results, it is recommended to go for DBS well before the symptoms become debilitating. In the later stages, the effectiveness of DBM tends to be lower.

DBS in Parkinson’s disease involves the application of continuous high-frequency electrical pulses through electrodes implanted in the subthalamic nucleus (STN) in the brain (though sometimes other locations may also be chosen). The STN is demonstrated to be over-activated in Parkinson’s disease. These electrodes are connected to the compatible pulse generating device. The pulse generator uses various pulses to achieve the optimal effect, where the right kind of settings can be chosen for a person by assessing treatment effectiveness.

Continuous DBS was shown to improve motor symptoms in more than two-thirds of patients, as compared to no stimulation or intermitted stimulation.

In one of the clinical studies, bilateral STN DBS was performed on patients that were not responding to the maximum dose of levodopa or to a continuous infusion of apomorphine. DBS showed marked improvement in motor function in 61% of cases. After the procedure, there was a 37.1% decrease in the daily dosage of levodopa in the patients. There was an almost 70% decrease in the need for apomorphine, with some patients not requiring apomorphine at all. Thus, the effectiveness of bilateral STN DBS in advanced Parkinson’s disease is well established.

Although the exact mechanism whereby DBS is effective is still unknown, it is believed to involve overcoming abnormal electrical patterns generated in the basal ganglia.

With the devices and surgical technique being constantly refined,  the effectiveness of this treatment may improve sufficiently enough to be widely used during the early stages of the disease in the future.

Deep brain stimulation in Alzheimer’s disease

In Alzheimer’s disease, DBS is still an experimental treatment. Lots of research with the use of various techniques has been done on animals, some with positive results. In one such study in monkeys, intermittent DBS was used with 60 pulses for 20 seconds with an interval of 40 seconds in between. The experiment demonstrated improvements in the memory of the primates. The experiment also showed deterioration of memory following continuous stimulation. The differences with results in the treatment of Parkinsonism might be explained by the differing pathological mechanisms involved.

After months of intermittent stimulation, the monkeys demonstrated improvements in memory even on discontinuation of stimulation. This lasting effect has not yet been explained. It is quite possible that such intermittent stimulation results in an improved connection between neurons, or higher levels of release of the neurotransmitter acetylcholine.

DBS has certain benefits over drugs, as it stimulates specific areas of the brain, while anticholinergic drugs used to treat Alzheimer’s have widespread non-selective action. Thus, DBM may prove to be a safer treatment option in the future.

It has to be noted that apart from DBS, non-invasive neurostimulation using transcranial magnetic stimulation has also demonstrated promising effects in animal studies.

References

Dubljevi?, V., Saigle, V., Racine, E., 2014. The Rising Tide of tDCS in the Media and Academic Literature. Neuron 82, 731–736. doi:10.1016/j.neuron.2014.05.003.

Elder, G.J., Taylor, J.-P., 2014. Transcranial magnetic stimulation and transcranial direct current stimulation: treatments for cognitive and neuropsychiatric symptoms in the neurodegenerative dementias? Alzheimers Res. Ther. 6, 74. doi:10.1186/s13195-014-0074-1.

Green, A.L., Bittar, R.G., Bain, P., Scott, R.B., Joint, C., Gregory, R., Aziz, T.Z., 2006. STN vs. Pallidal Stimulation in Parkinson Disease: Improvement with Experience and Better Patient Selection: STN vs. Pallidal DBS. Neuromodulation Technol. Neural Interface 9, 21–27. doi:10.1111/j.1525-1403.2006.00038.x.

Hansen, N., 2014. Brain Stimulation for Combating Alzheimer’s Disease. Front. Neurol. 5. doi:10.3389/fneur.2014.00080.

Little, S., Pogosyan, A., Neal, S., Zavala, B., Zrinzo, L., Hariz, M., Foltynie, T., Limousin, P., Ashkan, K., FitzGerald, J., Green, A.L., Aziz, T.Z., Brown, P., 2013. Adaptive deep brain stimulation in advanced Parkinson disease. Ann. Neurol. 74, 449–457. doi:10.1002/ana.23951.

Mallet, L., 2010. Deep Brain Stimulation in Psychiatric Disorders, in: Koob, G.F., Moal, M.L., Thompson, R.F. (Eds.), Encyclopedia of Behavioral Neuroscience. Academic Press, Oxford, pp. 376–381. doi:10.1016/B978-0-08-045396-5.00249-9.

Sharifi, M.S., 2013. Treatment of Neurological and Psychiatric Disorders with Deep Brain Stimulation; Raising Hopes and Future Challenges. Basic Clin. Neurosci. 4, 266–270. PMCID: PMC4202568.

Varma, T.R.K., Fox, S.H., Eldridge, P.R., Littlechild, P., Byrne, P., Forster, A., Marshall, A., Cameron, H., McIver, K., Fletcher, N., Steiger, M., 2003. Deep brain stimulation of the subthalamic nucleus: effectiveness in advanced Parkinson’s disease patients previously reliant on apomorphine. J Neurol Neurosurg Psychiatry 74, 170–174. doi:10.1136/jnnp.74.2.170.

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Detrimental Effects of Bright Screens on Sleep Patterns http://brainblogger.com/2017/10/13/detrimental-effect-of-bright-screens-on-sleep-pattern/ http://brainblogger.com/2017/10/13/detrimental-effect-of-bright-screens-on-sleep-pattern/#respond Fri, 13 Oct 2017 15:30:30 +0000 http://brainblogger.com/?p=22939 We often complain about people around us constantly being glued to their phone. Mobile technology is everywhere these days. When not on the go, we still tend to stare at computer screens both in the office and back at home. For many, this addiction to high-tech devices represents a way to be connected to friends and family. Many others think that these devices isolate us from real interaction with the world around us. One way or another, we do indeed spend too much time with our computers, laptops, tablets, and smartphones.

Apart from changing the way we communicate (for better or worse), all these devices have one more thing in common: bright screens. These light emitting screens can seriously affect our sleeping pattern. Moreover, the blue light (of a wavelength of ~470 nm) that is emitted by these devices is particularly harmful to normal sleep.

These days, an increasingly large number of people report problems with sleeping. Many people can’t fall asleep in the evening and then do not feel refreshed the next morning when they have to go to work. Lots of people complain about disturbed shallow sleeping and frequent awakenings at night. With normal sleeping hours often affected, people sleep less at night and if they can, compensate for this lack of sleep with daytime naps.

Disturbed sleep patterns are often linked to a diminished ability to focus on work, lack of motivation, and a generally low mood. This may lead to conflicts and stress at the workplace resulting, in some cases, in anxiety and depression. There are long-term negative consequences for other organs and systems of the body too. For instance, the link between chronically bad sleep and cardiovascular problems is well documented. Sleeping pattern disturbances also contribute to excessive body weight. It is estimated that around half of all Americans suffer from chronic stress at moderate or severe levels. Disturbingly, this number is growing in recent years.

Apart from many social and psychological factors, the growing level of stress in the general population can also be linked to the growing and excessive use of computers and smartphones. Exposure to bright screens in the evening hours is particularly harmful.

Our circadian rhythm (the sleep-wake pattern) is regulated by our exposure to light. There are several components of this system that are particularly important. First, we have specific cells in our eye retina that function as detectors of the duration and intensity of light. These cells, called intrinsically photosensitive retinal ganglion cells (ipRGCs), are particularly sensitive to short wavelength blue light.

Light-exposed ipRGC cells send signals to the suprachiasmatic nucleus in the brain. This region is responsible for setting the body clock, achieved by regulating the production of the hormone melatonin in the pineal gland. Melatonin plays a role in the adjusting mechanism: it synchronizes the body’s circadian rhythms with the real-life cycle of day and night experienced by the body. The problem is, this system can be easily fooled by prolonged exposure to artificial light. When you stare at your laptop screen late in the evening, you are also sending a signal to your brain that you are currently experiencing daytime. Your body will try to adjust accordingly to help you take advantage of daytime hours—it will reduce your desire to sleep. And once the screen is off, you don’t feel like sleeping anymore…

Recently published experimental data demonstrated that just two hours of evening exposure to bright computer screens emitting blue light decreases sleep duration and, more importantly, dramatically reduces its quality. People exposed to computer screens were awakening during the night much more often compared to those who did not use computers in the evening. The data also demonstrated that both the type of light emitted by the screens and its intensity is important for nighttime sleep quality. The screens with low brightness were less disturbing for sleep quality, and the screens emitting red light did not affect nighttime sleep at all.

Exposure to blue light-emitting bright screens in the morning is actually a positive thing: it can help to readjust the body to the correct time of the day. In fact, morning exposure to blue light is even used in a number of bright light therapy methods aimed at normalizing the circadian cycle, particularly in elderly people who often experience sleep-wake pattern disturbances.

It is quite unlikely that after reading this article anyone will immediately give up the habit of late-night internet browsing or chatting with friends via social networks before going to sleep. There are, however, several simple methods to reduce evening exposure to blue light emitted by screens. First, you can reduce the brightness of your screen. You can also change the background color while reading some types of documents. Text with white letters on a black background definitely reduces light exposure. If you anticipate working with documents in the evening, it might be a good idea to print them out. Paper is certainly much friendlier to the eyes. It is also possible to cover your computer screens with special filters that block out blue light. These small changes won’t require any major changes to your habits and routine but will help you to regain a normal sleep-wake pattern and bolster feeling refreshed the next day.

References

Arendt J. (2006) Melatonin and human rhythms. Chronobiol Int. 23(1-2): 21-37. DOI: 10.1080/07420520500464361.

Figueiro, M.G., Wood, B., Plitnick, B. et al. (2011) The impact of light from computer monitors on melatonin levels in college students. Neuro Endocrinol Lett. 32(2):158-63. PMID: 21552190.

Skene DJ, Arendt J. (2006) Human circadian rhythms: physiological and therapeutic relevance of light and melatonin. Ann Clin Biochem. 43(Pt 5): 344-53. DOI: 10.1258/000456306778520142.

Wright HR, Lack LC, Kennaway DJ. (2004) Differential effects of light wavelength in phase advancing the melatonin rhythm. J Pineal Res. 36(2): 140-4. DOI: 10.1046/j.1600-079X.2003.00108.x.

Image via simonwijers/Pixabay.

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Toxoplasma Gondii: Common Brain Parasite Behind Brain Disorders? http://brainblogger.com/2017/10/12/toxoplasma-gondii-common-brain-parasite-behind-brain-disorders/ http://brainblogger.com/2017/10/12/toxoplasma-gondii-common-brain-parasite-behind-brain-disorders/#respond Thu, 12 Oct 2017 15:30:15 +0000 http://brainblogger.com/?p=22937 Most people have never heard of the brain parasite called Toxoplasma gondii. We tend to think that creatures of such kind belong to the realm of exotic tropical diseases affecting people somewhere in miasmatic swamps of equatorial jungles. However, toxoplasma infection is remarkably common: it is believed that one in every three persons around the world have it. And not only in tropical regions, the prevalence of this infection in France is estimated at 84%! In fact, T. gondii is one of the most common parasites in the developed world. The majority of people reading this article have it in their brains.

If the infection is so common, why is it hardly ever mentioned? The reason is simple. As horrible as it sounds to have a parasite living in your brain, the infection with Toxoplasma gondii is asymptomatic and doesn’t seem to affect us in any obvious way. The initial exposure to the parasite may cause some flu-like symptoms, but very soon the infection enters latent stages and does not manifest itself. It can, however, become dangerous in people with weakened immune system, such as those with HIV/AIDS.

The parasite has a rather curious life cycle. It can live in almost any warm-blooded animal, but its major hosts are cats and other felines. In their bodies, the parasite can sexually reproduce giving rise to new generations of offspring. In other animals, as well as in humans, Toxoplasma gondii can only reproduce asexually. Thus, feline species are the definite hosts of T. gondii, while humans can only be intermediate hosts.

The oocysts produced in cats get excreted with feces and spread in the environment. This is where they can be picked up by rats and mice. In these animals, the parasite eventually reaches the brain, and here is where something really unusual happens. The parasite modifies the behavior of the rodents, making them less afraid of the smell of cats.

In addition, the brain infection affects the motor ability of animals, thereby making them easier prey for cats. These behavioral changes are achieved by introducing some epigenetic modifications affecting key neurons regulating the above behavioral characteristics. The behavioral modification of the host increases the chances of the parasite getting into the body of cats, and thus increases the chances of its reproductive success.

The important question is: does the infection with Toxoplasma gondii change human behavior as well? It appears that the answer to this question is yes. The results of psychological testing published in 2007 demonstrated gender-dependent changes in the behavior of humans affected by toxoplasmosis. Infected men had a tendency to disregard rule and were more expedient, suspicious, and jealous. Infected women, however, were more warmhearted, conscientious, and moralistic. The gender differences are related to different levels of testosterone in men and women.

Motor functions also appear to be affected in infected people. One study demonstrated a 2.65 times higher chance of traffic accidents among people with latent toxoplasmosis. The antibodies to the parasite were detected more often among drivers who were involved in traffic accidents, as compared to the statistical average.

Furthermore, a number of reports demonstrated a correlation between toxoplasmosis and the incidence of schizophrenia and bipolar disorder. Several studies have shown that the risk of attempted suicide is also higher among people affected by latent T. gondii infection. Correlation does not necessarily imply that the infection is the causative factor of neurological disorders, but it is likely to be a risk factor in the development of these conditions.

It is important to mention here that not all researchers believe that T. gondii infection really affects human behavior or the risk of diseases to any significant degree. Some recently published studies indicate that these risks are very small, and the previously published correlations with various behavioral changes are not as significant as we might think.

However, the most recent publication on this subject sounds the alarm again. Scientists used comprehensive systems analysis to look at the range of biomarkers generated by various parasites and to assess their impact in a large cohort of subjects. The data point to a correlation between toxoplasmosis and several neurodegenerative conditions including Alzheimer’s and Parkinson’s disease. The T. gandii infection was also positively correlated with epilepsy and a number of cancers. The scientists not only identified correlations, they also described the biochemical pathways that may actually lead to the increased risk of developing these conditions. They concluded that toxoplasmosis is a risk factor for many neurological disorders, and thus this infection has to be taken into consideration when developing strategies for preventing or delaying the onset of various brain diseases.

Can something be done to cure or at least prevent T. gondii infection? Unfortunately, not much. There are no drugs or vaccines to treat this infection. There is a number of simple strategies to decrease the risk of infection among healthy people. They include avoiding the consumption of raw or undercooked meat (among humans, this is the most common way of getting infected), as well as general basic food handling safety practices.

References

Berdoy, M; Webster, J; Macdonald, D (2000) Fatal attraction in rats infected with Toxoplasma gondii. Proceedings of the Royal Society B: Biological Sciences. 267 (1452): 1591–1594. doi:10.1098/rspb.2000.1182.

Flegr, J (2007) Effects of Toxoplasma on Human Behavior. Schizophrenia Bulletin. 33 (3): 757–760. doi:10.1093/schbul/sbl074.

Flegr, J; Havlícek, J; Kodym, P; Malý, M; Smahel, Z (2002) Increased risk of traffic accidents in subjects with latent toxoplasmosis: a retrospective case-control study. BMC Infectious Fiseases. 2: 11. doi:10.1186/1471-2334-2-11.

Kocazeybek, B; Oner, Y; Turksoy, R; Babur, C; Cakan, H; Sahip, N; Unal, A; Ozaslan, A; Kilic, S; Saribas, S; Aslan, M; Taylan, A; Koc, S; Dirican, A; Uner, H; Oz, V; Ertekin, C; Kucukbasmaci, O; Torun, M (2009) Higher prevalence of toxoplasmosis in victims of traffic accidents suggest increased risk of traffic accident in Toxoplasma-infected inhabitants of Istanbul and its suburbs. Forensic Science International. 187 (1–3): 103–108. doi:10.1016/j.forsciint.2009.03.007.

Torrey, EF; Bartko, JJ; Lun, ZR; Yolken, RH (2007) Antibodies to Toxoplasma gondii in patients with schizophrenia: a meta-analysis. Schizophrenia bulletin. 33 (3): 729–36. doi:10.1093/schbul/sbl050.

Arling, TA; Yolken, RH; Lapidus, M; Langenberg, P; Dickerson, FB; Zimmerman, SA; Balis, T; Cabassa, JA; Scrandis, DA; Tonelli, LH; Postolache, TT (2009) Toxoplasma gondii antibody titers and history of suicide attempts in patients with recurrent mood disorders. The Journal of Nervous and Mental Disease. 197 (12): 905–8. doi:10.1097/nmd.0b013e3181c29a23.

Sugden, K; Moffitt, TE; Pinto, L; Poulton, R; Williams, BS; Caspi, A (2016) Is Toxoplasma Gondii Infection Related to Brain and Behavior Impairments in Humans? Evidence from a Population-Representative Birth Cohort. PLOS ONE. 11 (2): e0148435. doi:10.1371/journal.pone.0148435.

Huân M. Ngô, Ying Zhou, Hernan Lorenzi, Kai Wang, Taek-Kyun Kim, Yong Zhou, Kamal El Bissati, Ernest Mui, Laura Fraczek, Seesandra V. Rajagopala, Craig W. Roberts, Fiona L. Henriquez, Alexandre Montpetit, Jenefer M. Blackwell, Sarra E. Jamieson, Kelsey Wheeler, Ian J. Begeman, Carlos Naranjo-Galvis, Ney Alliey-Rodriguez, Roderick G. Davis, Liliana Soroceanu, Charles Cobbs, Dennis A. Steindler, Kenneth Boyer, A. Gwendolyn Noble, Charles N. Swisher, Peter T. Heydemann, Peter Rabiah, Shawn Withers, Patricia Soteropoulos, Leroy Hood, Rima McLeod. Toxoplasma Modulates Signature Pathways of Human Epilepsy, Neurodegeneration & Cancer. Scientific Reports, 2017; 7 (1) doi: 10.1038/s41598-017-10675-6

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How Ketamine Acts on the Brain http://brainblogger.com/2017/09/29/how-ketamine-acts-on-the-brain/ http://brainblogger.com/2017/09/29/how-ketamine-acts-on-the-brain/#respond Fri, 29 Sep 2017 15:30:23 +0000 http://brainblogger.com/?p=22959 Ketamine is a medication mainly used for starting and maintaining anesthesia although it has also been used to provide rapid relief of treatment resistant depression.

The ability to rapidly stabilize severely depressed patients has been demonstrated in several studies and has led researchers to search for the exact mechanism by which ketamine works.

The effort is important as ketamine is sometimes illicitly used for its psychedelic properties and could also impede memory and other brain functions.

The multiple actions of ketamine has spurred scientists to identify new drugs that would safely replicate its antidepressant response without the unwanted side effects.

Now, emerging research from University of Texas (UT) Southwestern Medical Center scientists has identified a key protein that helps trigger ketamine’s rapid antidepressant effects in the brain. This is a crucial step to developing alternative treatments to the controversial drug being dispensed in a growing number of clinics across the country.

Researchers from the Peter O’Donnell Jr. Brain Institute have now answered a question vital to guiding future research: What proteins in the brain does ketamine target to achieve its effects?

As Dr. Lisa Monteggia, Professor of Neuroscience at UT Southwestern’s O’Donnell Brain Institute states:

Now that we have a target in place, we can study the pathway and develop drugs that safely induce the antidepressant effect.

The study published in Nature shows that ketamine blocks a protein responsible for a range of normal brain functions. The blocking of the N-methyl-D-aspartate (NMDA) receptor creates the initial antidepressant reaction, and a metabolite of ketamine is responsible for extending the duration of the effect.

The blocking of the receptor also induces many of ketamine’s hallucinogenic responses. The drug—used for decades as an anesthetic—can distort the senses and impair coordination.

But if taken with proper medical care, ketamine may help severely depressed or suicidal patients in need of a quick, effective treatment, Dr. Monteggia said.

Studies have shown ketamine can stabilize patients within a couple of hours, compared to other antidepressants that often take a few weeks to produce a response—if a response is induced at all.

As explained by Dr. Monteggia:

Patients are demanding ketamine, and they are willing to take the risk of potential side effects just to feel better. This demand is overriding all the questions we still have about ketamine. How often can you have an infusion? How long can it last? There are a lot of aspects regarding how ketamine acts that are still unclear.

Researchers will work to answer these questions as they plan two clinical trials with ketamine, including an effort to administer the drug through a nasal spray as opposed to intravenous infusions.

The results of these trials will have major implications for the millions of depressed patients seeking help, in particular those who have yet to find a medication that works.

A major national study UT Southwestern led more than a decade ago (STAR*D) yielded insight into the prevalence of the problem: Up to a third of depressed patients don’t improve upon taking their first medication, and about 40% of people who start taking antidepressants stop taking them within three months.

Ketamine, due to the potential side effects, is mainly being explored as a treatment only after other antidepressants have failed. But for patients on the brink of giving up, waiting weeks to months to find the right therapy may not be an option.

Dr. Monteggia touches on expected future developments, where:

Ketamine opens the door to understanding how to achieve rapid action and to stabilize people quickly. Because the (NMDA) receptor that is the target of ketamine is not involved in how other classical serotonin-based antidepressants work, our study opens up a new avenue of drug discovery.

This guest article originally appeared on PsychCentral.com: Researchers Learn How Ketamine Acts on the Brain by Rick Nauert PhD.

References
Suzuki, K., Nosyreva, E., Hunt, K., Kavalali, E., & Monteggia, L. (2017). Effects of a ketamine metabolite on synaptic NMDAR function. Nature, 546(7659), E1-E3. Doi: 10.1038/nature22084

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Older Age, Dementia, and Circadian Rhythms http://brainblogger.com/2017/09/22/older-age-dementia-and-circadian-rhythms/ http://brainblogger.com/2017/09/22/older-age-dementia-and-circadian-rhythms/#respond Fri, 22 Sep 2017 15:30:22 +0000 http://brainblogger.com/?p=22853 It is common knowledge that sleep patterns change with age. Older people tend to sleep less, their sleep can be shallow and fragmented. Often they sleep very little at night, spending few hours in bed during the daytime. The problem becomes serious in older people suffering from dementia, especially from the caretaker’s perspective.

Researchers discovered several brain processes that influence these sleeping pattern changes. One particularly interesting finding from this research (which may also inform approaches for addressing the problem) is the finding that light exposure has serious effects on the circadian rhythm in the elderly.

Our visual sensory system performs two major tasks: the gathering and processing of visual information (the visual response), and the control of the biological clock that regulates the production of several important hormones (the non-visual response). The majority of living organisms have a non-visual response to the day-night cycle, where body functions adjust to specific periods within a 24 hour day (circadian cycle).

Circadian rhythms regulate the sleep-wake cycle, body temperature, hormone release (e.g., melatonin and cortisol), and gene expression. Circadian rhythms are not set in stone and have to be fine-tuned to the actual experience of the timing and duration of day and night, which are subject to seasonal changes and geographic location. The importance of synchronized circadian regulation is obvious if we consider the physiological and behavioral disruptions caused by jet lag.

In 2005, our eyes were discovered to have a specific photosensitive cell type named intrinsically photosensitive retinal ganglion cells (ipRGCs) that are primarily involved in the regulation of circadian rhythms. These cells are sensitive to a broad range of wavelengths with maximal light absorption at blue light wavelengths of around 480 nm. It is believed that ipRGCs are tuned to the dominant wavelength of light at twilight. During twilight (i.e., at dawn and dusk) the sun is close to the horizon and there is a relative enrichment of ‘blue’ light in the dome of the sky because of the preferential scattering of short wavelengths of light passing obliquely through the atmosphere.

The signals from ipRGCs are processed in the suprachiasmatic nucleus in the anterior hypothalamus that is considered the key circadian pacemaker in the brain. The suprachiasmatic nucleus regulates the release of melatonin, a hormone crucial to the regulation of sleep and wakefulness, with blue light stimulating the most powerful changes in the melatonin secretion rhythm.

Visual and non-visual systems respond differently to the quantity of light and timing of light exposure. The quantity of polychromatic white light necessary to activate the non-visual circadian system is at least two orders of magnitude greater than the amount that activates the visual system. The reaction time of two systems is also different: while the visual system responds to a light stimulus very quickly (in milliseconds), the duration of light exposure needed to affect the circadian system can take minutes. The effects of light on the circadian system depends on the infusion of melatonin into the bloodstream, increasing the response time.

How circadian rhythms get affected with advanced age?

Our sensitivity to light stimuli reduces with the age. Multiple studies demonstrate that neuronal activity in the suprachiasmatic nucleus is reduced in the elderly, especially after the age of 80, and circadian rhythm amplitude is also reduced after the age of 50. This means that the intensity of the response of the non-visual system to light stimuli is reduced, sometimes very substantially. The direct consequence of this muted response is the lack of proper regulation and adjustment of circadian rhythms to the day/night cycle. Disturbances in circadian rhythms leading to poor sleep in older adults can be the result of dysfunctional circadian pathways or a pathway that cannot process light information with as much fidelity.

The first stage of phototransduction (when light signals are converted into neural signals) is negatively affected in older people: older adults have reduced optical transmission at short wavelengths that are maximally effective for the regulation of circadian system (i.e., blue light).

Older adults also tend to lead a more sedentary indoor lifestyle, with less access to bright light during the day, potentially increasing the risk for circadian disruption.

It is well-established that visual task performance improves with increased light levels, regardless of age. However, the need for light for visual task performance increases with age due to age-related losses in retinal illumination. These losses are reasonably uniform over time, with a 10% loss per ten years of aging. Thus, a ninety-year-old would require ten times the light of a 10-year-old for similar photoreception. The effect on circadian rhythmicity is further exacerbated with age because the shorter violet and blue wavelengths (400–500 nm) are most affected by yellowing of the aging eye.

It is also worth keeping in mind that older people often have reduced eyesight, suffer from blurred vision, and may have age-related eye diseases such as glaucoma, cataracts, macular degeneration, and other conditions.

How circadian rhythms get affected in neurological conditions?

Neurodegeneration caused by Alzheimer’s disease and similar conditions may affect multiple parts of the brain, including the parts involved in regulation of circadian rhythms. In Alzheimer’s disease, the suprachiasmatic nucleus deteriorates, contributing to alterations in circadian rhythms. This deterioration exacerbates the age-related loss of neuronal activity in the nucleus. Sleep disturbances, agitated behaviour, and depression are very common in people suffering from dementia.

What can be done to counteract these negative changes?

Bright light therapy has emerged as one of the most harmless and effective approaches to manage sleep disturbances in elderly people and patients with dementia.

Researchers have demonstrated that increased exposure to bright light may increase the amplitude of circadian rhythms, i.e., clearly enhances the intensity of the response to daily 24-hour cycles. Bright light exposure during the morning or evenings may help in consolidating circadian rhythms. Additionally, increased exposure to blue light may be beneficial, as photoreceptors in ipRGCs are more easily activated at these wavelengths.

The points above were incorporated into the development of a number of experimental light therapies aimed at stimulating the normal functioning of the non-visual system in the elderly and people with Alzheimer’s disease and dementia.

Light therapy may be delivered in a variety of ways, such as using a light box placed approximately one meter away from the participants at a height within their visual field; a headworn light visor; ceiling mounted light fixtures; or naturalistic light therapy—known as dawn-dusk simulation—that mimics outdoor twilight transitions.

Published research data suggests that circadian rhythm disturbances may be reversed by stimulation of the suprachiasmatic nucleus with light. Clinical research has shown that light therapy can consolidate rest and activity patterns in people with dementia.

There is a diverse choice of various electric light sources these days, and with proper selection, a balanced and circadian-effective lighting regime can be achieved in spaces with insufficient daylight illumination. The spectral characteristics and intensity of electric lights should be adjusted to the time of the day. Currently, the LED Luminaire™ is being developed that auto-tunes interior lighting to mimic the full spectrum of natural daylight throughout the day, with characteristics that can be “tuned” for older adults. This would provide quality illumination for visual tasks and help synchronize biological rhythms for better health, cognitive ability, and performance.

References

Abraha, I., Rimland, J. M., Trotta, F. M., Dellaquila, G., Cruz-Jentoft, A., Petrovic, M., Gudmundsson, A., Soiza, R., O’Mahony, D., Guatita, A., & Cherubini, A. (2017). Systematic review of systematic reviews of non-pharmacological interventions to treat behavioural disturbances in older patients with dementia. The SENATOR-OnTop series. BMJ Open, 7(3). doi: 10.1136/bmjopen-2016-012759

Dimitriou, T., & Tsolaki, M. (2017). Evaluation of the efficacy of randomized controlled trials of sensory stimulation interventions for sleeping disturbances in patients with dementia: a systematic review. Clinical Interventions in Aging, Volume 12, 543-548. doi: 10.2147/cia.s115397

Duffy, J. F., & Czeisler, C. A. (2009). Effect of Light on Human Circadian Physiology. Sleep Medicine Clinics, 4(2), 165-177. doi: 10.1016/j.jsmc.2009.01.004

Ellis EV et al. Chronobioengineering indoor lighting to enhance facilities for ageing and Alzheimer’s disorder. Intelligent Buildings International, 2013b Vol. 5, No. S1, 48–60. Ellis, E. V., Gonzalez, E. W., & Mceachron, D. L. (2013). Chronobioengineering indoor lighting to enhance facilities for ageing and Alzheimers disorder. Intelligent Buildings International, 5(Sup1), 48-60. doi: 10.1080/17508975.2013.807764

Figueiro, M. G. (2017). Light, sleep and circadian rhythms in older adults with Alzheimers disease and related dementias. Neurodegenerative Disease Management, 7(2), 119-145. doi: 10.2217/nmt-2016-0060

Hanford N, Figueiro M. (2013). Light Therapy and Alzheimer’s Disease and Related Dementia: Past, Present, and Future. Journal of Alzheimer’s Disease, 33(4), 913-922. doi: 10.3233/JAD-2012-121645

Weldemichael, D. A., & Grossberg, G. T. (2010). Circadian Rhythm Disturbances in Patients with Alzheimers Disease: A Review. International Journal of Alzheimers Disease, 2010, 1-9. doi: 10.4061/2010/716453

Image via TimHill/Pixabay.

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