Bipolar Disorder in Children- Efficient and careful diagnostic tools needed.

Bipolar disorder is generally defined as recurrent periods of mania and depression (Bipolar I) or hypomania and depression (Bipolar II). According to the website of National Institute of Mental Health (NIH), the lifetime prevalence of bipolar spectrum disorders is 0 to 3 % among adolescents, depending on assessment measured and the range of the spectrum considered. The prevalence of child onset bipolar is not well-established because there is no clear boundary of diagnosis and most of the symptoms overlap with other disorders such as Attention Deficit Hyperactivity Disorder (ADHD) and Schizophrenic disorders.
According to the article we read for class, ‘Bipolar disorder and mechanisms of action and mood stabilizers’ by Rapopart.et.al, 2009,  the mechanisms of bipolar disorder are believed to be due to imbalance neurotransmission, disease progression with worsening, cognitive decline, and progressive brain atrophy which can result in impairment of executive functioning, episodic memory, and sustained concentration. In neuroanatomical aspects, there is also thinning of the cortical mantle, widening of cortical sulci, and dilation of the lateral ventricles in bipolar patients. Neuroinflammation and excitotoxicity(incidence of  neural cell death due to over activation) are found to be underlying causes in Bipolar disorder. Neuroinflammation is due to increase Arachidonic Acid, a polyunsaturated omega-6 fatty acid derived from diet,  and excitotoxicity is  due to elevated brain glutamate/glutamine(excitatory neurotransmitter) ratio, and increase dopamine ,a  neurotransmitter that is usually found to be increased psychotic symptoms, levels.
In this blog, early onset bipolar symptoms and diagnosis in children will be discussed. Some general notable facts about bipolar disorder from the article, ‘The effect of the first manic episode in affective disorder: a case register study of hospitalized episodes’, by Kessing, Lars.1998. include –
–           “ Younger age at onset was associated with increased risk of developing a manic/circular episode for patients who presented with a depressive first episode “(Kessing, 1998)
–          “Courses of episodes were the same for patients for whom the first manic episode occurred later during the illness. Duration of intervals between episodes declined steadily with the number of episodes. “(Kessing, 1998)
–          The study found out that bipolar patients had the same rate of recurrence throughout the illness irrespective of at which episode or at what time their first manic episode occurred.
–          Patients who presented with depression but later developed mania were younger at onset than patients who remained unipolar. (Kessing, 1998)

http://www.additudemag.com/treating-depression-anxiety-bipolar.html

According to the article, ‘A Summary of Clinical issues and Treatment Options’, by Canadian Network for Mood and Anxiety Treatments (CANMAT), ‘early onset is often defined as occurring before the age of 25. The younger the age of onset of bipolar disorder, the more likely it is to find a significant family history of the condition. Early onset bipolar disorder most commonly begins with depression.’ (CANMAT, 1997) ‘Depression with psychotic features may be a predictor of future full-blown bipolar disorder in the early onset group. Rapid cycling, mixed states, and psychotic features are more common in early onset conditions.’ (CANMAT, 1997) Hallucinations and delusions are also common precursor symptoms associated with bipolar disorder.
Principal components analysis of early intervention symptoms in children with and without bipolar diagnosis in Children, according to Fergusa.et.al, 2003, include-

  1. Depression, II. Irritability/Dyscontrol, III. Mania, and IV, Psychosis/Suicidality.

Around age 7 and 8 –  “ The depression component (I) explained 14.2% of the variance and included nine symptoms (severe fatigue, periods of sadness, increased sleep, low self-esteem, more withdrawn, suicidal thinking, change in appetite, cries easily, and excessive guilt).
From age – 1 onward and greater incidence seen by age 3 – The irritability/dyscontrol component (II) explained 14.1% of the variance and included seven symptoms (temper tantrums, poor frustration tolerance, impulsivity, increased aggression, decreased attention span, hyperactivity, and irritability).
Around age 7 and 8 – Mania component (III) explained 11% of the variance and included six symptoms of mania (racing thoughts, extended mood elevation, pressured speech, grandiosity or delusions, bizarre behavior, and brief mood elevations).
Around age-9 onward – Psychosis/Suicidality component (IV) explained 10.2% of the variance and included five symptoms (hearing voices, paranoid thoughts, suicidal gestures, suicidal attempts, and obsessive thoughts).
According to the article, component II, ‘Irritability or dyscontrol‘ is the earliest symptom to discriminate the bipolar children from the other groups. This factor, according to the article, includes ‘temper tantrums, poor frustration tolerance, impulsivity, increased aggression, decreased attention span, hyperactivity, and irritability’. This factor is also supposed to be associated with later clusters of more classic manic and depressive symptoms that can lead to a diagnosis of bipolar illness. The symptoms in this category also overlaps with those of ADHD and they are believed to be the earliest precursors to classic bipolar see in adults and some adolescents, according to Fergus.et.al, 2003.
Diagnosing bipolar disorder, especially in children, is not a clear cut process and should not rely only on the established guidelines of symptoms. The diagnosis should take into consideration both the unique bipolar symptoms that are apparent in adolescents and adults and if necessary, also compare the symptoms with anatomical brain abnormalities from imaging brain scans.

Homelessness and Mental Illness: A Lethal Combination

This week, Fargo-Moorhead recognizes National Hunger and Homelessness Week, a time to raise awareness about the on-going problem of homelessness—not just in the big cities of New York, LA, and Chicago—but here in the frozen land of MN and ND, in our very own backyards. Whether or not it is acknowledged, homelessness is a problem in virtually every community. The National Coalition for the Homeless estimates that across the US on a given night, between 500,000 to 1 million Americans experience homelessness.
What people in our community may not know, however, is that an estimated 1,000 to 1,500 individuals in the Fargo-Moorhead area are homeless. The 2009 Wilder Research report, which gathered information from homelessness people in the Fargo-Moorhead area on one night in October by combing shelters, transitional housing, soup kitchens, and unsheltered areas like parking lots and alleys, found a total of 443 homeless people. Considering the total number of homeless individuals in our region, this figure is undoubtedly higher. Every year, local shelters like the YWCA and Churches United for the Homeless report maximum capacity and utilization.

While homelessness itself is a devastating experience, there’s evidence that mental illness is more prevalent among homeless individuals, compounding the problems they already face. The same Wilder report of the F-M area found that over 40% of the individuals surveyed had been recently diagnosed with schizophrenia, bipolar disorder, major depression, anti-social personality disorder, or PTSD. This finding reflects a host of social research that has found a nation-wide association between homelessness and mental illness, particularly bipolar disorder and schizophrenia. Based on this research, it is likely that mental illness is a factor that contributes toward homelessness. Being able to effectively diagnose mental illness and make treatment available to at-risk populations could potentially reduce the problem of homelessness.

What is bipolar disorder?
This week, the Concordia neurochemistry class discussed the issues with diagnosing and treating bipolar disorder, a condition that seems to be over-represented in homeless individuals. Bipolar disorder is characterized by uncontrollable and debilitating extremes of mood, which cycle between two states: mania (extremely high mood and energy levels) and depression. People with bipolar disorder are on a “roller coaster” of emotion, cycling between moods every few days, weeks, or months (depending on severity). Understandably, this can be very difficult to deal with personally, and can impair relationships and social functioning.
Diagnosing bipolar disorder is difficult. Like all mental illnesses, it cannot be detected with a quick-and-easy blood test or x-ray. Instead, a psychiatrist or psychologist needs to spend enough time with the individual in order to determine if the rapid cycling of moods is occurring and interfering with normal functioning. This can be tricky because the depression, mania, and sometimes psychotic behavior can look very much like other mental illnesses—like schizophrenia or certain types of personality disorders.
Treating bipolar disorder
The use of medication in treating bipolar disorder has been met with some success. Treating the disorder often involves a combination of medications in order to target both depression and elevated mood (mania). This is usually done through using anti-depressants and anti-psychotics. Another option that has shown relatively high success rates is the use of lithium carbonate, a natural element. Lithium is widely used now as an mood stabilizer in bipolar disorder, balancing the extremes of low and high mood. Exactly how lithium is effective in bipolar disorder, however, is still relatively unknown. What happens in the brain when a person takes lithium?

Drugs like lithium work in the brain by decreasing or increasing the activity of cells

Researchers have a couple of ideas. One suggestion is that lithium prevents too much of a substance in the brain called myo-inositol from being produced. Too much myo-inositol may contribute to the rapid cycling in bipolar disorder. Another hypothesis is that lithium decreases signaling in a biochemical pathway called GSK-3. This pathway is also believed to possibly contribute to the symptoms of bipolar disorder. Finally, lithium may also decrease the levels of arachidonic acid in the brain, an omega-6 polyunsaturated fatty acid found in cell membranes. This substance is important for a variety of biological functions, including chemical signaling and cell growth in the brain. Arachidonic acid causes inflammation and may damage cells of the nervous system if too much is released. Lithium may protect nerve cells by decreasing arachidonic acid.
So should doctors be prescribing lithium if they don’t even know how it works in the brain? Lithium has been in use for years and shown to be an effective mood stabilizer in many cases of bipolar disorder. While too much lithium can be toxic, doctors are aware of what they are dealing with and do their best to balance the potential benefits of the drug with the associated risk of harm. Most of all, it is important that people who take lithium are aware of both the benefits and possible risks, and make a choice they feel comfortable about.
Making treatment available
Medications like lithium or other treatment options like therapy have been shown to be helpful in treating bipolar disorder. Unfortunately, sometimes the people who need these resources the most do not have access to it. Many people, not just homeless people, can’t afford medical insurance to get the treatment they need. Additionally, not all insurance companies recognize mental illnesses equally as a legitimate condition. While drugs may be covered by insurance companies, other options like therapy and counseling may not be, limiting the options people have. This inaccessibility of treatment has made it very difficult for people with mental illness to get the help they need. Increasing awareness of mental disorders like bipolar disorder and their social implications may help increase the availability of treatment and services to people who need them the most.
Events this week in Fargo-Moorhead
Every October during the Homeless and Hungry campaign, local residents experience what it is like to be homeless



 
 
 
 
 
 
 
This month, the Fargo-Moorhead community is doing the Fill the Dome project for a fourth year in a row. Students around the area are collecting enough donations to fill the 80,000-square-foot Fargodome with food for local pantries and shelters. Each year, the project collects hundreds of tons of food. The project is wrapping up next week!
Students in Concordia College’s Echo Band are teaming up with the F-M Coalition for the Homeless to create awareness of homelessness as well as raise funds for local organizations. Their concert will be held Tuesday evening in the Centrum, Knutson Campus Center.
The Lake Agassiz Regional Library in Moorhead is holding Holiday Season Amnesty for patrons with overdue materials and fines! $2 will be forgiven per donated non-perishable food item. Donations will go to local food pantries serving the homeless and needy.
 
For the full 2009 Wilder Research report of the Fargo-Moorhead area, visit:
http://www.wilder.org/download.0.html?report=2354

Bipolar Disorder: We Need A Pokeflute

Bipolar disorder is one of the most well known neurological disorders, characterized by alternating states of prolonged depression or manic states (the term is often misused, such as to characterize a moody friend). Because two different states exist, it is difficult to administer one single drug that can alleviate both symptoms. Thus, mood stabilizers are often used to treat mania, while antidepressents seem to be the obvious choice for treating the depression stage.
Common mood stabilizers used today include lithium (administered as various salts), carbamazepine, valproic acid/valproate, and lamotrigine. These drugs have shown varied effectiveness in depressing the elevated mental state seen in mania or hypomania. However, these drugs were not designed with a certain mechanism of action in mind. Instead, hypothesises have to be made to predict how these drugs actually work neurologically. The paper our class reviewed this week put forth the “arachidonic acid cascade” hypothesis. Arachidonic acid is a polyunsaturated fatty acid that plays a role in many biological processse, including neurotransmission, gene transcription, sleep, memory, inflammation, and behavior. Too much arachidonic acid are linked with inflammation, ischeme, and convulsions. According to this AA cascade hypothesis, the aforementioned mood stabilizers may regulate mania by downregulating the arachidonic acid cascade, thus preventing some of the problems from its overexpression.
The paper only focused on treating mania. Treating the depressive state of BD is a whole new beast. Bipolar depression is three times more common than mania. The mood stabilizers mentioend above (except lamotrigine, to a small extent) are not able to treat depression effectively. It would be natural to assume that antidepressants would be a good treatment. However, most antidepressants increase the likelihood of switching back to mania, which is obviously not a desirable alternative, even when used in tandem with mood stabilizers.
An (not completely accurate) analogy would be considering a Snorlax, Pokemon #143. Consider the manic phase of Snorlax to be an aggravated, aggressive state (usually resulting in an intense pokebattle). Like in BD, this phase is much less common than the depressive state, the state we usually associate with Snorlax. In this “depressive state”, Snorlax is just sleeping and generally lethargic about the world around it. View an antidepressant as chucking a ton of apples at the Snorlax so it will wake up (come out of depression). If you do succeed in waking the Snorlax, it is likely it will instantly convert into a “manic state”, understandably angry from being disturbed so rudely. The antidepressant (apples) may have worked, but it resulted in another undesirable state. What BD needs is a Pokeflute: something that can gently bring the Snorlax out of depression but not bring it to an overactive state. However, since we regrettably don’t live in a fantasy world, this is much easier said than done. 


Images obtained from Google Images.

Working Backwards…

Bipolar disorder is a psychological disease characterized by extreme mood change. The highest point, termed mania, is a period of extremely good mood and impulsivity, while the lowest point, depression, is characterized by deep sadness or emptiness. Some of these intense emotional symptoms include poor judgment, spending sprees, very high self-esteem, and hyperactivity during mania which transitions into low mood, sadness, feelings of hopelessness, and thoughts of suicide during depression.[i] Interestingly, it is hypothesized that the famous historical figures Edgar Allan Poe, Vincent van Gogh, and Virginia Woolf all had bipolar disorder. In the U.S., the disorder is estimated to affect 5.7 million adults, but surprisingly only about 50% of these people are getting any treatment at all. [ii],[iii] What is stopping these people from getting adequate treatment for this debilitating disorder?
It would probably surprise you to know that bipolar disorder is one of the oldest known illnesses known today. In fact, according to some sources, its symptoms were recognized as far back as the second century.[iv] How does this make sense? How have we not figured out how to treat this disorder effectively?
Quite frankly, scientists simply don’t know what’s going on with bipolar disorder. The medications prescribed to patients for the disorder are essentially a shot in the dark. No one knows how or why they seem to work….sometimes. In fact, most scientific study into bipolar is essentially working backwards from treatment. In other words, maybe if we can figure out what the treatment is doing in the brain, we can figure out what’s wrong with the brain.
One of the front-running hypotheses as to what’s going on in the bipolar brain is called the “arachidonic acid hypothesis.” This hypothesis shows significant promise as to why mood stabilizers like lithium, valproate, and carbamazepine work to stabilize mood swings, especially in the mania stage.
Arachidonic acid, a polyunsaturated fatty acid found in our diet, plays a role in many cellular processes including neurotransmission, membrane excitability, long-term potentiation, gene transcription, membrane fluidity, neurite outgrowth, cerebral blood flow, sleep, and memory.[v] Furthermore, arachidonic acid has been implicated in the excessive neurotransmission of glutamate and dopamine observed in bipolar disorder. In one study, it was shown that NMDA activation increased arachidonic acid incorporation in controls while use of LiCl or NMDA agonist blocked this incorporation.
Lastly, it has been shown that mood stabilizers have some sort of neuroprotective effect over the brain. This makes sense in the context of the arachidonic acid hypothesis because increasing arachidonic acid levels can lead to cell damage and behavioral changes. Therefore, these mood stabilizers could be decreasing arachidonic acid’s cellular affects.[v]
There are still many unanswered questions surrounding bipolar disorder, and many psychological disorders in general. There really comes a point where you have to wonder – what is normal anymore? Will there come a time when we understand these disorders completely? Or will it take learning all the intricacies of the “normal” brain first? I don’t know the answers to these questions, but it seems like (for now at least) the arachidonic acid hypothesis is the best we’ve got.


[i] http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001924/
[ii] http://www.bipolarsymptoms.org/bipolar-statistics/
[iii] http://blogs.psychcentral.com/therapy-soup/2011/03/new-bipolar-study-statistics-suggest-serious-work-ahead/
[iv] http://www.caregiver.com/channels/bipolar/articles/brief_history.htm
[v] Rapoport et al. (2009) Bipolar disorder and mechanisms of action of mood stabilizers. Brain Research Reviews 61; 185-209.

Psychiatry by the Book: A cursory look at the mental disorder diagnostic process


Psychological disorder diagnoses have spiked dramatically in the last 30 years, bringing into question the environmental origins of these disorders.  Are there environmental factors such as pollution, high stress lifestyles of capitalist societies, and technological augmentations (i.e. television and the internet) which have changed the way humans function on a biological level?  In contrast perhaps progress has been made in the diagnoses of mental disorders, such that current diagnosis parameters include a wider range of symptoms than have been used to diagnose mental illness in the past.
A look into a psychiatrists office is enlightening and marginally nerve-racking.  Diagnostics often proceed with a psychiatrist, the subject seeking evaluation, and a friend or family member of the subject  in a question and answer style conversation.  The psychiatrist is often toting the Diagnostic and Statistical Manuals of Mental Disorders (DSM) “i.e. the bible of what is wrong with your brain”, referencing a diagnostic chart with specific questions aimed at assessing the presence/gravity of your mental illness.  For the subject this is not always the most self-esteem boosting activity because the evaluation can quickly unearth concerns that your friend has had all of this time about your quirks, which they have realized, through the course of the psychiatric evaluation, must be due to the mental disorder that the subject has.  In some cases a power complex can develop through comparison of the subject’s responses to the friend’s response to invasive questions about the subject’s personality.  For example, if the psychiatrist asks the subject if they obsess over certain aspects of their life, the subject might say “not really”, but the subject’s friend lapses through memories looking for the odd behavior and says “yeah you have been extremely focused on ______ since you were young.”  The friend’s response must be looked at subjectively due to the fact that they might not be interested in the subject’s interests, which can make them more prone to denoting certain behaviors obsessive as opposed to normal.
Throughout the diagnosis the string of question from the DSM are asked and the subject’s and friend’s answers about the subject are added up in a format that allows the psychiatrist to say “yes you have this disorder”, or ” no you don’t have this disorder.”  Either way the diagnostic process is far less empirical than medical science is used to employing.  The “shotgun approach” to mental disorder diagnosis that the DSM offers is crude and has shortcomings, however it is the best mechanism presently available to diagnose patients with a particular mental disorder and help the psychiatrist treat the patient in an optimal fashion.  Much progress is yet to be made in the realm of psychological disorder diagnostics, but the methods in use today are the best yet to surface.

Over Medicated and Undiagnosed

This week our topic focused around bipolar disorder.  Bipolar disorder is characterized by continual changes in mood that last over a long period of time.  These moods cycle between depression and mania and can last in one part of the cycle for weeks at a time.  The symptoms for mania include being easily distracted, little need for sleep, poor judgment, poor temper control, reckless behavior, elevated mood, extreme involvement in activities.  There are also two types of bipolar disorder, 1 and 2, bipolar 1 is characterized with the mania symptoms, while bipolar 2 still has mania symptoms, but not as intense.  Some of the other symptoms and possible treatments can be found on this link: http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001924/
It is often difficult to characterize and quantify the extent of the depression or mania symptoms so it is often challenging to diagnose true bipolar disorder.  It often takes many sessions over a long period of time to diagnose.  Often times doctors will ask about family history and ask about your recent behavior and mood swings to try to diagnose, but this is very difficult.  The official psychologist diagnostic manual called the DSM even states at the end that these episodes of depression/mania could be bipolar if they can’t be explained better through schizophrenia disorders, delusion disorders or other unspecified disorders.  Here is the link that include the descriptions from the DSM: http://www.fortunecity.com/campus/psychology/781/dsm.htm  This is extremely frustrating because there is no clear test or set of symptoms to declare that an individual definitively has bipolar disorder.  Simply put, it seems as though this disorder is diagnosed through the process of elimination.
Treatment is just as difficult if not more challenging to pinpoint.  Our article this week focused on three major medications for the treatment disorder, they include lithium, valproic acid and carbamazepine.  These medications are classified as “mood stabilizers” because they try to level out the mania and depressive symptoms however they work better on the mania symptoms and no one is sure why.  The different medications work differently on different individuals and the different types of bipolar disorder and since it is so hard to diagnose often times individuals are on these drugs on a “trial and error” method.  They will be prescribed one treatment and if that doesn’t work they move on to the next and the next and the next. Along with these mood stabilizers, doctors may also prescribe antiseizure medication, antipsychotics and antidepressants.  Some patients may even be on all of the drugs at once with many harmful side effects and when the treatment starts working and the symptoms lessen, doctors may be unable to pinpoint which drugs is the effective drug.  Treatments for bipolar disorder other than drugs include electroconvulsive therapy (small shocks to the brain), transcranial magnetic stimulation (sends pulses to a specific area of the brain) or even talk therapies and support groups. For more information about the drugs, side effects and other treatments please follow this link: http://mentalhealth.gov/health/publications/bipolar-disorder/complete-index.shtml

"Delayed Concussions"

I was a football student manager from 6th grade until I graduated high school so I saw my fair share of concussions but what I had never seen was a delayed concussion that happened days after the actual head trauma happened, until it happened to my cousin. That days practice started out like any other, with drills and running plays but throughout practice everyone kept asking where my cousin was and why he wasn’t at practice. The answer was that I didn’t know but not too much longer after we saw him coming down the hill but there was something off about him. His jersey was on backwards and he was having a hard time walking. When he got to the field he ran to the wrong group and continuously asked where the linemen where even after our coaches told him multiple times. When he finally got to the linemen group, where I was, he was in really bad shape. He could barely stand or talk and his coordination was extremely poor. Now in his past he had a history of drug use so everyone thought there was a chance he was high and that was why he was acting strange. Because of this thought and me being his cousin, everyone insisted that I take him home before the coaches realized that he might be high. So I did just that! I pulled him aside and, in my best stealth mode, started walking him up the hill back to the locker rooms. However, with the state he was in and his size (me=5’1″, 125 lbs, him= 6’2″, 275 lbs) carrying him up the hill was really hard. I knew something was really wrong when he looked down and asked why was the ground covered in ice cubes….there was no ice it was the grass. Luckily while walking with him a friend of ours saw us and offered to take him home. About 30 minutes later my mother called and said they were taking him to the hospital because they couldn’t come up with any reason why he was acting the way he was.
At the hospital, the ER doctor told us he was suffering from a closed head injury but when the neurologist came to see him he told us my cousin had a severe concussion. This was odd to us because we knew he hadn’t suffered a head injury in the few days preceding the incident. But then my cousin remembered that at our last game, almost  a full week before, he had a helmet to helmet collision with a player on the other team.
But the real question is what’s the difference between a closed head injury and a concussion?
There really isn’t a difference. A concussion is thought to be a form of a closed head injury along with brain contusions or bruising of the brain, intracranial hematomas or bleeding in the brain after being forced against the inside of the skull, and diffuse axonal injuries or damage to nerves in the brain. Closed head injuries are any injury to the head that does not penetrate the skull. They are usually caused by blows to the head because of traffic accidents, fall, assaults, or sports injuries.
Definitions of concussions themselves vary but according to the Mayo Clinic, concussions are any head injury that temporarily affects normal brain functions. Effects are usually temporary but can sometimes cause permanent problems. Most concussions are mild and do not result in loss of consciousness but this is not always the case. People suffering from a concussion can display immediate symptoms such as headaches, nausea, dizziness, slurred speech and vomiting. They can also be confused, have difficulty with coordination and difficulty with concentration. In some cases, like my cousins case, symptoms do not show up for hours or even days after the incident.
 
http://www.allabouttbi.com/closed-head-injury/

Concussions: A Big Impact on Life

Newsworthy
Concussions have been creating much fervor in the news recently. Increasingly, high schools, universities and other educational institutions have been implementing policies meant to protect athletes from lifelong brain dysfunction caused by concussions.  The NCAA requires that: all student athletes receive information about concussions, all NCAA institutions have a process in place to evaluate athletes for possible concussions, and that athletes exhibiting signs of concussion are removed from play and are not returned until cleared by a physician of physician designee.1 Students are not the only athletes affected by new policies shaped by awareness of the dangers of concussions. Both the NHL and NFL have been making changes to the equipment, policies and evaluation players undergo to avoid serious brain damage that has been associated with multiple concussions.
Concussion Symptoms
A concussion is caused by trauma to the brain and is by a loss of consciousness or altered level of consciousness, but people can have concussions and not realize it. Symptoms include headache, memory loss, nausea and vomiting, disorientation and experiencing a loss of time.2 Changes in behavior and mood are also indicators of a concussion. Much of the current discussion has revolved around the long-term effects of multiple concussions, which is also known as chronic traumatic encephalopathy (CTE). Although there are not many confirmed cases of CTE, more than 90% of them were seen in athletes and the symptoms are severe. In the earliest stages patients experience some psychotic symptoms and erratic behavior. Later stages include dementia, gait abnormality and symptoms associated with Parkinson’s Disease.3 what can be done to avoid these problems as an athlete or even just going through day-to-day life.
Your Brain on Concussions
The paper we read this last week described the timetable of events in the brain after experiencing a concussion. When the brain receives a traumatic injury it sets off the neurons, causing excitation in the brain and the movement of many ions, like sodium and potassium, out of balance within brain cells. To get things back on track the brain uses lots of energy to pump the ions back to their proper places. This creates an energy crisis within the brain, which likely is the reason for symptoms such as memory loss, disorientation and unsteadiness. There is also a reduction in the amount of blood flowing to the brain that only further exacerbates the energy crisis. It takes the body a number of hours to recover from the energy crisis and days to repair the damage done to brain cells due to the energy crisis and the trauma itself. Unfortuanatly, other than prevention there isn’t a good way to protect the body from concussions, yet.
Concussion treatment
So far, the best treatment for concussions is to rest and avoid overstimulation so the brain has time to fully recover. This is because there are a number of problems with treating a concussion with medications. One of the primary problems is with diagnosis. Most of the problems that a concussion causes in the brain happen in less than ten minutes. This leaves a very small window of time to evaluate the trauma, diagnosis the concussion, and administer the treatment. Because there are essentially no medications without side-effects it would likely not be appropriate to administer a concussion treatment every time a person gets knocked-around, “just in case.” A second problem with treating a concussion is finding the problem to treat. Should the excitation be treated, or the lack of blood flow, or the need for energy? Which is the underlying cause of the symptoms, and which if manipulated will cause the fewest side effects? As always, researchers are looking into these questions and any day a great discovery could be made. Until then, play hard, but play safe and protect your noggin.
1. http://www.ncaa.org/wps/wcm/connect/public/NCAA/Student-Athlete+Experience/Student-Athlete+Well+Being/Concussions
2. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001802/
3. http://www.sportsmd.com/Articles/id/44.aspx

"Spiritual Disorder" or Neurological disorder? What are we doing?

Neuro degenerative disorders were not always neuro degenerative disorders.  Before the enlightenment and its emphasis on naturalism and empirical study, neuro degenerative disorders were spiritual disorders.  These “spiritual disorders” were never naturalized, but were considered a distortion of the soul.  The naturalized language of modern day psychology and neuroscience did not make its appearance until the 19th century.  The disordered souls were ostracized by their respective communities.  And when rare help was called for, it was the religious healer, the back alley mystic, that answered the call.  The mystic may have had some balm or powder with its corresponding superstitions, but the primary method of cure was prayer or meditation, direct links to the soul.
Prayer, meditation, and an overall spiritual emphasis, are things modern medicine is slowly forgetting about.  Our reductionist understanding of the mind is taking over.  We have realized the power of direct intervention in the brain and with this we have reinvented “soul disorders” as neurological disorders; problems of the brain.  People are no longer inflicted with despair; they just have major depressive disorder.  People aren’t driven to great anxiety by past sins or moral infractions, they just have obsessive-compulsive disorder.  A new paradigm has brought with it new words and new treatments, but the ailment is the same, and the new treatment’s do not target the soul directly, but the brain directly.
Parkinson’s disease, although recently naturalized, was around long before neuroscience was.  Parkinson’s is understood as a loss of cells in the brain region called the substantia nigra that produce the chemical messenger dopamine.  Dopamine plays a vital role in muscle movement and coordination.  The loss of the dopamine producing cells in Parkinson’s causes its well known symptoms; the jerkiness, the shaking, the rigidity, and later cognitive decline.
Parkinson’s is a disease that the new paradigm cherishes.  Its origins are fairly obvious, and are under little scientific dispute.  Certain cells are lacking; this is something we can measure.  The new paradigm holds Parkinson’s up as a model of what neuroscience is capable of.  We can identify what’s wrong in the brain, theoretically go in, and fix it.  But Parkinson’s leads us down a path we have already started on.  Depression as a spiritual disorder is ignored.  A bad mood as a spiritual funk is ignored.  Every mental event is being fathered by the new paradigm and the spirit, the soul, which we cling to dearly, is taking a back seat.  Is something wrong here?  What should we think when a child is in a bad mood and the parents take him in for some anti-depressants?  Have we lost touch with ourselves?
The new paradigm should be put on a pedestal and it should be a guiding force in our decisions.  It works.  Without the new paradigm people with Parkinson’s would still be getting help from healing balms and ritualistic chants.  But we need to be aware of what the new paradigm is doing.  We need to be on our toes.  Neuroscience is progressing much faster than humanity’s intuition, and it seems to me that we do not know where we are headed with this technology.  Where do you think we are headed?  What do we make of the soul when all ailments are ailments of the brain?  What do we make of the soul, period?  It is the case that we still love and cherish our soul even though we ignore it.

Concussions in Elementary School Children

The topic of discussion this week was about the mechanisms underlying concussions and the many side effects that they can produce. The mechanical force of a blow to the head can cause chemical changes in the brain and alterations in signalling. These alterations can include influxes of calcium within cells that cause disruptions in metabolic functions that can cause permanent damages to cognitive functioning and memory systems.
The most heated area of discussion regarding concussions is in the area of professional sports and how to deal with athletes returning to play. However, an area that may hit a lot closer to home is concussions among elementary school aged children.  Some elementary schools now send notes home from the nurse’s office if children fall on the playground or seemingly knock their head too hard. While these measures are safeguards for parents to know what to look for in their children when they come home, the extremities of the measures that now days need to be taken may be seen as a little extreme. Nonetheless, concussions among elementary aged is an interesting and important topic during those formative years.
According to guides that are published by various school districts for educators, elementary kids are more likely to report physical problems or cognitive problems relating to anxiety or stress after an accident that may be due to a concussion. The key to this then is to collaborate with school teachers, nurses, playground staff, and parents to understand the nature of the injury and to help with recovery and improving cognitive learning side effects. Some classic symptoms that teachers can look for are students that get tired in class, are bothered by noise or light, easily distracted, trouble learning new material, problems with memory, or being easily overwhelmed with information. Teachers can help students during the time of experiencing cognitive difficulties by adapting classroom material, giving more time for assignments and tests, providing easier transitions, and allowing students to work in more quiet settings.
An understanding of these symptoms to look for and ways that they can aid in student recovery is important even for teachers of young children.

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