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Oh my god, getting manic after a concussion is a thing

And I think that is exactly what is happening to me 😦 I mean who posts 22 posts in 7 days? A manic person, that’s who! So anyway, I am increasing my lithium and Seroquel tonight, and getting a hold of my doctor tomorrow. And I will try not to post anything anymore, I have to calm down, relax and get better, I have a trip to Pakistan coming up, I have the holidays here to attend to, I don’t really have the luxury to get sick. Wish me luck, and look for a lot less from me. That will mean I am getting healthy again.

Happy Holidays my dear blogging tribe which includes but is not limited to Dyane, Laura, Kitt, Blahpolar, Jess, Deanne, Vic, And many others and to all my friends and family who read my blog. Love and peace and many hugs.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2424119/

Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment

“…. Although irritability, paroxysmal aggression, and mania may develop after a mild Traumatic Brain Injury (TBI) (Hibbard et al 1998) … The limited published case literature and expert opinions suggest that anticonvulsant mood stabilizers are preferable to lithium carbonate for the treatment of these problems (Arciniegas, Topkoff, et al 2000), although lithium carbonate may be of benefit in some persons with such symptoms following TBI (Zwil et al 1993). In general, when severe irritability, paroxysmal aggression, and mania are the predominant features of the clinical presentation in a person with TBI we recommend consultation with a neuropsychiatrist, behavioral neurologist, or neurorehabilitation specialist with expertise in the management of these postconcussive symptoms…”

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Concussion, I thank you!

pink lilyBuff Erie Co Bot Gardens.December 6, 1990

The day my son was born, the happiest day of my life!

 

There is a positive to having had this concussion for me. What? You may exclaim: What are you talking about!? How can whacking your head against rock hard ice and having your brain hit your skull, how can there be a positive in that?

Well, my answer to that would be: Endorphins!

With bipolar disorder, one has anxiety, one is depressed, one is manicky, in short there is no peace of mind.

When (I’m sure) my brain produced the endorphins (our brain produces these, our natural pain killers) after the concussion, et voilá, peace! My mind stopped chattering, the anxiety was gone, the ruminating thoughts disappeared. And miraculously, all was well. Nothing had changed in my life, only my brain was processing things differently! Everything was fine, no matter what, I was fine with it all. There was peace in my mind and my heart, my stomach was not tied up in knots. All was well with the world and everyone in it. My anxiety and depression were gone.

This is the gift that my concussion gave me. It reminded me that this kind of peace of mind was possible. Unfortunately, with bipolar d/o, it is rare to have this kind of mental wellness. No matter what was happening in the world externally, I was fine with it, I was at peace. I can still invoke that feeling to some extent, I can still remind myself that it is possible to feel this way, no matter what!

So thank you concussion, for reminding me that this “blissful” state was possible for me, no matter what was going on in my life!

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A genome-wide association study of kynurenic acid in cerebrospinal fluid: implications for psychosis and cognitive impairment in bipolar disorder

 

A variant of the SNX7 gene and its reduced expression, is associated with levels of a protein called kynurenic acid aka KYNA (an end metabolite in tryptophan metabolism.) This is associated with the psychotic (out of touch with reality) symptoms and cognitive impairment seen in bipolar disorder and schizophrenia. Interestingly, this pathway involves signaling via the immune cells (glia) of the brain! Another immune cell connection to mental illness! And KYNA could be targeted for drug development, as reducing it should lead to a decrease in psychotic symptoms as well as cognitive impairment.

http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2015186a.html

Abstract

Elevated cerebrospinal fluid (CSF) levels of the glia-derived N-methyl-d-aspartic acid receptor antagonist kynurenic acid (KYNA) have consistently been implicated in schizophrenia and bipolar disorder. Here, we conducted a genome-wide association study based on CSF KYNA in bipolar disorder and found support for an association with a common variant within 1p21.3. After replication in an independent cohort, we linked this genetic variant—associated with reduced SNX7 expression—to positive psychotic symptoms and executive function deficits in bipolar disorder. A series of post-mortem brain tissue and in vitro experiments suggested SNX7 downregulation to result in a caspase-8-driven activation of interleukin-1β and a subsequent induction of the brain kynurenine pathway. The current study demonstrates the potential of using biomarkers in genetic studies of psychiatric disorders, and may help to identify novel drug targets in bipolar disorder.

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Introduction

Elevation of brain kynurenic acid (KYNA) is a consistently found biochemical aberration in schizophrenia and bipolar disorder (BD).1, 2, 3, 4, 5, 6, 7 Brain KYNA is mainly produced in astrocytes as an end-metabolite of the kynurenine pathway of tryptophan metabolism. This pathway is highly inducible by inflammatory stimuli,8 and we have previously reported that cerebrospinal fluid (CSF) levels of the proinflammatory cytokine interleukin (IL)-1β are markedly increased in patients with BD or schizophrenia, although the majority of other cytokines measured in this study were undetectable.9, 10

KYNA is a neuroactive metabolite that antagonizes the glycine co-agonist site of the N-methyl-d-aspartic acid receptor (NMDAR).8 Administration of synthetic NMDAR antagonists causes psychotic symptoms in healthy individuals,11 and exacerbates psychotic features in patients with schizophrenia.12 Psychotic symptoms are core features of schizophrenia, and more than half of patients with BD will experience psychosis in their lifetime.13 Supporting that KYNA might be specifically involved in the pathophysiology underlying psychotic symptoms, we have found higher levels of CSF KYNA in BD-I patients with a history of psychosis compared with those who had never experienced psychosis.14 KYNA also noncompetitively antagonizes the cholinergic α7 nicotinic receptor, and animal studies indicate that increased brain KYNA might cause cognitive deficits.8 In rats, increased brain KYNA causes behavioral responses analogous to impaired set-shifting in humans,15 an index of executive function. Set-shifting dysfunction as measured by the trail making test (TMT) is indeed a feature of schizophrenia and euthymic BD,16, 17 especially in BD patients with a history of psychosis.18

Family history is the strongest risk factor for BD, but an important obstacle for progress in psychiatric genetics is that psychiatric syndromes—based solely on symptom clustering—do not necessarily reflect specific underlying biological dysfunctions and may be insufficient to delineate heritable phenotypes.19 Indeed, epidemiological and molecular genetic studies have blurred the diagnostic boundary between schizophrenia and BD by demonstrating that these disorders have partly shared genetic causes.20, 21 Complementary approaches to unearth causal genetic mutations are therefore needed. One approach is to focus on biomarkers, that is, measurable key components in biological pathways between genotype and disease.22 For this purpose, the use of CSF KYNA may be particularly rewarding given its biological links to distinct subdomains of pathology present in both BD and schizophrenia.

In this study of euthymic BD patients, we found CSF IL-1β and KYNA to be associated with a history of psychosis and set-shifting impairment. CSF levels of KYNA were also strongly associated with the dopamine metabolite homovanillic acid (HVA). We conducted a genome-wide association study (GWAS) against CSF levels of KYNA in BD that revealed a genome-wide significant association with the single-nucleotide polymorphism (SNP) rs10158645 within 1p21.3, a finding that was replicated in an independent cohort of BD patients. Furthermore, we analyzed this SNP in relation to CSF HVA, a history of psychosis (followed by a replication in a large data set of 565 BD patients) and set-shifting ability. As the minor allele in rs10158645 was associated with decreased expression of sorting nexin 7 (SNX7), we attempted to decipher the biochemical chain of events using a multipronged approach including causal inference analyses of clinical data, post-mortem data and cell culture studies. These experiments converged on the proposal that decreased SNX7 expression is linked to increased CSF KYNA concentration and ultimately psychosis and set-shifting difficulties in BD through caspase-8-driven activation of IL-1β.

 

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A baby doe

As I sit in the doctor’s  office for my follow up appointment for my concussion, what do I do but look at FB?  I saw this precious story of an injured baby doe, rescued by an amazing  young man and then reunited with her family. Very heartwarming for me. Who can resist babies, of any kind, especially  this little one! How kind and gentle of this man, who looks to be a hunter, to save this little one from  quite certain ruin. Yes nature is cruel, nature would have let this adorable, little mite die. If the weakness was the result of illness, then the illness genes would have been eliminated from the gene pool. But so would this wondrous, beautiful creature. As humans, we choose kindness over a better gene pool. I am human and I am all for kindness.
http://www.hlntv.com/shows/the-daily-share/articles/2015/10/27/man-rescues-injured-cute-baby-deer-and-returns-it-to-its-mother​

http://youtu.be/eStXV_TYFFw

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Word press shows me which countries my views came from!

Pretty amazing! This is from Dec. 11th, when I had 141 views. It only shows the countries, not the identity of the actual viewers. I only see the identity if someone comments, and then I only see the email they used to comment with.  Pretty cool still! Sometimes, I have a lot more countries in my views than even these ones. So cool to have a global audience. Blogging is definitely one good thing and rewarding thing I do. 🙂

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Extended release vs. Immediate release

This is my most looked at blog post ever! Who knew it would be so popular!

Bipolar1blog's avatarBipolar1Blog

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Many of the medications we take for our disorders come in immediate release or extended release forms.

Immediate release, as the name implies, dissolves immediately within our stomachs and is taken up into the bloodstream. This can cause side effects, it is also taken up quickly and then degraded quickly. So the concentration of the medicine does not stay constant in our bodies, we get a quick spike and the drug is quickly degraded. It is actually better to have a constant concentration as opposed to this increase and decrease. Lithium is one drug that is known to cause major gastrointestinal side effects if taken in large doses in an immediate release form and can be quite corrosive to the stomach.

Extended release, also known as Controlled release, has a coating that allows it to dissolve slowly either in the stomach or small intestine (enteric coated). These medicines are then slowly dissolved…

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The art of recovering gracefully

I am dedicating this post to my friend Dyane Leshin Harwood, whose amazing blog: https://proudlybipolar.wordpress.com/  has inspired me so much! And whose support and positive comments are so valuable to me. Love you my lithium sister!

Do you ever think you over react? Me? I say to myself, over react? Never! I am the modicum of tempered emotional reactions. Ummm no, actually I’m not. Happiness for me is joy, glee, giddiness. Sadness for me is ultimate doom, and blackness. Where is the middle ground? The happy medium? I do live there sometimes and sometimes I do not. Actually for someone with bipolar disorder, I am a fairly balanced person, but when something out of the ordinary happens, such as a concussion, well, I may lose it just a little, really, just a tiny, little bit.

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Actually after I hit my head, I felt so amazingly good LOL! I haven’t felt that good in forever. All the worry, the depression, anxiety, all of it was gone. In its place was a peace, an acceptance of everything, a pleasantness and an optimism, and happiness and a calm. This lasted for almost two heavenly days, after which the anxiety, depression, sadness, pessimism, all came rushing back. Sigh, I’m almost willing to hit my head again to get that feeling back. Is there any way to whack your head, just a bit, yet prevent brain damage? If anyone knows of one, by all means let me know! Please.

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I believe the good feelings were due to my brain producing endorphins to relieve the pain of the concussion. Yes, concussions are pretty painful. You, or in this case, I hit the back of my head against one of the most unyielding and hard substances in the world, ice! A whack of my head, against the ice, and my neck snapped back and my brain hit the wall of my skull. Luckily I fell backwards. Apparently that is the direction of choice. If I’d fallen sideways, I could have ruptured an artery, such as the middle meningeal artery, and that would have been a whole lot worse. As in subdural hematomas, coma, and death, if the pressure was not relieved by a craniotomy (a hole in your skull.)

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So I dodged a bullet there, Generally I’d say that I got away easy, as the CAT scan showed no bleeding and even my tail bone was not fractured, though it feels like it is. Even the headaches I had for two days in Buffalo weren’t as bad as the worst migraines I have ever had.

The plane ride seems to have exacerbated the symptoms a bit in that I’m having headaches again, but not really, really bad ones.

I count myself as lucky, that even though I did do something as stupid as not wearing a helmet, and very ungracefully falling on my butt and then thwacking my head against the crystalline, diamond hard ice, I came thorough it quite well.

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Concussions are not good for anyone, especially I might add, for people with bipolar d/o, as emotional disturbances can occur. Even in this aspect, I feel I am doing fine.  Although, I do realize now that I was a bit up, just a bit, mind you, even before the concussion, and I did have a little emotional down spike a few days after the concussion as well, but since then, calm.

And of course, my mantra is “Wear a helmet!”

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After I come back from Pakistan, yes my next adventure, I will buy a helmet, hire an instructor, and learn how to ice skate, really well 🙂

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If at first you don’t succeed, try, try again. That is also a mantra of mine 🙂

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Plant compound found in spices and herbs increases brain connections

“Apigenin, a substance found in parsley, thyme, chamomile and red pepper, improves neuron formation and strengthens the connections between brain cells….

The research team conducted by Rehen demonstrated that apigenin works by binding to estrogen receptors, which affect the development, maturation, function, and plasticity of the nervous system. This group of hormones is known to delay the onset of psychiatric and neurodegenerative disorders such as schizophrenia, depression, Alzheimer’s and Parkinson’s disease. However, the use of estrogen-based therapies is limited by the increased risk of estrogen-dependent tumors and cardiovascular problems.”

http://www.neuroscientistnews.com/research-news/plant-compound-found-spices-and-herbs-increases-brain-connections

Brazilian research shows that the flavonoid apigenin has potential to treat diseases like schizophrenia, depression, Alzheimer’s and Parkinson’s –

Brazilian researchers from D’Or Institute for Research and Education (IDOR), Federal University of Rio de Janeiro (UFRJ) and Federal University of Bahia (UFBA) have demonstrated in laboratory that apigenin, a substance found in parsley, thyme, chamomile and red pepper, improves neuron formation and strengthens the connections between brain cells.

Previous experiments with animals had already shown that substances from the same chemical group as the apigenin, known as flavonoids, positively affect memory and learning. Many studies highlight the potential of flavonoids to preserve and enhance brain function. While the effectiveness of flavonoids for brain health is not an entirely new concept, this research is the first to show the positive effects of apigegin directly on human cells and the first to unraveling its mechanism.

The scientists observed that just by applying apigenin to human stem cells in a dish they become neurons after 25 days—an effect they would not see without the substance. Moreover, the neurons that were formed made stronger and sophisticated connections among themselves after being treated with this natural compound.

“Strong connections between neurons are crucial for good brain function, memory consolidation and learning”, says neuroscientist from IDOR and UFRJ Stevens Rehen, leader author of the paper published today at Advances in Regenerative Biology.

The research team conducted by Rehen demonstrated that apigenin works by binding to estrogen receptors, which affect the development, maturation, function, and plasticity of the nervous system. This group of hormones is known to delay the onset of psychiatric and neurodegenerative disorders such as schizophrenia, depression, Alzheimer’s and Parkinson’s disease. However, the use of estrogen-based therapies is limited by the increased risk of estrogen-dependent tumors and cardiovascular problems.

Researchers believe apigenin can be used as an alternative approach on future treatments for neurodegenerative diseases as well as in neuronal differentiation strategies in laboratory.

“We show a new path for new studies with this substance”, points out Rehen. “Moreover, flavonoids are present at high amounts in some foods and we can speculate that a diet rich in flavonoids may influence the formation of neurons and the way they communicate within the brain.”

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At last, hope for migraine sufferers?

“… Now we may have true cause for hope.

At least four large companies are holding clinical trials to study something called monoclonal antibody therapy. This therapy uses genetically engineered antibodies to stimulate the immune system and attack a nasty compound that is elevated in the brain during migraine headache pain. The treatment would be injected periodically. It has had excellent results in early trials, and could be available within a few years. “Not only is this the most hopeful thing on the horizon,” said Dr. Joseph Safdieh, a neurologist at Weill Cornell Medical College who is not involved with the trials, “it is the only hope on the horizon.”

But why has it taken so long to find a fix for an ailment that so many millions suffer from? The answer may be that what looks like one syndrome could actually be a symptom of a number of different conditions.

According to Dr. Steven B. Graff-Radford, the director of the Headache and Orofacial Pain Program at Cedars-Sinai Medical Center in Los Angeles, “most migraine sufferers are undiagnosed or given the wrong diagnosis.” He said, “They go to their general doctor — when they should be seen by specialists — and are told they have sinus or tension headaches, which are treated with antibiotics or psychological management, when they have other kinds that should be treated another way.”… “