Bipolar Disorder - Science topic

This is a question that needs a literature search rather than a question on RG. There's a systematic review from but it rates the evidence for traumatic head injury as tentative. A review this year doesn't mention it as a risk factor at all.

And I found those in three minutes. I'd recommend you head off and do some lit searching.

Stopping medication in the treatment of bipolar disorder is possible, but it should only be done under the guidance and supervision of a qualified healthcare professional. Abruptly discontinuing medication can be dangerous and may exacerbate symptoms or trigger a relapse. Therefore, it's essential to consult with a psychiatrist or mental health professional before making any changes to your treatment plan.

I would rather ask, why you want to combine it? MAOIs are very potent Antidepressant, in adequate dose and duration, i think will be sufficient for your patient. I also hold the same opinion like others who opined , better to avoid adventurous practice rather play safe.

check this out:

Low levels of lithium do appear to confer some protection against suicidality. Please see here for a recent supporting review -

I have used lamotrigine a great deal and have not seen this side effect. Is it dose-related?

Dear Emily

I thin this site can be useful for you:

Thank you Michael Uebel ... this was very helpful! I am trying to identify potential sources of random noise so I will have to consider other things that could be random noise instead.

Thanks again.

In my understanding, both the terms are NOT mutually exclusive. So a case control study can be cross-sectional too and vice versa.

Please see here:

Hans-Ulrich Iselin

Thank you for your insightful comment. I have read Cassiers et al (2018) as well as 3 other insightful articles: 1) Nemeroff CB.(2016). Paradise Lost: The Neurobiological and Clinical Consequences of Child Abuse and Neglect. In Neuron; 2) Aas M et al. (2019) Childhood maltreatment and polygenic risk in bipolar disorders. In Bipolar Disorders; and 3) Stevelink et al. (2019) Childhood abuse and white matter integrity in bipolar disorder patients and healthy controls. In European Neuropsychopharmacology.

I am interested in causation and the interplay of genetics and childhood trauma as I am trying to write a book on childhood trauma and how the different types of trauma at different times explains the behaviors of survivors, the mental health challenges caused by childhood trauma and toxic stress, and how people can "overcome" (I hate this word but can't think of another) trauma. My story of childhood trauma, developing several mental illnesses including bipolar disorder, and how I was able to get a PhD and have a successful career while growing and healing is being used as the backdrop to tell the scientific story to a lay audience.

Lastly, here is a paper that describes switch failure when the switch was to aripiprazole due to dopamine supersensitization. They describe “Dopamine supersensitivity psychosis (DSP)“ as being ”characterized by the need for high antipsychotic dosages for the treatment of patients with schizophrenia, tardive dyskinesia,, and/or an abrupt relapse triggered by the reduction or discontinuation of antipsychotics.

Hope that these resources help!

Tremor is a typical and common side effect of lithium. It can be alleviated by reducing the dose of lithium, reducing the amount of coffee you drink, stopping other tremor drugs, or by using regular or appropriate beta-blockers (eg 10 to 40 mg of propranolol 1 to 3 times a day). If tremor occurs only when lithium plasma levels peak (1 to 2 hours after dosing), tremor may be avoided by taking the entire dose in a single evening dose. (M Huttunen, 2017)

Interested

I think things are a bit unclear here. Xanax and Clonazepam are benzodiazepines which are anxiolytics. They are not antipsychotics. They can be addictive, though as Schedule IV drugs, they are classified by FDA to have relatively low addiction potential (I personally think they are more addictive).

Antipsychotics include drugs like Haldol, Zyprexa, and many others that treat symptoms of psychosis, e.g., hallucinations, and I would not consider these addictive; actually the opposite as most people do not particularly like taking them, but find the relief from psychosis to be the reason to do so.

All of the above fall under the more general categorization of psychotropics.

As I interpret the decision to select a statistical test depends upon the type of study, pattern of data & most importantly your objective.

Regards

I think bipolar disorder is triggered by sleep disorder in persons with unstable circadian rhythms (see my RG question on this).

First of all I should know the daily doses of all drugs he takes daily and the serum litiemia dosage as well. Anyhow I would never give a bipolar patient an amphetamine. The antidepressant drugs themselves should be used with caution. In principle in this particular case I would try to add paroxetine 10 mg /day after breakfast, increasing to 20 mg /day after 1 week if needed.

Ronan Michael Conroy, no worries, I already used Jane to find something. And I edited the question, because I realized it was not clear enough.

Regards,

Milena

done

Ok Anthony. You have some very good questions and a valid idea, but our approaches are not mutually exclusive. Oftentimes more than one cause can be attributed to the same outcome. Which came first the chicken or the egg? And then of course you have to throw in the environment. If sleep disorder is the driving force for bipolar disorder, schizoaffective disorder, anxiety, schizophrenia, and other illnesses how do you explain that particular force setting off so many different diseases and not a specific disease, unless losing sleep function stresses the body to trigger a predisposition for a particular mental illness.

I was wondering whether you've ever worked in medical research setting and what your background knowledge is other than the reading that you do? Do you have a medical background that allows you to understand physiology and illness? I have worked with simple organisms, bacteria (E. coli, Streptomyces species), that have one chromosome. My background is bacterial genetics and molecular biology with a veterinary nursing background. Humans are logarithmically more complex than bacteria. They have 23 pairs of chromosomes for a total of 46. Based on my journey, personal experience, knowledge, and research experience either theories are possible.

1. Occam's razor doesn't always apply in biological systems, and though it is obvious to me that you are a thinking type (Jungian types) and you will never accept this possibility I have to throw that out there. An endocrine imbalance is just a plausible as the beginning of the process of developing bipolar, schizoaffective disorders as what you are postulating, and either could lead to the same conclusion.

2. The progression that a relative experienced was first hyper-vigilance (I believe that can be attributed to home environment growing up that induced overactive adrenal glands. Whenever the patient was faced with being with a person she could feel the adrenaline surge followed by fight, flight, freeze), as a teen self imposed sleep interruptions, hypothyroidism late twenties, then a few years later a psychotic break, then extremely notable sleep disturbances as time went on. Another relative experienced hypothyroidism as a teen, then eventually developed a series of psychotic breaks in the twenties, after having children the sleep disturbances became pronounced, developed severe pathology of the pituitary gland and now has severe sleep disturbances and sleep apnea. I must admit, I have no idea when the sleep disturbances started because I didn't ask. I simply know that at this point they are severe.

3. I'm not sure that we would necessarily know whether bipolar disorder was an endocrine disorder by now. I don't think that physicians necessarily communicate with research counterparts all that well. They don't even have time to communicate with their patients other doctors and so inadvertently incompatible drugs are prescriptioncribed by two different doctors. I think that an endocrine homeostatic imbalance could be a stressor that could lead to bipolar illness. I also believe that a sleep disorder could be a stressor that could lead to bipolar illness. I also believe that the stress of having a bad home life, being a scapegoat for bullies, having some sort of traumatic experience could all lead to bipolar illness if the person was genetically predisposed. "According to one study, the often-debilitating sleep disorder insomnia can be genetic and for some, insomnia may be hereditary. Scientists say some people's genes increase their stress-reactivity. And that increased stress response increases the likelihood of poor sleep and developing insomnia." There is a population of people having sleep disorders that are not mentally ill. About 18% of people in the population are not considered mentally ill. Between 50% and 80% of mentally ill people have sleep disorders.

By going through this exercise and finding this last piece of information about "Scientist say some people's genes increase their stress-reactivity. And that increased stress response increases the likelihood of poor sleep and developing insomnia." I'm not sure that we would necessarily know whether bipolar disorder was an endocrine disorder by now. I don't think that physicians necessarily communicate with research counterparts all that well. They don't even have time to communicate with their patients other doctors and so inadvertently incompatible drugs are prescriptioncribed by two different doctors. I think that an endocrine homeostatic imbalance could be a stressor that could lead to bipolar illness. I also believe that a sleep disorder could be a stressor that could lead to bipolar illness. I also believe that the stress of having a bad home life, being a scapegoat for bullies, having some sort of traumatic experience could all lead to bipolar illness if the person was genetically predisposed. "According to one study, the often-debilitating sleep disorder insomnia can be genetic and for some, insomnia may be hereditary. Scientists say some people's genes increase their stress-reactivity. And that increased stress response increases the likelihood of poor sleep and developing insomnia." There is a population of people having sleep disorders that are not mentally ill. About 18% of people in the population are not considered mentally ill.

By going through this exercise and finding this last piece of information about "Scientist say some people's genes increase their stress-reactivity. And that increased stress response increases the likelihood of poor sleep and developing insomnia." I would say that bipolar disorder is probably triggered by stressors rather than saying it is a sleep disorder. It is a chicken-egg question though because once you have a mental illness there is an all consuming quality that leads to avoiding sleep.I would say that bipolar disorder is probably triggered by stressors and predisposition to the disease rather than saying it is a sleep disorder. It is a chicken-egg question though because once you have a mental illness there is an all consuming quality that leads to avoid sleeping that seems to worsen over time.

National Comorbidity Survey Replication data indicate that bipolar disorder is characterized by high lifetime rates of co-occurring anxiety and substance use disorders (SUDs) (Merikangas et al., 2007). Increasing evidence suggests that medical illnesses also frequently co-occur in bipolar disorder (Beyer et al., 2005; Kilbourne et al., 2004; Krishnan, 2005; McIntyre et al., 2006) and may contribute to an increase in premature mortality from natural causes of death (Osby et al., 2001). Although an increased prevalence of medical comorbidity affects nearly every organ system, the high rate of cardiometabolic conditions such as diabetes, cardiovascular disease, and dyslipidemia is particularly alarming (Angst et al., 2002; Kilbourne et al., 2007).

"National Comorbidity Survey Replication data indicate that bipolar disorder is characterized by high lifetime rates of co-occurring anxiety and substance use disorders (SUDs) (Merikangas et al., 2007). Increasing evidence suggests that medical illnesses also frequently co-occur in bipolar disorder (Beyer et al., 2005; Kilbourne et al., 2004; Krishnan, 2005; McIntyre et al., 2006) and may contribute to an increase in premature mortality from natural causes of death (Osby et al., 2001). Although an increased prevalence of medical comorbidity affects nearly every organ system, the high rate of cardiometabolic conditions such as diabetes, cardiovascular disease, and dyslipidemia is particularly alarming (Angst et al., 2002; Kilbourne et al., 2007)."

Hyperlipidemia (dyslipidemea) can also be related to a hormonal disease such as diabetes, hypothyroidism (low levels of thyroid hormone), polycystic ovary syndrome (PCOS), metabolic syndrome, and Cushing syndrome.

Endocrine disorders include hypothyroidism, congenital adrenal hyperplasia, diseases of the parathyroid gland, diabetes mellitus, diseases of the adrenal glands (including Cushing's syndrome and Addison's disease), and ovarian dysfunction (including polycystic ovary syndrome), among others.

"...Now, preliminary data concerning 7 drug-naïve DSMIV- TR bipolar I patients who underwent an oral glucose tolerance test suggest that bipolar disorder may be highly associated with abnormal glucose metabolism irrespective of pharmacotherapy. The patients were evaluated at the time of their first clinical contact for psychotic symptoms at a general academic hospital. The patients were initially classified as first episode of non-affective psychosis, but their diagnosis was changed over a year time for an affective diagnosis, namely bipolar disorder type I. All subjects gave informed consent for participation in the study, which was conducted under the supervision of the authors’ respective hospital ethics committees, and came from a larger study of metabolic abnormalities and glucose dysregulation in neuropsychiatric disorders (4). The results after an overnight fast showed a high incidence of glucose metabolism abnormalities, including impaired fasting glucose in two of seven patients and impaired glucose tolerance in six of seven patients. Abnormal glucose metabolism, measured as an increased two-hour glucose load, reflects that bipolar I disorder is associated with an elevated risk of death from cardiovascular pathologies and all causes, independently of other known risk factors.

Our data and the actual state of knowledge suggest that glucose abnormalities are linked to the diagnosis of bipolar disorder before the effects of medications and other confounders had taken place. Indeed, glucose abnormalities are the basis for the reportedly high number of medical comorbidities found in patients with bipolar disorder. The concept of ‘Allostatic Load’ has received considerable attention as a theoretic explanation of its medical burden. Allostasis is a term that describes a multisystemic view of the physiologic toll that is required for adaptation to different situations; these processes are adaptative to internal or external circumstances and so maintain the homeostasis of the organism. However, when extra loads appear pointy or over time (the adaptative mechanisms are repeatedly activated), the allostatic response becomes excessive or inefficient and the organism develops an allostatic load (overload) that can direct to abnormal responses through insulin dysfunction such as T2DM, hypertension, or arteriosclerosis (5).

The pathophysiology that underlies the association of bipolar disorder and T2DM or glucose abnormalities is far from being understood, but several explanations have been developed over time. These include possible common pathophysiological processes, genetic and epigenetic links, and environmental factors.

Dysregulation in the hypothalamic–pituitary–adrenal axis is a highly consistent finding that would explain through cortisol disturbances the abnormalities in glucose homeostasis, increased body fat deposition and atherosclerosis, although in our sample, cortisol value was in the normal range, and in another naïve bipolar I study, it was lower compared with matched controls. Dysfunction in the purinergic system has been associated with both bipolar naïve patients (6) and T2DM, as purines play a crucial role in energy homeostasis and neuroregulation. Indeed, Kraepelin already described in 1921 an association between uric acid and manic-depressive illness. Evidence implicates also mitochondrial dysfunction, impaired phospholipid metabolism and fatty acid-related signal transduction, and dysregulation of glycogen synthase kinase-3, in the common pathophysiological processes that underlie bipolar disorder and T2DM (2). Common genetic abnormalities and shared susceptibility loci have been described between T2DM and bipolar disorder; however, genetic-wide association studies have not yielded conclusive results.

However, we would like to highlight the physiology of early environmental processes (7) and its epigenetic programming in the development of metabolic disturbances. Bipolar disorder, from a gene-environment model, is associated not only with familial risk but also with a certain number of early environmental factors. Birth and gestational-related problems appear to be risk factors for both bipolar disorder and diabetes, low birth weight being the most notable example, suggesting neurobiological adaptative changes that might underlie both pathologies. Obstetric, prenatal disturbances, and early growth patterns predict an increased risk of developing T2DM (8) and other cardiovascular pathologies over time, through epigenetic pathways, a finding that could also partially explain part of the increased risk of morbidity and mortality found in patients affected with bipolar disorder.

Understanding the onset of a severe mental illness not only as psychiatric but also as a medical condition would imply a metabolic control independent of the type of treatment. Hence, all physicians should be aware of the need of implementing primary preventive strategies in an effort to reduce the overall medical burden and mortality of bipolar patients."

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Acknowledgments

The work leading to these results have been supported in part by Grant RO1 DK069265 from the National Institute of Diabetes and Digestive and Kidney Diseases (Dr. Kirkpatrick), NARSAD (Dr. Fernandez-Egea) and by the Instituto de Salud Carlos III, FEDER, Centro de Investigación Biomédica en Red de Salud Mental, CIBERSAM, Government of Catalonia, Secretaria d’Universitats i Recerca del Departament d’Economia i Coneixement (2009SGR1295) and by Esther Koplowitz Center-Barcelona (Dr. Bernardo).

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References

1. Osby U, Brandt L, Correia N, Ekbom A, Sparen P. Excess mortality in bipolar and unipolar disorder in Sweden. Arch Gen Psychiatry. 2001;58:844–850.  [PubMed]

2. Calkin CV, Gardner DM, Ransom T, Alda M. The relationship between bipolar disorder and type 2 diabetes: more than just co-morbid disorders. Ann Med. 2013;45:171–181.  [PubMed]

3. McIntyre RS, Mancini DA, Pearce MM, et al. Mood and psychotic disorders and type 2 diabetes: a metabolic triad. Can J Diabetes. 2005;29:122–132.

4. Fernandez-Egea E, Bernardo M, Donner T, et al. Metabolic profile of antipsychotic-naive individuals with non-affective psychosis. Br J Psychiatry. 2009;194:434–438. [PMC free article]  [PubMed]

5. Grande I, Magalhaes PV, Kunz M, Vieta E, Kapczinski F. Mediators of allostasis and systemic toxicity in bipolar disorder. Physiol Behav. 2012;106:46–50.  [PubMed]

6. Salvadore G, Viale CI, Luckenbaugh DA, et al. Increased uric acid levels in drug-naive subjects with bipolar disorder during a first manic episode. Prog Neuropsychopharmacol Biol Psychiatry. 2013;34:819–821. [PMC free article]  [PubMed]

7. Vaag AA, Grunnet LG, Arora GP, Brons C. The thrifty phenotype hypothesis revisited. Diabetologia. 2012;55:2085–2088. [PMC free article]  [PubMed]

8. Hales CN, Barker DJ. The thrifty phenotype hypothesis. Br Med Bull. 2001;60:5–20.  [PubMed]

So it appears that at least some endocrine disease have been shown to be associated with bipolar disorder.

Thanks for the alternative methods and sugestions from James and Taussif. They were very kind and I will try to choose the best that I can do. I will tell you the results. Thanks a lot.

You are right that researchers rarely wrote about the many challenges involved in conducting methodologically sound clinical trials. Recruitment is definitely one, which is why many studies use samples from different sites, which introduces its own challenges. The challenges are written about, but they are not highlighted in titles and abstracts and so may be difficult to search for.

Hi,

Maybe, this paper could help:

A cross-sectional survey of stigma towards mental illness among medical students: a focus on bipolar disorder By: Atienza-Carbonell, B.; Hernandez-Evole, H.; Balanza-Martinez, V. BIPOLAR DISORDERS Volume: 20 Special Issue: SI Supplement: 1 Pages: 109-109 Meeting Abstract: P-124 Published: MAR 2018

I suggest

Thank you so much....

ADHD is a loosely defined behavioral syndrome. It is a common mistake to assume it has single cause implying common treatments will work for all diagnosed with ADHD. Many factors including being the youngest in a school class can result in a child being diagnosed with ADHD. Some children have basically nothing wrong with them others have wide variety of problems. 

In short-term research trials pharmacological interventions invariably appear more effective than non-drug treatments for two reasons. First, drugs alter behaviour much faster than non-drug treatments, and trials most often measure improvements by short-term symptom management (often for no longer than a few weeks). Second, while the behaviour-altering effects of stimulants are almost universal, other forms of treatment are not. Family counselling, for example, will be of little or no benefit if the underlying cause of behavioural problems is exposure to environmental toxins.

In many cases there is nothing to ‘treat’. Many children are naturally inattentive, impulsive and hyperactive. In these cases normal childhood behaviour is pathologised and healthy children are ‘medicated’. Perhaps subconsciously for many busy, stressed adults, being able to control their child’s challenging behaviour is their main concern. If so, stimulant medication wins hands down.

Dear 

we have a dataset of depression paients and we use them. For determining treatment response as well as developing diagnostic indexes. We also have EEG of healthy individuals performing attention task.  

I have not found a good and big size database of EEG of mood disorders. Perhaps the good way is exchanging dataset or using datasets of other research groups. We welcome such exchange and collaboration 

David, I fully agree that there is a connection between affective disorder and conditions characterized by fatigue and chronic pain, including fibromyalgia, chronic fatigue syndrome, and cancer-related fatigue. And there is plenty of evidence suggesting that the immune system is a mediator. However, I would add to this the role of sleep, particularly REM sleep. It is well known that REM sleep suppression can rapidly reverse depressive symptoms, so one should ask if too much REM sleep (which is determined by our sleep behaviors) might cause depressive symptoms, including fatigue (see attached poster on fibromyalgia and sleep). Since sleep affects the immune system, and vice versa, I submit that the starting point for these conditions may be excessive sleep, especially morning sleep. A hypothesis for why this relationship may have evolved, can be found in the attached poster on cancer fatigue. 

All the best,

Henry Olders

Dear Sarika Srivastava

Can you give some information about the project so that we may be able to give more specific information. 

Any drug causing severe mental side effects would/should not be used as a contraceptive.

Dear Kayleigh Owens,

Bipolar disorder, also known as manic-depressive psychosis, is a mental illness characterized by atypical mood changes, energy swings and the ability to function. Unlike normal mood changes, with their ups and downs, which are inherent in everyone, the symptoms of bipolar disorder can lead to very serious consequences. They are able to destroy personal relationships, affect the quality of work or school performance, and even lead to suicide. Fortunately for us, bipolar disorder still gives in to treatment, and patients with this disease are able to lead a full and productive life.

Specialists at Cambridge University argue that rap music can be a real salvation for diagnoses such as schizophrenia, bipolar disorder, dependence, depression.

Thus, under the influence of rap patients who are not easy to tell about their condition, feel more motivated to communicate, helping to identify their problems. There are reasons to believe that people with mental disorders are comforted by rap, helps to put in order thoughts and feelings, makes more contact, the researchers concluded.

Regards, Shafagat

A very interesting question. I know that a lot of work now around identification of biomarkers for bipolar disorder focus more around inflammatory cytokines; some of these studies reference Na-Li counter transport. You may be able to track down more recent research by searching for this type of inflammatory biomarker research as a backdoor to answering your question. Good luck!

Dear Béatrice. Thank you for the paper suggested.

Dear Vladimir! Thank you very much for your words and reference suggestions. I will read the papers and then I'll give a feedback.

Best regards,

Amilcar

One of the major psychosocial concerns in bipolar relapse is "Expressed Emotion," which is characterized by a high level of negative interaction/criticism and overinvolvement of family members.  Although there are some problems with the construct, it does seem to predict relapse after initial recovery.

Dear Amilcar,

I fully agree with Jordi's comments. I think that a diagnosis of Anti NMDA Receptor Encephalitis should be, always, a differential diagnosis in young patients with neuropsychiatric symptoms, specially if the patient has a history of a prodromal phase of fever, diarrhea or flu-like symptoms followed by a psychotic/manic phase with changes in his/her personality and behavior.

I attached here two articles that may be of interest to you.

Best wishes,

Julio

Thanks, Beatrice and Mary.  Mary, that's what I was thinking, even though I was hoping for a way to have a bit more diagnostic clarity, esp. to engage these FEP pts. who are often ambivalent they even need help.

See work of Boris birmaher

Hello, Maria.  I believe Chris is correct.  Do you have access to that technology?  You very well might in the Chemistry department or even in your own.  If not, do you have access to clinical laboratory in medical pathology department or a veterinary lab?  Either way, you are likely to find friendly colleagues who would treasure the chance to participate in your research.  I agree with your thinking that lithium concentration will afford the most reliable way to compare results both for therapeutic effects and toxicity.

Dear Farooq,

You're welcome. Please keep me informed about your CBT-based group program for bipolar disorders.

Regards,

Stephen

It is always difficult to distinguish "endogenous" psychotic phenomena from externally-induced psychotic phenomena, whether from toxins, fevers, social isolation, emotional trauma, immune reactions, withdrawal reactions, starvation...etc. The only way is to wait until the external stressor is over. But, even when over, the reaction can persist. Is it even a worthwhile distinction to make?

I think that you may use TMS firstly and if it is not effective you can use ECT

Jan

I have used pramipexole at a dosage of .5 to 2 mg in patients also taking tranylcypromine, usually prescribed at 40 mg/day or lower.  No problems have ensued.  However, on a few occasions with pramipexole alone, but at higher doses; 3-4 mg, have seen various types of increased risky behavior.

Charlie

Thanks Beatrice. This is not exactly what I am looking for - rather I'm after an article that shows how one can convert a CARSM score to a YMRS score i.e., a score of 15 on CARSM is roughly equivalent to a score of ? on YMRS.

Thank you, Beatrice

Hi, Kostas!

There is an extensive literature on the deficits in both expression of emotion and emotion recognition in Parkinson's Disease patients. These deficits occur in facial expression of emotion, speech prosody, and body habitus. Many bipolar disorder patients are treated with antipsychotic medication, which in many cases cause a parkinsonian syndrome as a side effect, typically 2 or 3 months after starting the medication. Valproic acid, sometimes used as a mood stabilizer in bipolar disorder, has also been implicated in occasionally producing a parkinsonian syndrome, although in my experience this may take a year or longer to manifest. 

I suspect that emotion recognition through the various modalities is intimately tied up with the neural networks for emotion expression; that is to say, the circuits for pattern recognition of emotion may be "primed" to recognize certain emotions by inputs from the emotion expression mechanisms. This is what seems to occur in other areas of perception; for example, individuals learning to read frequently say the words aloud, then mouth the words silently, and finally suppress the motor expression entirely, as their reading skills improve. The circuits responsible for generating the motor output likely continue to be functional in priming the recognition circuitry, but only their final motor output is suppressed.

If this hypothesis about how perception is linked to expression is valid, one would be able to more easily identify individuals with perception deficits by looking for expression deficits in the first instance. Studying emotion perception is difficult, because the process is not conscious and does not depend on consciousness to function (or not function). Thus, asking someone about their interpretation of a facial expression is already flawed because it requires conscious awareness. Better are paradigms that do not require conscious participation, such as EEG or other physiologic responses like heart rate, BP, skin conductivity, etc. Artificial intelligence approaches to pattern recognition may improve our capacity to link multiple physiologic responses to specific emotions (e.g., Yuvaraj R, Murugappan M, Acharya UR, Adeli H, Ibrahim NM, Mesquita E. Brain functional connectivity patterns for emotional state classification in Parkinson’s disease patients without dementia. Behav Brain Res. 2015 doi: 10.1016/j.bbr.2015.10.036 )

Hope this helps, and good luck with your investigations!

Henry

Eugen Bleuler's Textbook of Psychiatry (1924) has two pages on Thyreogenic Psychoses.  There is no uniform picture, but mania and depression can occur. 

I have used the Conners 3 but the Conners has come out with some new rating scales that are more specific than the Conners 3.  They are published by  Multi Health Systems Inc.  The Conners 3 also has an early childhood version for young children as well.  The Conners 3 measures for more than just mania.

Because parents may have relationship concerns regardless of parenting stress, you could identify a covariate that also may be contributing to stress to help eliminate some bias. For example, self-reported status of the relationship as a) married-coparenting well, b) divorced or separated-co-parenting well, c) married- we fight all the time, d) divorced-we fight all the time.  How they perceive the other parent as well as their efforts in parenting may play a role in how stressed they feel.

Hi Kostas,

You may want to look into these:

Best wishes,

Stephen

From my experiences doing epidemiological research studies in different countries (Japan and US),  the predictors are culture dependent.  Because each culture/country has different tendencies in terms of frequencies across age groups, gender differences, reasons for attempt, method of attempt, religious affiliations etc.  I'd be careful to generalize findings from other cultures.  Good luck with your research!

Lithium is the best option, if needed valproate can be added in a second step, you can read this: Lithium therapy in bipolar disorder: a balancing act? (Lancet, 2015)

For rapid treatment of acute mania on an inpatient unit, consider an accelerated oral loading of divalproex sodium, 30mg/kg for days 1 and 2, then followed by maintenance dosing at 20mg/kg. Here is the study which validates this approach: http://www.ncbi.nlm.nih.gov/pubmed/10665626

Hi Ahmad,

When the body and mind enter stillness, what is already there - experiences held in  mind memory and tissue-held memory in the body, may emerge.  In my studies and practices in bodywork, energy work, mindfulness/meditation, yoga, etc., there has always been reference to these possibilities and recommendations to seek professional medical assistance, i.e. counseling services to work through what may bubble up.  The consequences you are contemplating are really a person's baggage unpacking, and that movement is a path toward wholeness. At the same time, special attention is prudent because a flood is not so healthy rather a gentle peeling of the layers as the person is ready.  In short, it's not so much the methods that pose risk (in my opinion) but the resistance to acknowledge what's there, the readiness/committment to "do the work", and the willingness to seek appropriate services  which may include a variety of providers, strategies, and most importantly, timing. Your thoughts?

Best,

Victoria

Very interesting discussion. It's interesting that the literature really does not try to parse out when stressors lead to either depression or anxiety, as they are highly comorbid with each other, and they overlap with multiple symptoms. Even their treatments with CBT and antidepressants are similar, and making determinations if this is anxiety or depression really does not matter much, as it does not inform further clinical treatments. In my clinical experience, stressors are either handled via adaptive coping skills, or they aren't via maladaptive ones. These patients may then start having adjustment problems, and you notice the specifiers for adjustment disorder includes -with anxiety, -with depressed mood, and -with anxiety and depressed mood. If the stressors continue, then either a depressive disorder or an anxiety disorder emerges, and this tends to go back to CBT theory about thoughts and appraisals about the fearful stimuli and stressors, and this seems to be a significant variable which in turn determines which disorder emerges.

It also appears that anxiety and depression share the same neurobiology: it comes down to the interaction of genetic vulnerabilities (family history) with environmental influences (major life stressors), and it is this interaction which leads to abnormal processing circuits in the brain (hyperactivity of the amygdala to fearful stimuli and stressors). This hypothesis has been supported by a recent study which revealed that people with increased reactivity of their amygdala to fearful stimuli (as measured on fMRI), when they also experience a major life stressor, are more at risk to developing either anxiety or depression up to 4 years into the future: http://www.ncbi.nlm.nih.gov/pubmed/25654256. Further research should examine how the differentiation is made between the development into depression or anxiety, following study subjects with high amygdala reactivity to fearful stimuli who have also endured a major life stressor. I hypothesize that it is the thoughts and appraisals of the stressors which differentiates anxiety from depression, as discussed previously by other researchers who have replied to this interesting thread.

I'd like to join others in saying "Yes" to your question, Ahmad.

Indeed depression is a universal phenomenon and there are subtypes of depression. However, from the perspective of multicultural psychotherapy and international/global psychology, there are differences in one’s symptom manifestations, cultural explanations, and impact of depression on oneself and one’s intimates, depending on one’s cultural identification, acculturation to the Western cultural worldviews, and diverse backgrounds (Falicov, 2014; McGoldrick et al., 2005; Sue & Sue, 2013).

In terms of treatment, there are also differences in one's expectations of the treatment goals, processes and relationship with the healer (Cheung, 2009; Hong & Ham, 2001).

DSM-5 has provided an excellent outline for cultural formulation (OCF) and Cultural Formulation Interview (CFI).

Self-injury could be accidental (e.g. starting a fire from a cigarette). Prevention would be  to try to accident-proof  the house, set up smoke alarms etc. Preoccupation could be secondary to psychotic phenomena so medication would help as long as it does not sedate.

Self-injury could be deliberate because of depression. Screen for depression and institute antidepressant treatment including a heavy dose of social support.

Self-injury could be secondary to a delusion or command hallucination - antipsychotic medication will help.

Self-injury could be a desperate cry for help, Try to attend to the person's needs.

Self-injury could be inadvertent - e.g. scratching dry itch skin. Try to determine the cause.

One area that CBT is focussed in the last2 decades is Bipolar  Disorder

Please check David Miklowitz papers for Family Focussed Treatments for Bipolar Disorder. I believe you will find them very useful.He is the expert on this topic and you can contact him directly. Please do not hesitate to give my name if you contact him directly

I was listening to a Seminar by William Dodson about the difficulty in diagnosing bipolar disorder in children. In the UK, it is said, they do not diagnose children with bipolar disorder--they can call it an otherwise specified mood disorder, oppositional defiance disorder, etc.

Yet, with bipolar symptoms in children can come ADHD comorbidity. This is a bit difficult to tease out at a young age. So, due to this, counselors and psychiatrists have to observe over time the mood fluctuations that occur for a month or two. Sadly, children with ADHD have a high chance of comorbidities.

Link: http://www.additudemag.com/adhd/article/2511.html

Again, he has some free webinars and a plethora of other information on the topic.

Diagnosing younger people with bipolar disorder is questionable at best, and it remains controversial on the ethics side of things. In America it is a bit more acceptable though.

I found this a week or so ago. It's just an abstract, but it is some interesting news.

Link: http://www.pnas.org/content/early/2015/02/09/1424958112.abstract

And here's an article on it : http://isbmolecularme.com/a-breakthrough-in-understanding-the-genetic-architecture-of-bipolar-disorder/

Additionally,  here are some sources for the polymorphism question you had.

Link: http://www.futuremedicine.com/doi/abs/10.2217/14622416.9.11.1589

You may already have read these, but I hope they help!

Consider iatrogenic etiologies secondary to either dopamine antagonists or SSRIs.

my idea is that when there is sodium deficiency of any cause, lithium levels arise. Therefore, it s effective in lower dosage. But this has nothing to do with the pathophysiology of Bipolar Disorder, which is hardly understood. 

Epidemiology shows that there is (and biologically it makes sense); clinically most of these people - not being "sick" by the dysfunction model, do not come into treatment. Therefore clinical studies don't easily capture them. DSM-V is not helpful in identifying this group.

Tony,

My late husband died from suicide. Though I do not know if he had bipolar or any kind of mental health illness at the time.  I do know towards the end he was showing signs of risky behavior with drinking heavily and keeping to himself.  He was in the navy for 15 years divorced with two small children who lived in another state.  We dated for six years and married for only 13 months.  Your topic is very interesting I would love to learn more about it.  Thanks for sharing. 

I agree with the previous answer, starting the question with how or also rephrasing a question to state "Which relatives, if any, have mental illness?" versus "Do you have relatives with mental illness." 

There is a significant risk for false positives and false negatives.  I would not advise use in the primary care setting without further evaluation by a psychiatrist or psychologist.  If the plan is to use it as a screen and not diagnostically to start treatment (which should be the case) either could be used.  

This paper may be of help for you:

Seasonality and bipolar disorder: A systematic review, from admission rates to seasonality of symptoms. Geoffroy PA, Bellivier F, Scott J, Etain B.. J Affect Disord. 2014 Oct 15;168C:210-223. (email: pierre.a.geoffroy@gmail.com)

RESULTS:

Fifty-one papers were identified of which 32 addressed hospitalization rates by season, 6 addressed categorical diagnoses, and 13 explored symptom dimensions. Seasonal peaks for different BD mood episodes are observed worldwide and widely replicated. Manic episodes peak during spring/summer and, to a lesser extent, in autumn, depressive episodes peak in early winter and, to a lesser extent, summer, and mixed episodes peak in early spring or mid/late summer. There was a high frequency of SP for manic episodes (15%) and depressive episodes (25%), the latter being associated with a more complex clinical profile (BD II subtype, comorbid eating disorders, more relapses and rapid cycling). Finally, there was evidence for greater seasonal fluctuations in mood and behavior in individuals with BD than in those with unipolar depression or 'healthy' controls

The hypomania checklist has been developed as a screen by angst and colleagues. What specifically are you looking to measure? I know few more which might be relevant 

Thankyou for your thoughts everyone much appreciated. Im looking for a questionnaire as a baseline measure of depression symptom severity rather than to be used to make a diagnosis (participants will already have an established diagnosis). These are useful questionnaires to consider thanks again

The same applies to many other conditions, e.g.  depression, migraine, OCD, autism, ME/CFS, back pain, motion sickness, etc.

In my experience working with chronic pain patients, the ongoing pain associated with migraines and the way in which it disrupts people's lives will trigger depression. I have worked with people who are suicidal due to chronic pain because it isolates them and they are frequently treated poorly in the medical community. (I include people with migraines into the category of chronic pain)

"Hypomanic switch induced by antidepressant was found to be higher in SAD patients with ADHD comorbidity (26.5%)" Did this group have additional medication for ADHD?

Melanie,

The second edition of Frederick K. Goodwin's and Kay Redfield Jamison's "Manic Depressive Illness (not the first edition) has a chapter on children/adolescents concerning bipolar disorder.  I am reading the compilation of information gathered from the body of research over the past 27 years, but I have not gotten to that chapter.  You might look at it to gather information on your subject if you can't find what you are looking for.

I personally do not think that true bipolar disorder can be treated effectively without prescription drugs in conjunction with some type of psychological therapy.  At the very least with prescription drugs.  A minimum of the mood stabilizer lithium, which is the gold standard, or an anticonvulsant such as depakote would be very helpful, especially in conjunction with some type of non-pharmaceutical therapy Kraepelin (mid nineteenth century to early 20th century differentiated manic depressive illness from schizophrenia). Therapy is also a viable way to treat bipolar disorder: 

Non-pharmaceutical

Clinical psychology Electroconvulsive therapy Involuntary commitment Light therapy Psychotherapy Transcranial magnetic stimulation Cognitive behavioral therapy. 

There are some papers from 2014 on this issue:

Blood levels of brain derived neurotrophic factor in women with bipolar disorder and healthy control women.

Kenna, Heather A.; Reynolds-May, Margaret; Stepanenko, Aleksandra; Ketter, Terence A.; Hallmayer, Joachim; et al. Journal of Affective Disorders156 (Mar 1, 2014): 214-218.

 

Increased platelet intracellular calcium ion concentration is specific to bipolar disorder.

Dubovsky, Steven L.; Daurignac, Elsa; Leonard, Kenneth E.. Journal of Affective Disorders164 (Aug 1, 2014): 38-42.

Blood–cerebrospinal fluid barrier dysfunction in patients with bipolar disorder in relation to antipsychotic treatment.

Zetterberg, Henrik; Jakobsson, Joel; Redsäter, Mikael; Andreasson, Ulf; Pålsson, Erik; et al. Psychiatry Research217.3 (Jul 30, 2014): 143-146.

Serum level of brain derived neurotrophic factor (BDNF) among patients with bipolar disorder.

Rabie, Menan A.; Mohsen, Manal; Ibrahim, Mona; El-Sawy Mahmoud, Rania. Journal of Affective Disorders162 (Jun 20, 2014): 67-72.

The relationship between impulsivity and lipid levels in bipolar patients: Does temperament explain it?

Tatlıdil Yaylacı, Elif; Kesebir, Sermin; Güngördü, Özlem. Comprehensive Psychiatry (Feb 12, 2014).

Early apoptosis in peripheral blood mononuclear cells from patients with bipolar disorder.

Fries, Gabriel Rodrigo; Vasconcelos-Moreno, Mirela Paiva; Gubert, Carolina; dos Santos, Barbara Tietböhl Martins Quadros; da Rosa, André Luiz Schuh Teixeira; et al. Journal of Affective Disorders152-154 (Jan 2014): 474-477.

 

 

There is no date. You can use it and write n.d. instaed of the year.