Science topic

Bipolar Disorder - Science topic

A major affective disorder marked by severe mood swings (manic or major depressive episodes) and a tendency to remission and recurrence.
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I an looking for an resting state (eyes closed) EEG datasets for any kind of psychiatric disorder. These can include, but not limited to
  • Alcohol use disorder
  • Acute stress disorder
  • Addictive disorder
  • Anxiety disorder
  • Behavioral addiction disorder
  • Schizophrenia
  • Post traumatic stress disorder
  • Depressive disorder
  • Bipolar disorder
etc.
I would prefer if the datsets contain raw EEG data eg EDF files but. If anyone can assit i would really appreciate that. Thank you in advance
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It seems accepted that lithium can induce anti-suicidal effects. Does this require the typical dosages utilized in mania or bipolar disorder maintenance?
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Low levels of lithium do appear to confer some protection against suicidality. Please see here for a recent supporting review -
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Lamotrigine is an anti-epileptic medication and a very good mood stabilizer, especially for bipolar disorder type 2. Tactile hallucination of bugs crawling on the skin can be a very annoying side effect. This can lead to discontinuation of this medication, despite significant improvement of mood symptoms. It will be very helpful to know its prevalence and if there is any remedy to minimize this side effect so that the patient can continue to use it.
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I have used lamotrigine a great deal and have not seen this side effect. Is it dose-related?
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Hi,
I am hoping someone can inform me as to how the SCID-5-CV is scored? I have been looking online but can't find too much without purchasing handbooks from the DSM.
I am looking at hypomania symptoms in patients with bipolar disorder and want to know if I can use the SCID to measure hypomania symptoms between time points (e.g. at baseline, 6 months, 12 months etc). As such, I want to be able to determine episodes, duration, severity etc. from one time point to the next. Moreover, I would like this to be in a way that is quantifiable, for statistical analysis.
Can the SCID-5-CV allow for this? Or alternatively, is there a more appropriate measure?
Thanks,
Emily.
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Hi,
I have identified two things that I deem to be random noise in a hypothetical study. I just want reassurance these are sources of random error, as opposed to confounds.
The study is looking at the effect of exercise intensity (low, moderate, high) on hypomania symptoms in patients with bipolar disorder over time (before, mid-way through, and after a 12 week exercise programme, as well follow-up at 6 months and one year from baseline). We were interest in whether any conditions improved, or exacerbated hypomania symptom severity.
What I identified as random noise:
- A potential socialisation effect if participants were coming into the lab and exercising alongside other participants (BD is associated with increased social anxiety and so the experiment could increase stress, which can be a cause of hypomania symptoms). I said this was random noise as it would not affect one condition more so than any other, but it would make it harder for us to detect a significant effect.
- Time of day effects on exercise session and hypomania symptom measurement. Disruption to routine can increase the potential for manic episodes, and this would also add noise to the sample, making it harder for us to detect the effect of exercise intensity on hypomania symptom severity. Again, we did not believe that these effects would impact one condition more than others, and as such, identified it as noise.
Can anyone confirm that these factors are indeed sources of random noise, as opposed to confounds?
Thanks.
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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.
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I am measuring sleep spindle activity in 3 groups: schizophrenia, bipolar disorder and healthy individuals.
I aim to compare their activities and the sleep study will only do once.
Do you think this is a cross-sectional study since I measure it at one-time point?
Or do you think it is a case-control study?
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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:
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Can you identify differences between your experience of love when you are healthy or manic? For individuals with bipolar disorder this knowledge may be elusive and change with different stages of life.
Some people believe when a person is in a manic state, he/ she is also more likely to feel in love!
What is your opinion?
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Yuppppp
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I am trying to discern whether, in the brain (structure & function) of people with bipolar disorder/MDD/schizophrenia who experienced childhood trauma, there are:
1. already differences in children's brain structure & function that trauma further modifies and the person develops a mental illness OR (genetics first then trauma)
2. trauma changes the structure and function of the brain that the child's genetics further modifies and the person develops a mental illness (trauma first then genetics)
Has anyone researched this & if so, can you please share your findings or references you know of?
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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.
  1. In Cassiers et al (2018), their review of the literature supports the hypothesis that the brain changes are a protective adaptation in response to abuse, they did not discuss the genetic components that may be predisposing to or responsive to abuse so it doesn't directly answer the question.
  2. In Nemeroff (2016), he suggests (based on my assessment) some brain changes are due to the moderating effects of genetics (so genetics first) (eg, carriers of 1 or 2 copies of the "short" allele of the serotonin transporter promoter polymorphism have greater rates of depression vs those with the "long" allele homozygotes with equal childhood trauma) and other changes are in response to the trauma and predispose the person to the mental illness (eg, reduced hippocampal volume in depressed women with a history of childhood maltreatment but not in equally depressed women without maltreatment).
  3. Aas M et al (2019) reported that polygenic risk score (PRS) and CTQ were inversely correlated so those with lower PRS reported more severe abuse and vice versa, so the based on this (my interpretation) is that in a brain/body with more "imbalances" due to genetics (brain structure/function and physiology that is predisposed to BD), abuse does not need to be severe to make the changes sufficient to cause BD wherein people with low PRS have brain structures and physiology is more "balanced", greater severity of abuse is needed to sufficiently change the brain structures and physiology to cause BD. They did not also look at brain or physiology so we can only infer based on genetics.
  4. In Stevelink et al (2019), their study findings suggest "that childhood abuse results in poor white matter integrity in a subset of people who are then possibly more vulnerable to development of psychiatric disorders, including bipolar disorder" and "that childhood abuse, in particular, is associated with FA, possibly due to its effects on HPA-axis activity." But as pointed out in the limitations, their cross-sectional study design does not allow for establishing causation "Based on our results, we cannot differentiate whether decreased integrity of white matter in patients is caused by childhood abuse, or whether this decreased integrity was already present prior to experiencing childhood abuse."
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.
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I am attempting to write a paper on the relationship between left-handedness and psychopathology, including PTSD, bipolar disorder and schizophrenia.
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Sommer, I., Aleman, A., Ramsey, N., Bouma, A., & Kahn, R. (2001). Handedness, language lateralisation and anatomical asymmetry in schizophrenia: meta-analysis. The British Journal of Psychiatry, 178(4), 344-351.
Chicago
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Switching antipsychotics to minimize risk of side effects one should also inform the patient of risk of relapse
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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!
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Lithium is first line therapy for Bipolar Disorder, mainly in acute manic face, after initiating lithium therapy, most common side effect is tremors.
1. why tremors, mechanism?
2. treatment for tremors - propranolol?
3. most accepted mechanism of action of lithium?
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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)
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Is there a link between onset of Isotretinoin treatment with the onset of psychiatric symptoms (depressive disorder, bipolar affective disorder, suicidal ideation)?
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Interested
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Please let me knows about squizophrenia and bipolar disorders and this kind of therapies....
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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.
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My topic of thesis is “ mental health & media literacy: analyzing the role of social media regarding mental health awareness”
I have selected twitter to analyze what type of information has been posted about depression, stress, anxiety and bipolar disorder. I want to study the media literacy level of people by evaluating their perception, participation on twitter regarding the issue and role of twitter in changing public perception about mental health as stigma and help seeking behavior for it.
I want to ask what type of spss test will be applied to my hypothesis? My hypothesis is if people participate more in discussion of mental health issues, the less will be the stigma.
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As I interpret the decision to select a statistical test depends upon the type of study, pattern of data & most importantly your objective.
Regards
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Particles, such as lithium and ethanol are known for their strong action on CNS. Little diameter of these particles, enables them to migrate and act directly on many cerebral structures. Similarity of lithium to another ions prone to check if high efficacy of lithium treatment is only the result of impaired ion- balance repair...
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I think bipolar disorder is triggered by sleep disorder in persons with unstable circadian rhythms (see my RG question on this).
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Patient has bipolar depression, on Lithium carbonate, quetiapine and propranolol, has residual symptoms of depression such as fatigue, and attention deficit. I am thinking if adderall is a good CNS stimulant for her? any recommendations?
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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.
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Can you tell me about the connection between variability heart rate and bipolar depressive disorder (or pharmacoresistant unipolar depression)? I would be very thankful for the publications you know of about this topic which applied fractal and nonlinear measures, apart form frequency analysis. I know of some finding about the link between the outcome of ECT and VHR in depression, but the sample was small. We are trying to understand our data and it is difficult to find newer publications apart from Goldberger, Pincus, Costa et al on nonlinear measures illustrating that connection.
Thank you
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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
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Dear all,
We invite you to participate in PROCEED, an international scientific survey with the goal to identify your expectations for treatments of depression.
You are eligible if :
you suffered or you are currently suffering from an episode of depression
• you are an informal caregiver, that is to say a family member or a friend of someone who has suffered or is suffering from depression
• you are a healthcare practitioner working with of depressed patients (for instance : psychiatrist, psychologist, nurse, general practitioner/family doctor, etc)
To make your voice count, please connect to the survey's dedicated website and answer the anonymous questionnaire. It will take less than 10 minutes.
The more participants will be included, the more we will be able to make things change in the improvement of treatment for depression.
This survey has been approved by an ethic committee IRB00003888.
Thank you for your participation !!
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done
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Joseph Williams wrote in 1846 (Med Times 15:140): "Puerperal insanity occurs after parturition, and is generally observed in those cases where there has been considerable exhaustion; and in this respect it somewhat resembles delirium tremens". Sleep disorder or deprivation has often been noted in bipolar disorder, but rather than regarding it as a symptom of the disease, could it not simply be a universal trigger for it?
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I have found in patients with severe mental disorders, particularly psychosis, schizoaffective and bipolar, that if they take melatonin at night there is a definite improvement in cognitive processing, processing speed and emotional processing. It is idiosyncratic though, as no clinical trials have been done per se, however it indicates that neural repair etc that occurs during sleep plays an important role in functioning.
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I want to test the GSK3 activity in neuronal cells. Since the isotope is not authorized in our lab, I wonder whether there is an isotope-free  method for detecting GSK3 activity.
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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.
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Many articles on psychological treatment of bipolar disorder (and anxiety in bipolar disorder) report small samples. However, very few describe or raise the question about the challenges in recruiting patients with bipolar disorder. Please help me find articles about this topic or write what you know if you are an expert! Thank you
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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.
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I am seeking research studies and statistics regarding the graduation rates of students diagnosed with bipolar disorder. In particular, I am interested in what accommodations are made by colleges and universities for the symptoms of bipolar disorder which may be, at face value, seeming violations of typical Code of Conduct policies, and how these accommodations have been applied to assist with bipolar student success to graduation. Specifically, these symptoms are recognized as (1) extreme irritability, (2) provocative, intrusive or aggressive behavior and (3) denial that anything is wrong.
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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
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I need it for my thesis in Psychology.
I can read material in English or Italian.
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I am seeking databases that includes variables for women that have been diagnosed with postpartum psychosis or postpartum bipolar disorder or major depressive mood disorder with psychotic features in the first year postpartum.
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Thank you so much....
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What are effective and long-lasting treatments for ADD (attention deficit disorder) / ADHD (attention deficit/hyperactivity disorder), excluding stimulants (like amphetamines, SNRIs, NRIs, or NDRIs)?
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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.
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I'm trying to use EEG signals to feed an artificial neural network in order to diagnose mood disorders (specially major depressive disorder, but it would be interesting to try with bipolar disorder, schizophrenia etc).
However, I'm having a hard time finding quality databases of EEG with annotations of mood disorders.
Anyone knows where I could find it?
Thanks in advance.
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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 
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Since my early career research focused on the search for biomarkers, particularly red blood cell Li-Na countertransport levels in bipolar patients and alcoholic patients, and many of my bipolar patients also had clinical complaints consistent with what is now called fibromyalgia; and my mid-career research focused more on the epidemiology and mental health aspects of HIV infection, through the Multicenter AIDS Cohort Study (the MACS), it is interesting to see other researchers interested in immune function in both affective disorders and fibromyalgia. Have you or any other researchers following your research also seen similarities in the immune profiles of patients with bipolar disorder and fibromyalgia and the state-dependent changes in immune markers?
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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
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Hi everyone, I am searching for a drug having contraceptive or anti fertility properties but induces a severe mental disorder like depression, bipolar disorder etc. 
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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.
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I'm a 3rd year nursing student looking to do a musical representation of rapid cycling bipolar for my alterations in neuro-psychological health course. I would appreciate any input.
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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
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Reports of altered cation transport genes and their transmembrane protein transcripts in cultured cell lines from bipolar patients were judged as irreproducable by other research groups, and the original report was eventually withdrawn by Gershon and colleagues. In the 15-25 years since, have there been in vitro studies that either support or further debunk the theory that hereditary differences in Na+ Li+ countertransport levels in peripheral blood or cultured cell lines from patients might be useful surrogate markers for the clinical diagnosis of affective disorders or clues to their pathophysiology?
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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!
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Abnormal brain oscillations have been related to some of the underlying mechanisms of psychiatric disorders including unipolar depression and bipolar disorder.  Adverse life events are well-known factors that can trigger or worsen the symptoms of depression. Are adverse life events related to abnormal brain oscillations? If yes, how?
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Dear Béatrice. Thank you for the paper suggested.
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It is well known that adverse life events can trigger or worsen depression. It has been reported abnormal brain oscillation in depression and also hypothesized that at least, in part, this abnormal brain oscillation might share some features with the neurophysiology of epilepsy. 
Are there any connections between reduced serotonin levels, adverse life events, and abnormal brain oscillations? 
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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
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How do key pychosocial factors exert their effects via biological and behavioural pathways to influence key illness outcomes 
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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.
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Not every psychosis or manic episodes are functional. Some are due to organic causes. Should a deeper organic screening be introduced in the psychiatric clinical practice?
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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
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I am concerned about differentiating first episodic psychotic break (in schizophrenia, schizoaffective d/o, or mania w/ psychosis) from substance-induced psychosis due to:
-energy drinks (poss. distinct in effects from caffeine due to other substances added such as taurine, ginseng, l-theanine, etc.)
-nutritional supplements, esp. androgenic substances and those used by bodybuilders
-any combination of these, or with other substances, esp. nicotine, alcohol, and stimulants.
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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.
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I've been looking on some data on epidemiology of mood disorders among adolescents, but practically all the information I can find in textbooks is that in case of younger patient, it is more likely that he/she suffers from bipolar disorder rather than depression. Where can I find the newest data on prevalence and characteristics of mood disorders among young adults/adolescents? Thank you for your response.
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See work of Boris birmaher
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I'm working with animal models for bipolar disorder to investigate lithium mechanisms of action. However i've been using lithium dosage based only in the suggestions from the literature. Indeed, I would like to check if the dosage i've been using is catching the right blood concentration that i'm expecting or not. How could I measure lithium levels in the blood?
Thanks!
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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.
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I am helping with development of a CBT based group program for the bipolar disorder. NICE Guidelines are rather disappointing in this regard. There are a few old meta analyses. Any help and guidance will be heplful. 
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Dear Farooq,
You're welcome. Please keep me informed about your CBT-based group program for bipolar disorders.
Regards,
Stephen
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Bipolar I Disorder can include psychotic symptoms, including auditory hallucinations. Patients with any type of Bipolar Disorder (I or II) not uncommonly abuse alcohol. Some people who abruptly withdraw from alcohol may experience auditory hallucinations.
Is this a distinction without a true difference?
Can anyone offer any useful references or clinical experience?
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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?
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The lack of significant differences in adverse pregnancy and birth outcomes in treated versus untreated women with bipolar disorder is a reassuring piece of data for clinicians weighing the risks and benefits of medication during pregnancy. However, this study could not adequately address risk for malformations, which have been documented in many other studies. Importantly, women with bipolar disorder had worse pregnancy outcomes than women without bipolar disorder. Many factors were statistically controlled for; however, others, such as psychosocial stress and instability and substance use not meeting diagnostic criteria, might contribute to these group differences
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I think that you may use TMS firstly and if it is not effective you can use ECT
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Fawcett, J et al. Clinical experience with high-dose pramipexole in treatment resistant depression in unipolar and bipolar patients. Am Journal Psychiatry, 2,2016
Fawcett, J et al. Adding Stimulants of Monoamine Oxidase Inhibitors, American J of Psychopharmacology, 1991
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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
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Does anyone know of any papers in which the authors converted scores between the Young Mania Rating Scale and the Clinician Administered Rating Scale for Mania, or between the Montgomery Asberg Depression Rating Scale and the Hamilton Rating Scale for Depression?
I'm looking to compare scores across datasets, in which different measures have been used. I know this type of conversion has been done with the BPRS/PANSS (Leucht et al., 2013). Is it possible to do the same with the above mentioned scales?
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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.
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There was a wonderful article about schizophrenia and insomnia in the October 2015 Journal of Nervous and Mental Disease written by Chiu, Harvey, Sloan, Ree, Lin, Janca, and Waters.
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Thank you, Beatrice
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Are there articles for the neuropsychological deficits in perception of emotion in bipolar disorder in patients depending on the medication?
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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
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I am seeking research on any areas that would give false positive results for Bipolar Affect Disorder (BPAD). I have not been successful finding current studies. I am curious if Thyroid evidence would impact results?
Also, knowing that Chromosome 18, with parental linkage has impact, has anyone completed research on parental/patient (nuclear family) testing for significance? I did find one study regarding this latter topic. Thank you. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1801428/
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Eugen Bleuler's Textbook of Psychiatry (1924) has two pages on Thyreogenic Psychoses.  There is no uniform picture, but mania and depression can occur. 
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Can anyone direct me to a Spanish version of the Young Mania Rating Scale or Spanish and English versions of  PGBI-10M, for use with my community mental health center clients?
I'm also happy to be directed to any other bilingual/Spanish version available psychiatric rating scales for children and adolescents that might be more difficult to find (i.e. anything not a PHQ scale, Vanderbilt scale, or SCARED.)
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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.
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I am looking to conduct a qualitative exploration of co-parenting when the other parent has a diagnosis of BPD but wanted to include some measures or concurrently run a quant study looking at parenting stress in the non-diagnosed parent. I don't know whether to ask retrospectively about when the partner was 'ill' or if this biases the data too much away from how well they co-parent most of the time potentially?
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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.
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There are articles on this?
It is said that in emotional level autism with bipolar disorder are connected 
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Hi Kostas,
You may want to look into these:
  • Examining the comorbidity of bipolar disorder and autism spectrum disorders: a large controlled analysis of phenotypic and familial correlates in a referred population of youth with bipolar I disorder with and without autism spectrum disorders by G. Joshi, J. Biederman, C. Petty, R. L. Goldin, & S. L. Furtak, & J. Wozniak.
  • Bipolar Spectrum Disorder Comorbid with Autism Spectrum Disorders by Jay A. Salpekar & Peter Daniolos.
  • Others.
Best wishes,
Stephen
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Greeting!
Could you please suggest any additional expected predictor of suicide among hospitalized psychiatric patients to be investigated for a future research?
This is the initial list:
1- being young,
2- male gender.
3- high level of education.
4- history of prior suicide attempts.
5- presence of depressive symptoms.
6- presence of active psychotic symptoms.
7- good insight to illness
Kind regards,,,
Ahmad.
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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!
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Is Lithium or Valproate a better option in case of bipolar and substance dependence? I thought that Valproate would be better as it would play a role in treating withdrawal seizures as well, but, I am not getting literature to support this point.
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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)
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I understand that sleep is important and may help ease the state for some people (since lack of sleep has been seen to induce mania). I also understand that mania may be treated with certain medications.
What I am looking for are studies or any experience on how to quickly and effectively manage manic episodes. Thanks in advance!!
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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
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Mindfulness is now widely accepted practice for improving physical and psychological well-being. Recently, one participant in mindfulness-based interventions who is trying to integrate mindfulness in every-day life experiences reported to me that she had experienced palpitation and headache during her mindfulness practice. This rare observation leads me to ask about the risks (negative consequences) of mindfulness practice!  
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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
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Chronic stress can lead to anxiety in some people, while it can lead to depression in others. Some people with chronic stress may experience both anxiety and depression. It seems not clear how stress, anxiety, and depression contribute to each other. How can we interpret these different combinations of co-morbidity?
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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.
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Signs and symptoms of depression in mothers of children with autism are frequently reported. However, based on extensive clinical observations and self reported data, I constantly observed that these mothers report specific depressive symptoms more than others. I did not observe this phenomenon in patients with schizophrenia or bipolar disorders. Is there any evidence supports this??? or it is a merely chance?  
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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).
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What can you do to prevent it? What are the risk factors? What is the prevalation?
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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.
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A commonly noted factor causing BPD is reported to be environmental stress.  How much of a contributor is stress from the patient's immediate family in initially triggering the onset of the disease,  Until diagnosed and treated, would immediate family conflicts and tensions from reactions to the emerging behaviour symptoms further aggravate the patient's conditions ? Finally, can the patient's immediate family positively contribute to the diagnosis, treatment, recovery and rehabilitation phases.
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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
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I am writing an argumentative essay exploring the validity and ethics of diagnosing children with bipolar disorder.
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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.
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.
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To be very specific I need to know about some gene expression studies on bipolar disorder. Is anyone working with polymorphism studies of any psychiatric disorders?
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I found this a week or so ago. It's just an abstract, but it is some interesting news.
Additionally,  here are some sources for the polymorphism question you had.
You may already have read these, but I hope they help!
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I am interested in knowing more about the endurance of anhedonia in BPD patients after they have suffered a depression. I can't find relevant literature on this topic, so perhaps someone here can help me out?
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Consider iatrogenic etiologies secondary to either dopamine antagonists or SSRIs.
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I've seen anecdotal evidence of a potential relationship between bipolar and sodium deficiency, but I'm looking for empirical evidence of such a correlation. Can anyone recommend articles or other resources?
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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. 
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Most doctors do not think it exists, because very happy people rarely seek treatment, but a few researchers suggest that 15-20% of patients diagnosed with bipolar disorder may be unipolar manic. Are there any studies on this?
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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.
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There is a sizable literature on the incidence of suicide and suicide risk in those with bipolar disorder. However, the nature of the disorder, particularly the manic phase, there would seem to be conducive to fostering severe suicide risk in those with intimate relationships with bipolar sufferers, especially spouses. Lavish spending sprees, unwise financial decisions and resultant debt, quitting jobs, other consequences of grandiosity, impulsive sexual indiscretions, dangerous substance abuse and other risky behavior, hostile put-downs, may create suicide risk in spouses. Rapid cycling more common in women may be a contributing factor to suicidality in male partners.
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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. 
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Asking about demographic details (age, sex) and family history, how can we format questions that are open ended?
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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." 
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MDQ? HCL-32? Both have Spanish validated versions. However, to my knowledge, they have not been used in primary care settings.
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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.  
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I have recently seen a middle aged female from rural Kashmir who has had episodes of mania or hypo-mania every three months from the last 20 yrs starting 2 days before cycle and ending three days after it. The only time she didn't have an episode is during her pregnancies.
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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
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Interested in finding out any new questionnaires for bipolar disorder. I am familiar with the mood disorder questionnaire.
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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 
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Hi there I'm planning some research with bipolar disorder and need a self-report measure of depression symptoms (which is free to use!)
One's that fit the bill are PHQ-9 (designed for primary care) and Centre for Epidemiological Studies Depression Scale (designed for general population research). Can't find any studies validating them with bipolar.
Any thoughts on which one I should use? Many thanks!
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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
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There has been an ongoing difference of opinion among researchers about the classification of Bipolar Disorder. Some believe its etiology and genetic relationship is closer to Schizophrenia than to Major Depression.
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"There is no illness as there are no biological markers apart from behaviour, there is no disease as there is no pathogens, viruses or bacteria's, there is no evidence of brain disease and chemical imbalance is simply a marketing slogan which has become urban myth.."
The same applies to many other conditions, e.g.  depression, migraine, OCD, autism, ME/CFS, back pain, motion sickness, etc.
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With a family history of MDD as well as Bipolar disorder, could this be a reason for the constant reoccurence of high pain scale migraines on a daily basis?
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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)
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I think that there might be an association between hypomanic switch in SAD patients and ADHD.
In our study (Koyuncu et al. 2012) that includes 108 SAD patients, bipolar disorder occurred under antidepressant treatment in 14 of 16 patients with bipolar disorder comorbidity. Hypomanic switch induced by antidepressant was found to be higher in SAD patients with ADHD comorbidity (26.5%) than those without comorbidity (0%). Fifty-six of 108 social phobia patients (51.8%) were under antidepressant treatment for at least one month. Fourteen of those 56 patients (25%) had hypomanic switch. Interesting part of the picture was that switch occurred only in SAD group that had ADHD comorbidity.
There are studies regarding switching in patients with SAD. It was reported that 18 out of 32 patients treated with a monoamine oxidase inhibitor (MAOI) have remitted while 14 of those patients developed hypomanic symptoms (Himmelhoch, 1998). Among patients with major depression, antidepressants were more related to hypomanic switches in the presence of SAD comorbidity (Holma et al., 2008). In our study, the switch rate was lower than in Himmeloch’s study.
As it is known, the validity of the antidepressant induced hypomania concept is controversial. Is it induced by antidepressant or caused by nature of disorder? (Levis and Winokur, 1982; Tondo et al. 2010 )
Akiskal and Malya included antidepressant induced hypomania in soft bipolar spectrum in 1987. Himmelhoch suggested that a group of social phobia patients who had switch might be within the bipolar spectrum and that bipolar characteristics might appear by antidepressant treatment (Himmelhoch, 1998). In our study, we found that social phobics with ADHD comorbidity had switched with antidepressant treatment.
Antidepressants might increase the likelihood of mood elevation in some sensitive patients regardless of the clinical diagnosis. (Wehr & Goodwin, 1987; Ghaemi et al., 2004; Tondo et al., 2010). Considering these publications, ADHD patients who have similar symptoms with bipolar disorder might be one of the sensitive patient groups for the switch mentioned in those studies. It means that those with ADHD comorbidity might switch from ADHD to bipolar spectrum under antidepressant medication regardless of the primary diagnosis.
Although it is claimed that antidepressant induced hypomania should not be classified in a different category because it belongs to the course of bipolar disorder (Chun and Dunner , 2004), it might take place in the border between ADHD and bipolar disorder. Antidepressants might be taking patients from ADHD to bipolar spectrum.
Our patients who went through a hypomanic switch under antidepressant treatment (especially patients with a combined or hyperactive type ADHD comorbidity) claim that they come back to the way they used to be. They report becoming hyperactive, impatient and very talkative people who can not stand still, who talk and take risks without much thinking. They say to me “These characteristics were diminished, but now they came back but this time I am very happy and more self-confident.” Our theory is that antidepressant induced hypomania might be an exacerbation of ADHD in patients with SAD. Prescribing antidepressants to an ADHD patient might exacerbate ADHD like pouring gasoline on fire. ADHD comorbidity in SAD must alert clinicians regarding the occurrence of possible switches or bipolar disorder. New studies that explain these issues are warranted.
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"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?
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In particular, teens under 18, and who have a history of manic episodes.
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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.
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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. 
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Dr. Peter D'Adamo, naturopathic doctor has previous research data relating to this topic. Also, with correlations to food allergies and psychiatric conditions which can be greatly improved through diet (i.e. gluten free diet). Has anyone come across correlations in blood testing and bipolar/depression/schizophrenia?
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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.
 
 
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I am looking for articles or research that will aid in a psychodynamic understanding of addiction, especially in individuals diagnosed with bipolar disorder.
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There is no date. You can use it and write n.d. instaed of the year.
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Imagine you have a 35-year old childless woman with bipolar disorder currently in remission on lithium. She and her partner want to have a child. Considering her history you feel that discontinuation of lithium is highly risky and her getting pregnant would exponentially increase the probability of disastrous outcomes for her, her partner and the future pregnancy. How are you going to do the decision making involving her and her partner?
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The main teratogenic effect of lithium is a tenfold increase of a very rare severe cardiac malformation which is caused around the 10 gestational week. Thereafter lithium-loss of effect (or intoxication after adjustment) may be a problem because of a large increase in body water especially if pre-eclampsia develops (which seems more common in bipolarity). Therefore body weight should be followed nearly on a daily basis. When an increase of more than 20 kg has been witnessed pre-eclampsia is very likely and magnesium therapy should be instituted. Pregnancy is a state of tolerance with inhibition of adaptive immunity and increase in innate immunity which is related to bipolar disorder. Risks of pregnancy are closely related to mucosal infections anywhere and therefore these should be treated. Lithium possibly inhibits innate immunity.
That's the way I would see it. Kr gt
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We are designing a neuroimaging study to test hypothesised circadian moderation of reward function in humans. Seems like our hypothesis is best tested using resting state methods, ideally with the hypothalamic suprachiasmatic nucleus as a 'seed region' to investigate correlations with brain reward centres (particularly ventral striatum).
I understand that small, deep brain centres are difficult to image.
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Hi Greg,
Interesting idea. In theory, almost any brain region can be used as a seed region for resting-state functional connectivity studies. In practice, I think the SCN is going to be tricky. Maybe not impossible, but certainly difficult.
Your two main problems are going to be:
1. Localisation - getting an accurate SCN ROI for each of your subjects. I'm only aware of one paper which tried to localise the SCN in humans (http://onlinelibrary.wiley.com/doi/10.1111/j.1460-9568.2008.06582.x/abstract;jsessionid=1DDF475BBC25A93E627D75AD61392F59.f04t04?deniedAccessCustomisedMessage=&userIsAuthenticated=false) and they did it basically by anatomical means - using the optic chiasm as a landmark. Since the SCN is so small (about 2mm^3) they admitted in the paper that their ROI probably included bits of the surrounding structures i.e. the anterior hypothalamus. I would imagine that this is probably the only option for such a small structure. Functional localisation would be extremely difficult given that typical fMRI resolutions are 3mm^3 - you'd be looking at a single voxel. Possibly you could try a functional localiser (i.e. a visual stimulus) with some very small voxels (2mm or 1.5mm) and just a few slices in that region, but you'd be losing so much signal that you might have to scan your subjects for hours to get anything reliable. Which leads me on to...
2. Signal-to-noise. You're right in saying that small, deep structures like this are difficult to image. The SCN in particular is right on the bottom of the hypothalamus, next to a pocket of CSF - this means you're going to get some pretty nasty magnetic susceptibility artefacts and partial-voluming effects, which will essentially serve to reduce your signal and inflate the noise. Plus, it's a very small area, so even if you localise anatomically (and manage to do it accurately) you're probably only going to be looking at a handful (5-10?) of functional voxels that are forming your ROI - this will give you a noisy estimate of the time-course of that area, which means when you feed that in to a functional connectivity analysis, your power to detect results will be reduced.
One solution might be to go the other way around, and localise the reward areas to be used as the seed region in your FC analysis - this can be pretty easily accomplished either anatomically, or using a functional localiser like the MID task.
Hope that helps!
M.
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Therapeutic communities have had some success in reducing socially aberrant behaviour associated with conditions defined as personality disorders. What evidence exists for their efficacy in patients presenting with acute psychosis, including paranoid delusions and explosive anger?
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A plain no. TCs do not largely work with a full time Psychiatry MD. Having said that, people with a Mental Disorder, including most psychotic, anxious and bipolar cases, who are able to understand what is going on, stabilized on medication and followed up by a Psychiatrist or trained clinician, can easily find a place in a TC to receive appropriate care in several other domains of their lives. Here in Brazil, TCs are specially meant to alcohol, crack and other drugs dependents and the group is considered a quite important therapeutic aspect of them. I recommend reading George De Leon' books and papers.
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I am looking for Japanese versions of the following scales:
Bipolar Spectrum Diagnostic Scale (BSDS)
Hypomania Checklist-32 (HCL-32)
Hirschfeld's Mood Disorders Questionnaire (MDQ)
Temperament Evaluation of Memphis, Pisa and San Diego Autoquestionnaire (TEMPS-A)
Altman Self-Rating Mania Scale (ASRM)
Unfortunately, despite searching, I could find neither open-to-public versions of this test nor works with these tests enclosed.
I would be very thankful for any help.
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Please find it enclosed
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How is the relationship?
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There is an informative new paper written by Mark Zimmerman on the relationship between bipolar disorder and BPD. Full-text version can be found here:
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The first line of treatment for BD is mood-stabilizing medication, such as lithium or anticonvulsants, but is ECT a valid alternative treatment, perhaps even used fairly early on in the treatment course?
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Dear Neil;
There is no clear answers emerge from the literature: But there is a growing body of evidence to suggest that for those patients who have not responded well to medications but have responded to ECT, Maintenance-ECT must be presented as an option to the patient.
Rabheru K. demonstrated that relapse rates after discontinuation of ECT are very high. But M-ECT is an underused treatment option that can substantially reduce risks of relapse in patients with major depressive disorder and likely in bipolar disorder and schizophrenia as well.
Review: Rabheru K. Maintenance electroconvulsive therapy (M-ECT) after acute response: examining the evidence for who, what, when, and how?
J ECT. 2012 Mar;28(1):39-47. doi: 10.1097/YCT.0b013