Science topic

Biological Psychiatry - Science topic

An interdisciplinary science concerned with studies of the biological bases of behavior - biochemical, genetic, physiological, and neurological - and applying these to the understanding and treatment of mental illness.
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Hello,
I would love to receive some recommendations from experts in regards to the topic, whether there are valid findings in research on biological markers for anxiety disorders. I am trying to gain some stable insight and be able to argue in favor of the notion, that no anxiety disorder "comes from a malfunction/sickness of the brain".
Thank you in advance!
Best
Ivo
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What are the pharmacological risks?
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Thanks you, Dr. Miky Timothy
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In the aftermath of the 1918 Spanish Flu pandemic there was a marked increase in incidence in psychological and psychiatric illness incidence. These conditions now often referred to generically as post-viral syndrome increased hospital admissions and treatment of mental health disorders in the years following the outbreak in 1918.
Population studies in countries that did not take part in World War One seem to indicate that the possible post war melancholy could be ruled out as a confounder as this increased incidence was seen in all countries affected by the flu that had been non-combattants in WW1.
Could there be a lasting and chronic element to all SARS type respiratory disorders?
SARS genome sequences have been detected in the brain of earlier SARS autopsies with LM, EM, and with real-time RT-PCR. The signals were confined to the cytoplasm of numerous neurons in the hypothalamus and cortex. Oedema and scattered red degeneration of the neurons was identified in the brains of 80% of the confirmed cases of SARS examined.
SARS viral sequences and pathologic changes have not been found in the brains of unconfirmed cases or control cases.
We may have a longer lasting health care problem that will affect those 'recovered' from Covid-19 for some years to come.
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Of course: YES !!. The Covid-19 coronavirus is neurotrophic, but -in addition- it is generating thousands of behavioral and psychopathological disorders due to the infinity of biopsychosocial problems that it is generating ... not to mention the so-called "pandemic fatigue" that the entire population is suffering. in general because of the "anti-Covid control" measures (confinements, border closures and perimeter closures of cities, time controls, curfews, etc.) that are influencing a lot and changing our lifestyles ... phobias are skyrocketing. , paranoid and catastrophic ideations, Post-Traumatic Stress Disorders -PTSD-, sleep problems and disorders, over-stress, anxiety, depression, pathological grief for the deceased, problems of schooling and socialization of children and a long etcetera (without going any further far, the Separations and Conflicts of Couple have increased in the West by 135%).
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A study on Biological Psychiatry found that aging is successfully linked with a choice to live happy and productive life. Any one who limits his vision to memories of yesterday is already dead - Lillie Langtry.
Is it important to know that happiness stems from heart and a cheerful heart is linked to cheerful mind and long lasting body?
Inviting to share your own experiences in this context.
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Yes, I think this is true because many heart attacks are the result of sadness or upset, but a person who has hope in life easily overcomes those obstacles and sad situations.
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Prudent prescribing of antimicrobial drugs to hospital inpatients may reduce the incidence of antimicrobial drug resistance and healthcare-associated infection. Despite strenuous efforts to control antimicrobial drug use and promote optimal prescribing, practitioners continue to prescribe excessively; it is estimated that up to 50% of antimicrobial drug use in hospitals is inappropriate. Antibiotics have several drug-drug interactions (DDIs) with psychotropic drugs (mainly antidepressants, antiepileptics, antipsychotics), which can lead to adverse events, treatment failure and significantly rise the costs of treatment. 
Currently, very little is known about antibiotic prescribing patterns in psychiatric hospitals, including the frequency of potential DDIs between antibiotics and psychotropic drugs.
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Regardless if you have a psychiatric diagnosis and not, you can have infections and other p0hysical disorders. My experience is that too little focus is put on these patients' physical disorders. In the early years alcohol and penicillin was recommended not to be taken together. This was not due to any interaction between alcohol and penicillin but it was a precaution that sailors and others with sexually transmitted disorders could forget to take their antibiotics when drunk.
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This is for a theoretical project, so I have to describe what statistical analysis I would, rather than actually calculate it. 
I'm looking to see if the combination of propranolol and virtual reality exposure has an interaction on reducing PTSD symptoms, meaning that the combo therapy is more effective than either therapy alone. 
2 IVs: exposure (virtual reality or control), medication (propranolol or placebo)
2 DVs: CAPS-5 (psychological measurement of PTSD symptoms) and EDA (physiological measurement).
So, I have 4 treatment groups, and I know I do a 2-way MANOVA, followed by two 2-way ANOVAs (looking at each DV in turn). But what else do I do, in terms of follow-up tests or post-hoc tests, to show that the virtual reality-propranolol group is significantly more effective than the others? 
Many thanks for an help, I can't find the answer online or in my books. 
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When the MANOVA model is significant, use descriptive discriminant analysis (DDA) for the post hoc analysis, not any ANOVA or post-hoc Tukey’s etc. Such wrong concept has been around for decades.
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In recent decades, the role of psychopharmacological treatment in psychiatry has become more and more central. Critical voices in this regard are increasing significantly
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Yes indeed. The attached slides include a study with some startling results on acute/chronic variations in drug therapy in psychosis.
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Can you help me with some database for neuroscience, for example fMRI database, or database which show underlying mechanisms of the brain, show the connection between brain and behavior, psychiatry database and other things which related to brain, if you were familiar with genetics we have for example Reactome, KEGG, STRING and other database which show lots of pathway and cell connection, I wonder if we have sth like that in neuroscience, a big database which help us to better understand the brain.
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Actually you can use those databases that you mentioned to conduct research and understand mechanisms of brain activity in health and disease in computational neuroscience!
We recently used KEGG and STRING to study gene networks in different psychiatric diseases.
However, if you are mainly interested in using fMRI and imaging databases in your research, please check the following as well:
1. Blue Brain project by EPFL has a great database in at circuit level that can be used:
2. Human Connectome Project (HCP) is a great database comprised of scans and analyses of more than 1100 subjects:
3. Allen Brain Atlas
and many other databases that you may find and use depending on your main focus in neuroscience.
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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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DNA structure and activity can change with environmental factors. But does experience such as sexual abuse create significant biological effects on DNA?
These type of researches are so important in detecting crime.
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Just like environmental factors, psychological factors may have an impact on gene expression and its regulatory mechanisms but the extent of impact would be depndent on multifactorial aspects and would need to be ascertained in a case to case basis.
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I am a psychiatrist writing a book on mindful eating. Does anyone have a mindful eating scale that I may publish?
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Dear colleagues, we are validating the Brazilian version of the MES, here you find the scale in Portuguese: https://www.mindfulnessbrasil.com/center-mente-aberta/mindful-eating-brasil/mes-mindful-eating-scale/
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Is that ok with using high-risk suicide in MINI (mini international neuropsychiatric interview) as outcome in major depressive disorder ?
If no, is there any  clear or general definition for the outcome of high-risk suicide in major depressive disorder ? Such as suicide attempt ?
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I suggest suicidal ideation, I attach our paper:
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It is surprising how we (in general) mindlessly believe that depression (and other mental-health conditions including anxiety) are purely a chemical imbalance in the brain and that it does not have environmental/social factors.
""It is a bio-psychosocial problem; there are biological factors and psychological and social factors. What Hari is talking about are the social drivers of depression.""It's good to challenge how the drug companies and the DSM and the FDA oversimplify not just depression, but all mental disorders,"
Professor McGorry said. "They try to reduce them and American psychiatry is really responsible for that; they turned away from psychoanalysis to biological psychiatry and regarded everything as just a brain disease.""
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I have worked in poverty/high crime areas most of my 35+ career in psychiatry. Good practitioners know the difference between grief, situational and chemical depression and treat accordingly.
I don't just give someone a pill if depressed, we both process severity of depression, reasons for such and ways to make it better. I find Professor McGorry's assumptions insulting. Most patients see a psychiatric provider and a thearpist as well as a case manager. I am a therapist but consider myself a brain chemist but I do know the difference between depression/grief, etc. which should be treated with medication and what should not be treated/won't respond to medication even if taken. I usually say, "I wish I had a pill for the sadness and stress that you are going through, but if it gets too severe or you get thoughts of harming yourself or others, we can try medication." I let the patient decide from there and usually they agree that it is situational and they can get through it.
In Professor McGorry's defense, I find that about 50% of people are incompetent in their jobs and sadly that includes medicine and psychiatry.
Remember too that if someone has prolonged stress it can cause chemical depression and medication may be able to help the person get through troubling times if too severe i.e suicidal thoughts, aggression to others, not able to function at work, etc. Now days, no one can afford to take time off of work to heal.
In regard to drug companies PR campaigns, maybe there would be less suicides if people knew that treatment was available. I like when my patients ask me about medications seen on TV, we discuss the pros and cons of that one and others in the same category and the patient choses which one (if indicated) i.e. some cause weight gain, some help with sleep, increase in blood sugar, etc.
Most of my patient's stress is around not having money, housing, and in limbo waiting on a "disability" decision in order to get money.
PTSD is also common due to terrible childhood traumas and adult traumas as well (the stories I hear would make you sick).
Genetic loading is a big factor in my patients with mental illnes on both sides of the family. I find a lot of patients coming to me with depression who failed multiple antidepressants because he or she acutally has Bipolar II whcih is bipolar depression (often misdiagnosed for 15 years).
Malnutrition can also play a role which is why my patients get a B complex and Vitamin D3 daily from me.
Substance abuse is another factor.
I hope you find this helpful i.e. it isn't just one way or the other, a good clinician knows the difference between situational/transient/manageable depression and something that only time, lifestyle changes, therapy can heal. Continued monitoring for need of medication is also important.
Dr. Kelly Gardiner PhD, PMHNP, CNS, BC
Board Certified Psychaitric Clinical Nurse Specialist
Psychiatric Mental Health Nurse Practitioner
PhD Public Health: Community Health and Education
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In real clinical practice some patients are treated with combination of clozapine and another depot antipsychotic. Although we have a positive evidence of clozapine combination with some antipsychotics, clozapine should not be combined with depot antipsychotics, because of several adverse events, which can not be discontinued very easy in patients treated with depot. In clinical practice we often have problem that we have positive symptoms (residual) with only clozapine and therefore combinations could be used. In my point of view many combinations should be used first (e.g. combination with lamotrigine, combination with another antipsychotic non-depot, combination with N-acetylcysteine) before this potentially risky combination.
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Before combining with other antipsychotics, it might be helpful to control serum levels, because particularly in clozapine, non-compliance or only partial compliance is a frequent cause of treatment resistance.
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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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I'm not a psychiatrist, but I wonder if it is possible to reliable identify the presence of hallucinations. And if the method can be translated to the animal models. I would greatly appreciate the variety of opinions.
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Sometimes darting eyes, hands over ears or plugs in ears, loud music on ear phones, head shakes, holding the head, banging the head, talking back, unprovoked smiles or laughs or shouts, frightened looks, looking over one's shoulder, listening attitude, dazed look. Not sure whether any of this applies to lab animals.
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KINDLY HELP OUT;
Table 1 Genotype distribution and allele frequencies in fluvoxamine-responsive and nonresponsive patients. ;
                      GENOTYPE FREQUENCY               ALLELE FREQUENCY
RESPONSIVE         24(68.6)    11(31.4)           0(0.0)      59(84.3)    11(15.7)
NON RESPONSIVE 6(31.6)       9(47.4)            4(21.0)    21(55.3)    17(44.7)
Frequencies are shown in parentheses.
OBTAINED FROM: (K. Yoshida et al. / Progress in Neuro-Psychopharmacology & Biological Psychiatry 26 (2002) 383–386)
MY QUESTION IS
1. HOW CAN I USE THE INFORMATION FROM THE ABOVE STUDY TO DETERMINE THE SAMPLE SIZE FOR MY STUDY WHICH WILL HAVE A POWER OF 80% CONFIDENCE OF 95% AN ALPHA OF 0.05 TO IDENTIFY AN ODDS RATIO OF 2 BETWEEN RESPONSIVE AND NON RESPONSIVE PATIENTS. 
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Miyuru Chandradasa AND Béatrice Marianne Ewalds-Kvist 
THANKS FOR YOUR RESPONSES
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According to the evidence and some reports and suggestions amisulpride is very effective antipsychotic with medium effect size (Cipriani; Lancet). Because of its pharmacological profile and mechanism of action amisulpride could be combined with another antipsychotics, when there is a lack of efficacy (or small efficacy better) of first antipsychotic (especially in patients with positive symptoms of schizophrenia). There are also studies, where positive effects in combination with clozapine are described. Its pharmacological profile shows that it could be used as antidepressant in small doses (e.g. until 100-150 mg), because of its action on presynaptic receptors (antagonist on D2/D3). By blocking these autoreceptors amisulpride is preventing neurons to stop firing dopamine, leading to an increase of dopamine concentration in the brain. However, there is support to prescribe this agent in a real clinical practice pharmacoepidemiological data shows that a consumption of amisulpride is very small. Why?
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Amisulpride might indeed be very effective in the elderly patients. However, to my experience, the potential of inducing EPS is not that small. I have seen parkinsonism even after very low doses and if dose goes up to 200 mg and a patient is older than 75... Well, the drug becomes problematic. On the other hand, the use as an augmentation in MDD could be bigger. Low doses (usually up to 100 mg/day) are quite effective, particularly in cases with lack of energy / apathy / anhedonia. 
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I am looking for questionnaires and tests that apply to clinical assessment of novel psychoactive substances addiction.  Is there visual analogue scale for craving?
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Dear Dr. Béatrice Marianne Ewalds-Kvist
Thank you very much!
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In the case of major depressive disorder treatment (MDD) a full remission is main goal of the treatment, however about 2/3 of patients fail to achieve remission in first year of the treatment with antidepressant. In this point of view achieving remission is often connected with use of 2 different antidepressants (e.g. bupropion and SSRI, trazodone and SSRI, mirtazapine and venlafaxine ... ) or switching. In real clinical practice antipsychotics are also often added (e.g. aripiprazole, quetiapine and olanzapine). 
When you make decision which way (combine or switch) is more appropriate for the patients with MDD?
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This is a huge question and virtually with no simple answer. Partially responsive patients often represent a mixture of biological, psychosocial, personality, addictions and even economic or legal problems. Drugs provide no real benefit then. However, generally speaking, I try to keep treatment simple and prefer multiacting drugs over combinations. What I always try to add are BDNF-related therapies (such as fitness training or yoga:-) and CBT elements.
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Serotonin (5-hydroxytryptamine, 5-HT) is a chemical found in the human body.It carries signals along and between nerves - a neurotransmitter. It is mainly found in the brain, bowels and blood platelets.Serotonin is thought to be especially active in constricting smooth muscles, transmitting impulses between nerve cells, regulating cyclic body processes and contributing to wellbeing and happiness.Serotonin is regarded by some researchers as a chemical that is responsible for maintaining mood balance, and that a deficit of serotonin leads to depression.
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Several lines of evidence implicate decreased serotonergic activity in anxiety and major depression, but its importance in the etiology and severity of these disorders remains unclear. Acute tryptophan depletion studies support a role for decreased serotonin in depression, or at least in relapse of recovered depressed patients. Imaging and post-mortem studies indicate altered activity of discrete regions within the prefrontal cortex (PFC) and their atrophy are associated with depression. Genetic polymorphisms in serotonin genes [e.g., 5-HT transporter (5-HTT), 5-HT1A receptor] have been associated with depression, but these associations are weak and not always reproducible, suggesting that serotonin may be a predisposing factor rather than a cause of depression or anxiety. Pl. refer following thread for further details:-
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According to the many well designed trials and reports, there is an important correlation between hypertension and psychiatric disorders. Psychiatric patients are often treated with antihypertensive agents. If we know that treatment with antidepressants and antipsychotics is often long-term we should be very careful, which antihypertensive agent is appropriate for these special patients. These patients are often treated with different specialists and many drug-drug interactions (e.g. indapamide-clozapine) occur within pharmacotherapy.
My opinion with the use of EBM:
- ACE inhibitors should be used first and those with longer half life (especially those with appropriate pharmacokinetics accroding to the kidney failure; e.g. Fosinoprilat). Because psychiatric patients are usually treated with antidepressants (e.g. trazodone) and antipsychotics (e.g. clozapine and quetiapine), which can make hypotension it is very important to use ACE inhibitors with longer half life (to avoid serious short hypotension and falls).
- diuretics (e.g. Indapamide) should be avoided. Although these agents are second line in many international guidelines for hypertension treatment they can incude serious prolongation of QTc, which can have very bad consequences (e.g. death, torsade). We know that many psychiatric patients are treated with those drugs and we can expect additional action, when many 'dangerous' drugs are used together (e.g. TCA, clozapine, quetiapine, amisulpride etc ... ). Instead of diuretics use CA-antagonist for example (e.g. amlodipine, because is cheap and effective).
- sartans are second line treatment (ACE inhibitors first line). However valsartan could be a good idea in patients where Fosinoprilat is not effective and we have psychiatric patients with kidney failure.
- beta-blockers are very useful in these patients, especially where we can avoid polypharmacy (e.g. propranolol for tremor and hypertension) and add additional efficacy (e.g. pindolol in depression and hypertension). However use of these drug should be with great caution especially in the elderly psychiatric patients.
Especially a great caution is required, when used these drugs in patients with ADHD. In these patients avoid of the use of beta blockers because serious hypertension can occur, especially when withdrawal is taking place.
- Moxonidine could be a good option in some patients, however drug drug interactions can be very dangerous. To add moxonidine to ACE inhibitors and CA-antagonists could be a better option as add diuretic indapamide.
- Alpfa blockers are not first line treatment, especially in elderly psychiatric patients. Many DDIs can be very dangerous (e.g. pharmacodynamic) and serious hypotension can occur, when used together with antidepressants and antipsychotics.
If i sum up, it is very important to check all possible DDIs before prescribing. It is also very common that psychiatric agents with its mechanism of action have potential to lower blood pressure and usually in these patients antihypertensive agents can be reduced. However, a cooperation among clinical pharmacists and clinicians can be beneficial for these patients.
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Dear Matej
Thank you for sharing your extensive knowledge and indeed experience in this complicated topic. 
As for treatment of hypertension, HIV, cautious combination (yes I avoid the term polypharmacy) therapy has important role in effective treatment of individuals with psychiatric disorders.
Given the risk of DDIs, its important to have access to all the relevant information.
I use an app (for smart phone) called Epocrates.
Happy to learn about any other useful apps colleagues use.
Rashid 
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Any suggestions for available databases for DNA methylation in psychiatric patients? And if available, any suggestions regarding software for analysis of these data?
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you may be aware of this publication:
Whole genome methylation analyses of schizophrenia patients before and after treatment.
available here:
To me it's the first methylome  wide association study.
I don't know it the publication contains the whole genes methylation list.
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In the last few years many prescribers do not prescribe IR-MPH in their practice, although clinical guidelines do not support this practice, especially in the titration phase. A pharmaceutical industry is very strong towards newer forms and atomoxetine, which is lower in term of efficacy (effect sizes obtained from meta-analyses). How IR-MPH should be used that patients with ADHD are treated more appropriate? Easy question but hard to answer.
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At the end of the day, despite what treatment guidelines say about what is first line treatment for ADHD, it comes down to cost and value. Industry-sponsored articles from thought leaders in association with industry will not be able to answer this without bias. For patients without the resources to buy more expensive, patented, long-acting medications, then this is an easy answer- MPH-IR is a cost-effective solution. For 3rd-party payers that pay for more expensive, patented, long-acting medications, they should do their own cost-analysis and not be swayed by the biased literature regarding ADHD treatment guidelines.
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According to the many trials and guidelines the use of antipsychotic polypharmacy is not recommended, however more than 1/3 of patients are treated with antipsychotic polypharmacy (APP). Risperidone was often used in many trials and many of them are negative (N Engl J Med. 2006 Feb 2;354(5):472-82.). In last years paliperidone is available, however there is a big lack of studies with APP, where paliperidone is included, although is often used in clincal practice. It is interestingly why these studies have not been conducted yet; if it is because of negative trials with risperidone and 'afraid' or another reasons have been existed.
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It is certainly worth having data on all combinations to guide us.
One reason I sometimes choose other second generation antipsychotics over risperidone (R) and paliperidone (P) is because both cause clinically significant increases in serum prolactin. And as regards hyperprolactinemia, P is worse than R, probably because higher doses of P are required to pass the blood brain barrier...but the pituitary is not 'protected' by the blood brain barrier and is therefore exposed to high levels of P
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Usually the antipsychotics are titrated very fast in first 1-3 weeks. However there are several reasons for non-response and one of them is also 'pharmacokinetic failure', when usually even higher doses are used as recommended. Often, because of non-optimal titration (too fast) patients are treated with high doses to fast and serious adverse event (e.g. EPS) are often occured. Although is known from EBM trials that for optimal effect prescriber should wait smth until 8-12 weeks of monotherapy within the maximal recommended dose, usually in clinical practice doses are too fast titrated and consequences are often seen in antipsychotic polypharmacy, which has not many support in EBM and clinical guidelines for management of schizophrenia. Easy question, however very hard to answer ...
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It would be a good idea to establish if the patient was actually metabolising the drug before titration.  'Pharmacokinetic failure' is frequently associated with the inability of the patient to metabolise the drug and also in an alarming number of cases where the wrong drug is being administered.  
The often cited and utterly unscientific nonesense of 'treatment resistant schizophrenia'  is nothing of the sort.  The reason the patient 'resists' the medication is because it is the wrong medication.  Psychiatrists and psychiatric nurses should be required to complete a full course in pharmacology before being allowed to prescribe. the fact remains that many prescribers have little more than a rudimentary understanding of pharmacokinetics and pharmacodynamics and simply follow the pack when it comes to treatment.
The death rate from faulty prescribing is an alarming testimony to the pharmacological ignorance of many practitioners.
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Dear experts,
I am encountering some problems while doing PPI analysis in SPM8. In my study, subjects participated an intervention, and they watched 2 types of pictures in the scanner before and after the intervention.
I have chose a brain region that is critical to intervention as a seed, and I am intersted in connectivity changes of the seed with other regions that interacted with the ratings for 2 types of pictures in pre-post intervetion contrast, like the procedure in Schmaal et al., 2013, Biological Psychiatry (Effects of modafinil on neural correlates of response inhibition in alcohol dependent patients).
In Schmaal's paper, she achieved this goal using the generalized form of PPI (gPPI; McLaren et al., 2012). However, I failed to do the same analysis in classic PPI module in SPM8, because SPM8 can not do pre-post (intervention) test at the 1st level analysis, whereas PPI analysis need VOIs and SPM.mat that generated from the 1st level analysis.
I will be really appreciated if you could help solve this question!
Best,
Yuan-Wei
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Hi Griffis,
Thank you for your helpful comments! I really appreciate that.
Best,
Yuan-Wei
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According to the few studies and reports there is a big lack of reports in psychiatry and neurology, where medical errors and inappropriate prescribing are reported. In most countries worldwide there are no appropriate systems within health systems in terms of inappropriate prescribing detection and appropriate solutions. One of the most important question in this field is ... Who will protect patients from medical errors and inappropriate prescribing ... Clinical pharmacists and/or pharmacologists with practice in psychiatry, GPs, psychiatrists with practice with inappropriate prescribing or whole team, where all specialists will be included. On the end, it is very interesting that we do not have studies or reports on this topic in the most European countries.
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Hi Matej
The literature shows that the error rate in medication administration is about 10% (not counting errors in timing). That means about 500 errors each day for a hospital with 600 beds. The reporting rates run at 200 per year which is a tiny percentage. I have come to appreciate that it is better to concentrate on those errors that are reported than to expend energy on increasing the reporting rate. Much can be learned from each error and implementing a change to prevent the error will also prevent many of the other unreported ones. In my own hospital there is a committee dedicated to analysis of error reports and making corrective suggestions. There are two doctors, two nurses and two pharmacists. Each brings their own experience and perspective to the discussions. This could be extended to the problem of inappropriate prescribing. Multidisciplinary groups are ideal and it should be implemented through each discipline with reports back to the committee. An essential part of this kind of activity is to have the full support of the management.
Regards
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Dear all,
There is an expectation that understanding the neural substrates of mental disorders will revolutionize the field of psychiatry, in terms of improving diagnostics and treatment. However, the clinical value of neurobiological research into mental disorders has so far been minimal.
What are your opinion on this matter?
Do you agree that an understanding of the biology of psychiatric disorders (genetics, molecular, brain circuits etc) will lead to improved diagnostics and treatment, or are the expectations of a ”revolution” exaggerated?
I’m interested in hearing your opinions on this matter.
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I think that there is indeed a great deal of potential for a "revolution," but that what has held back the field back is the decidedly non-biological approach that has traditionally characterized psychiatric genetics, neuroscience, and related fields.  That is, the object of study is biological, but the approach and assumptions are not (or only so in a very limited way).  That is, there has been a general lack of anything resembling a systems or organismic approach when it comes to matters of the mind.  Brains nonetheless don't exist in vacuums (or vats) and will never be understood purely in reference to themselves and the occasional stimulus that impinges upon some sensory organ.  Zing Yang Kuo and Jaques Le Magnen are notable, past critics of the mainstream, dualistic (and reductionistic) approach.  For recent reviews hammering on this issue in the domain of depression, read:
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Does anyone have any views on a biological basis for PTSD? C-reactive protein (CRP) a marker in inflammation has been associated with combat related PTSD in soldiers. Biological factors in chronic psychiatric illness have been elusive but this might give us an insight into why some people are more negatively responsive to stress than others.
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As others have mentioned, there are genetic polymorphisms that can make one more vulnerable to PTSD, but you don't necessarily need to have these differences to develop PTSD.
Here's how I wrap my head around this type of genetic/environment interaction situation. Stay with me, I swear I'll connect it :). Wine. Grapes are the best fruit to make wine with; the natural properties of grapes allow the fruit to create wine without any additives during the fermentation process. However, wine can be made without grapes... it can be made with all sorts of fruit and even rice, but these materials are not as easily converted into wine and require special additives and/or processes during fermentation.
In this illustration, wine is PTSD; grapes are the serotonin transporter genes with one or two shorter alleles. The other types of fruit and the rice are the genes with the long alleles, they can make wine (develop PTSD) but it's easier with the grapes (shorter alleles). That being said, just because you have grapes (short alleles) doesn't necessarily mean you are going to make wine (develop PTSD), you could always have a nice fruit salad. :)
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My background is in mental health, however I am new to the study of asthma. What are the key conversations regarding the interaction of these two elements should I get myself up to speed on?
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On the epidemiology side, one of the important issues concerns the bidirectional (one could even say pluripotential) nature of the associations. As with many long-term medical conditions, asthma has mental health consequences. On the other hand, mood and anxiety disorders may increase the incidence of asthma (see General Hospital Psychiatry. Volume 30, Issue 5, Pages 407–413.). 
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Hi all,
I am currently analysing data from an fMRI study, with a 2x2 between-within design. Patients vs controls reflect the between factor, and congruent and incongruent trials reflect the within factor (this is a Stroop task).
After seeing an interaction effect between the two factors in several brain clusters, I wanted to extract the beta-weights from these clusters to explore the underlying effects.
I used Marsbar to extract the raw beta-weights from congruent and incongruent trials, separately (so no contrast between conditions performed), and plotted the results for my two groups.
Many of the resulting beta-weights are negative, and I wonder what this means? Does it reflect a sort of 'deactivation'?  
Any input will be highly appreciated!
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Most likely, in your case, when you run a general linear model (GLM) analysis, you are attempting to predict the voxel signal using a vector of onsets convolved with some hemodynamic response function. It's fundamentally the same as when you are carrying out any other linear regression: You are predicting some variable (Y) as a function of a predictor variable (X): Y = B(X)+E -- Y is a function of X, plus some variance, (E). B is simply the coeffcient of the predictor variable that leads to the best estimate of Y. In the case of fMRI, X is the idealized time course for the onsets of a particular condition. When B is high for a voxel, that means that the activation for that voxel closely follows the idealized time course for that condition. If B is near 0, that means there is little to no relationship between voxel activity and the idealized time course. B can also be negative, meaning that it is inversely related (e.g, whenever that particular condition occurs, activation actually decreases).
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How emotions injure your heart? What are the pathophysiological factors involved?
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Dr Blake Jane, I was hypothesizing about molecules released by the brain under acute or chronic stress, still under study or yet undiscovered, which could directly affect the heart, causing aging, arrhythmias and sudden death.
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A lot of us are investigating the pathophysiology associated with mental disorders. One popular method is fMRI, which would be one example of measuring macro properties of the brain, at the regional / circuit level.
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Bassett, D. S., and Gazzaniga, M. S. (2011). Understanding complexity in the human brain. Trends in Cognitive Sciences, 15, 200-209. doi:10.1016/j.tics.2011.03.006 provided an interesting discussion along these lines. We have now published a series of articles suggesting the appropriate level to understand higher cortical functions is based on dynamic cortical columns that are in circuits. These in turn interact with subcortical structures, consistent with Luria's views that higher functions can only be understood as whole brain activity. The same theory provides information on serious neuropsychiatric disorders, depression/anxiety, the metatraits of plasticity and stability of the Big 5, the process variables in psychotherapy, and a structured approach in dealing with influential relationship-based negative emotional memories. I have attached one article from June that discussed the microcircuitry allowing the theorized manner of column formation. The other articles are available at my page, with the first being in 2006.
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Autism and ASD undoubtedly have a multitude of risk factors, which lead to somewhat similar symptoms. What biological mechanisms do you think are converging from different risk factors to produce ASD symptoms?
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Theory of mind is affected in a range of conditions and I'm not sure that the fact that it is abnormal in people who are congenitally deaf really advances your argument. My experience of people with autism, and I've treated a lot of them, is that they are unusual in a broad variety of ways, many of which are hard to relate even indirectly to sensory pathology. Cognitive abnormalites such as weak central coherence are inexplicable in purely auditory-vestibular terms.
Autism research is littered with single aetiology theories, the most infamous of which was the now utterly discredited MMR theory. In the current state of knowledge we need to be circumspect in our evaluation of the aetiological evidence. My last word on the matter.
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It is well accepted that schizophrenia has many different causes that presumably lead to similar symptoms/syndromes. What do you think the convergence mechanisms and pathways are in schizophrenia?
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@ Nathanael Yates: I deem that 1) altered (alleviated) PI3K/Akt-mediated CREB activation and further decrease in BDNF and/ or c-Fos expression(s) as well as activated GSK-3beta and declined beta-catenin mediated neuronal apoptosis might have a role in diminished dopaminergic functions and consequent schizophrenic pathology. 2) Besides, neuropsychologicalimmunology based hypothesis (Stress - Fas/TNF/Interleukin/Caspase activation-mediated dopaminergic neuronal apoptosis) is also proposed as an upstream pathway underpinning schizophrenic pathology. But, the additional role of these upstream signals in the GABA-ergic and Glutaminergic neurons could not be ignored.
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How strong is the evidence that ECT causes mania and are there any studies to support it?
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In my experience some depressed patients may experience mild hypomania during ECT. However, this is no real clinical problem, since ECT is effective for mania as well.
Therefore, my advice is to continue ECT, it is very likely that the hypomania will resolve.
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Has anyone seen patients developing symptoms of hyperammonemia and encephalopathy while on valproate and what's the management ? What are are the common signs and symptoms ?
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From my clinical experience, hyperammonemia is not that frequent with sodium or magnesium valproate up to 1500mg/2000mg day in healthy adults receiving monotherapy, especially for the acute management of mania. In case of epilepsy it may be used up to 3gr/day but the risks for toxicity do increase proportionally. So, from my own experience with patients IT IS (!!!!) largely dose dependent. Hyperammonemia may cause central hyponatremia and could be associated with cognitive and cardiological toxicity. Also bare in mind that a major metabolism pathway for the drug is UGT and CYP2C9 and CYP2C19: although you may exclude in most of the cases any clinically relevant pharmacokinetic interaction which could RISE the levels of valproate (on the opposite side, valproate may INDUCE CYP3A4 substrates including lamotrigine, but this is an another story), in some cases valproate could rise the pancreatic functioning (a specific parameter is represented by the pancreatic lipase), so you could monitor it too. Most importantly, the clearance pathway for valproate is the GI, not just the urinary trait, and that patients with severe constipation may be at higher risk to reach toxic levels of valproatemia (which you could monitor by blood sampling). A rapid and effective way to manage valproate intoxication (including: fever, hypothermia, hypotension, cardiac arrest and respiratory depression) is represented by the withdrawal (sudden w. if fine in case of acute toxicity) plus the administration L-carnitine, which is very important in case of life-threatening valproate intoxication. But apart from specific cases (e.g. PCOS in fertile women) or specific pancreatic conditions, I find valproate a cornerstone treatment for a number of mood disorders, so I always use it with confidence and I many patients (including bipolar I and II and/or epileptic ones) who tolerate 2000 or even 2250mg/day since years. I rarely go beyond such doses, and I prefer reducing valproate to add a second agent (including SGAs or lithium) to enhance both safety, efficacy and long-term tolerability.
To sum-up: hyperammoniemia may lead to both toxic encephalitis and permanent damages to liver, kidney and pulmonary functions. USE valproate with confidence BUT if you really suspect toxicity is occurring (valproatemia may help), suddendly remove it and introduce creatine/L-carnitine which counterbalances the effects of ammonia.
Michele.
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Contents of our dreams can reflect our personality and sometimes they are related to some diseases.
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Given the fact that the discussion about the ([neuro]biological) relevance of dreaming and consequentially dream content is still controversial (see, e.g., the works of Allan J. Hobson), you could perhaps find some hints here:
1: Pagel JF. What physicians need to know about dreams and dreaming. Curr Opin Pulm Med. 2012 Nov;18(6):574-9. doi: 10.1097/MCP.0b013e328358bf42. Review.
2: Stumbrys T, Erlacher D, Schädlich M, Schredl M. Induction of lucid dreams: a
systematic review of evidence. Conscious Cogn. 2012 Sep;21(3):1456-75. doi:
10.1016/j.concog.2012.07.003. Epub 2012 Jul 28. Review.
3: Hill CE, Knox S. The use of dreams in modern psychotherapy. Int Rev Neurobiol.
2010;92:291-317. doi: 10.1016/S0074-7742(10)92013-8.
4: Blagrove M, Pace-Schott EF. Trait and neurobiological correlates of individual
differences in dream recall and dream content. Int Rev Neurobiol. 2010;92:155-80.
doi: 10.1016/S0074-7742(10)92008-4. Review.
5: Schredl M. Characteristics and contents of dreams. Int Rev Neurobiol.
2010;92:135-54. doi: 10.1016/S0074-7742(10)92007-2. Review.
6: Vandekerckhove M, Cluydts R. The emotional brain and sleep: an intimate
relationship. Sleep Med Rev. 2010 Aug;14(4):219-26. doi:
10.1016/j.smrv.2010.01.002. Epub 2010 Apr 2. Review.
7: William Domhoff G, Schneider A. Similarities and differences in dream content
at the cross-cultural, gender, and individual levels. Conscious Cogn. 2008
Dec;17(4):1257-65. doi: 10.1016/j.concog.2008.08.005. Epub 2008 Oct 4. Review.
8: Rosa A, Poyares D, Moraes W, Cintra F. Methodology in clinical sleep research.
Cell Mol Life Sci. 2007 May;64(10):1244-53. Review.
9: Stickgold R, Hobson JA, Fosse R, Fosse M. Sleep, learning, and dreams:
off-line memory reprocessing. Science. 2001 Nov 2;294(5544):1052-7. Review.
10: Revonsuo A. The reinterpretation of dreams: an evolutionary hypothesis of the
function of dreaming. Behav Brain Sci. 2000 Dec;23(6):877-901; discussion
904-1121. Review.
11: Kramer M. Manifest dream content in normal and psychopathologic states. Arch Gen Psychiatry. 1970 Feb;22(2):149-59. Review.