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.
Questions related to Biological Psychiatry
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!
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.
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.
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.
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.
In recent decades, the role of psychopharmacological treatment in psychiatry has become more and more central. Critical voices in this regard are increasing significantly
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.
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...
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 ?
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.""
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.
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?
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.
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.
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?
I am looking for questionnaires and tests that apply to clinical assessment of novel psychoactive substances addiction. Is there visual analogue scale for craving?
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?
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.
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.
Any suggestions for available databases for DNA methylation in psychiatric patients? And if available, any suggestions regarding software for analysis of these data?
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.
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.
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 ...
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!
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.
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.
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.
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?
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!
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.
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?
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?
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 ?