Questions related to Clinical 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!
As often in medicine animals are ( SADLY) used in experiments .A new study of mice shows there are important links between human and mouse minds in how they function -- and malfunction. Researchers at Washington University School of Medicine in St. Louis devised a rigorous approach to study how hallucinations are produced in the brain, providing a promising entry point to the development of much-needed new therapies for schizophrenia.
The study that was published in the journal Science, lays out a way to probe the biological roots of a defining symptom of psychosis: hallucinations. The researchers trained people and mice to complete a computer-based task that induced them to hear imaginary sounds. By analyzing performance of the task, the researchers were able to objectively measure hallucination-like events in people and mice.
This approach allowed them to study the neural circuits underlying hallucinations, potentially fully opening up the study of mental illness to the kind of scientific studies that have been fruitful for diseases of other parts of the body. My concern is that despite the positives and even if there are similarities, can a study like this be of great value when it comes to humans who has a fundamentally different cognitive ability and brain structure? I agree that we can see tendencies and the study gives an insight, however can this ever fully be transferred to humans? also see other risks as well as grave ethical concerns that applies with all experiments on animals. What are your thoughts?
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.
I performed a moderation test and I found a significant moderation effect. The post hoc tests showed that both +1SD and -1SD lines are significant. How can I interpret this? Is it correct to assume that any levels of the moderator can increase (in my case) the relationship between x and z? Can I assume a moderating effect for the variable that was entered as a moderator?
I have been diagnosed and medicated over twenty years with a psychiatric condition that medication works well for me.
I was on 100 mg of Seroquel for a long time with no problems, then had to be hospitalized. The Dr. told me it wasn't a therapeutic dose, even though it had been working just fine for years. He raised my dose to 300 mg. When I went home I felt like I would die every time I went to sleep went back to the hospital then the same Dr. gave me Geodon, which did not even work at all and then I was threatened if I did not take an injection to go to court. They messed my medication up, not me.
I understand the holistic approach, but requiring services the client does not want, does not benefit the client in any way other than someone to talk to. I don't think Social Workers should be making diagnostic decisions anyway. It is a waste of time and money and Paternalistic.
I have not found many studies about this treatment. It has been approved by FDA based on very preliminary evidence. How much time does FDA take in general to approve a treatment in mental health field?
I just came across a really interesting point of view in a clinical manual by a leading author in clinical treatment in Spain, Miguel Ángel Vallejo. He claims, based on a study by Rude and Rehm (1991)*, that psychotherapy is most effective when it boosts already-existing capacities and skills, rather than when it focuses on ameliorating deficits. That seems to run counter to much of what I have seen before in psychotherapy; does this idea match your clinical experience, or do you have any additional bibliography that might support this claim Thanks a lot!
*The citation to this article is given as "Rude, S. S., & Rehm, L. P. (1990). Cognitive and behavioral predictors of response to treatments for depression. Clinical Psychology Review, 11, 493–514"; however, all I can find online is this other article, with a different name, although (apparently) similar content: https://psycnet.apa.org/record/1992-06180-001
The symptoms described by Freud were : episodic episodes of "psychosomatic" dyspnea, cough, afonia (without a medical explanation and then " conversion" symptoms ) but also : depression, " hysterical "
social withdrawal, and "taedium vitae" ( i.e. for the modern " emptiness" ? )
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 ?
Cycloserine is an antibiotic used to treat tuberculosis. It has several side-effects, including irritability and anxiety. It is an analogue of D-alanine. It has been used as an anti-depressant, based on its effect on NMDA receptors.
I am being asked to provide psychiatric support to a patient who is facing 8 months of treatment with cycloserine, and wonder if someone has experience of psychopharmacological interventions that might reduce the negative effects of the cycloserine?
As part of our investigations into the current state of psychiatry, I would like to ask how academics and practitioners, researchers and clinicians, and of course professors of psychiatry, see contemporary psychiatry and its future. My colleague Drozdstoj Stoyanov, MD, PhD, and I are writing a book called "Psychiatry in Crisis" (see Research Project on "Psychiatry in Crisis") in which we pose and will try to answer the following question:
Is psychiatry a social science (like psychology or anthropology), is it better understood as part of the humanities (like philosophy, history and linguistics), or is the future of psychiatry best assured as a branch of medicine (privileging genetics and neuroscience)?
This is on APA Psychnet for purchase. However, I don't think it is the actual questionnaire. Any help appreciated. Thanks.
Salovey, P., Mayer, J. D., Goldman, S. L., Turvey, C., & Palfai, T. P. (1995). Emotional attention, clarity, and repair: Exploring emotional intelligence using the Trait Meta-Mood Scale. In J. W. Pennebaker (Ed.), Emotion, disclosure, & health (pp. 125-154).
Is it in the best interest of the patients , not to highlight certain side effects of medications or procedures which might have a Nocebo response?
For example: Do we highlight to a man that beta blockers can cause impotence before starting beta-blocker??.
More patients are having negative responses to various medical interventions when they are told more than they should know about the treatment.
Are we here to in this profession to help patients benefit from the treatment modalities or are we here to do the job and safeguard our self without having to worry about what happens to the patient?
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.
Must we change their anti-epileptic treatment before ECT ?
Any risk of dangerous sides effects like status epilepticus ?
Must we adapt the protocole of ECT ?
Have you clinical experience about that or any evidence based ?
You wrote in the abstract of your article (Overreactivity of the psyche or the soma? Interindividual associations between psychosomatic symptoms, anxiety, heart rate, and end-tidal partial carbon dioxide pressure. Psychosomatic Medicine 56(6):533-40.) “The findings suggest that reports of psychosomatic symptoms represent two distinct components: one that is primarily psychological (and is unrelated to physiological factors) and a second that reflects objective variance in physiological functioning. The influence of the first component is probably greater than that of the second.”
My answer: We can prove that physiological events (after chronic hyperventilation) are the causes of the psychosomatic symptoms and psychological factors are only their consequences.
We discussed the topic: how we think that chronic hyperventilation (and its metabolic compensation) can cause "physiological panic attack," which may be intensified by the fear of attacks. (A quotation from Sikter A, Faludi G, Rihmer Z.: The role of carbon dioxide (and intracellular pH) in the pathomechanism of several mental disorders. Are the diseases of civilization caused by learnt behaviour, not the stress itself? Neuropsychopharmacol Hung. 2009;11:161-73.)
“We made an attempt to integrate the three main theories (Sikter et al., 2007b. See attached the full text article: Sikter A et al.: The role of hyperventilation: hypocapnia in the pathomechanism of panic disorder. Rev Bras Psiquiatr. 2007; 29:375-9.) about the relationship between hyperventilation and panic disorder, even though according to Wilhelm et al. (2001a), these theories would include antagonistic contradictions. The three statements are: A/ hyperventilation is a protective/preventive mechanism against panic attacks; B/ it is a physiological response to hypercapnia; C/ it can induce panic attacks. We think that panic attack is a cascade of events where hyperventilation has different roles in different times. Chronic hyperventilation is probably a precondition of (respiratory subtype) panic attack, although it defends against panic. While it exsists, spontaneous panic attacks cannot arise (see statement A). Chronic hyperventilation can be generated by either organic diseases (e.g. asthma bronchiale) or mental conditions (e.g. sighing or crying for a tragedy). Compensational mechanisms set off metabolic acidosis that neurtralizes hyperventilational alkalosis, this compensational process lasts at least for a week. In the state of compensated hypocapnic alkalosis extra- and intracellular pH stays in the normal range. The depressed pCO2 level starts to go up to the normal level (or slightly higher) before the attack. The elevating carbon dioxide promptly diffuses into cells and causes acidosis, which increases catecholamine release from different cells (e.g. noradrenaline release from locus coeruleus) (Filosa et al.). On the other hand, elevating carbon dioxide level also evokes acute hyperventilation (through a brainstem reflex), which may be more vigorous than previously. (see statement B). At this point hypercatecholaminemia (induced by previous acidosis) and alkalosis (abruptly decreasing pCO level) evolve at the same time. Alkalosis multiplies CNS-responsiveness to catecholamine levels, and it lasts for several minutes to break down catecholemines. This coexistence means an intense sympathicotonia, a very high arousal. (The cascade of events is similar to Steen’s animal model – a hypercapnic period is followed by a hypocapnic one) (Steen et al.). High catecholamine level/sympathicotonia can provoke panic attacks (Cameron et al.). Panic attack is precipitated by this second (acute) hypocapnia (see statement C) plus catecholaminemia induced by previous acidosis. We have illustrated panic attack on a theoretical diagram. According to this panic theory intra- and extracellular pH is thoroughly compensated before the attack, but the acidosis would be overcompensated by acute hypocapnic alkalosis during the attack. The main problem is that the different compensational mechanisms work out at different rates. Carbon dioxide level can change in the whole organism in a few seconds, the elimination of catecholamines lasts for several minutes, and the clearing of blood from metabolic (“titratable”) acidity takes at least one week. This is one of the many reasons there is no perfect compensational mechanism.”
Physiological events of the respiratory type of panic attack (a hypothetical model) See the attached figure (jpg)
· Period A/ Chronic hypocapnic alkalosis is compensated by chronic metabolic acidosis (pH is in the normal range). The arousal is normal.
· Period B/ The pCO2 level starts to normalize (is elevating): intracellular acidosis arises, catecholamine output increases. The arousal is normal or decreased.
· Period C/ The pCO2 level reflexively decreases, the responsibility of neurons to the catecholamine levels increases AND the catecholamine level is still high – a panic attack can arise
· Period D/ Feeling and fearing of somatic sensation elevates catecholamine level and decreases pCO2 level
The periods A/, B/, and C/ are single physiologic events. Only the period D/ is a psychic phenomenon. Without chronic hypocapnia, there is no respiratory panic attack. If the breathing results in eucapnia and it is regular, there are no hyperarousal, anxiety, and somatic sensations (e.g. GAD)- or they exist only on a minimal level.
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?
Seems that they have higher nocebo effect. Did you know researchs about most frequent nocebo signe and symptoms in panic disorder?
In a very disturbing outcome last week, a young woman was found unconscious in her car on Staten Island in New York City. The responding police took her to the nearest ED (SIU Hospital) where the treating physician correctly diagnosed opioid overdose, and administered naloxone. The pt became conscious, and was discharged into police custody 6 hours after receiving IM naloxone and showing "healthy" vitals. She was incarcerated and died a few hours later in jail of an opioid overdose. My initial reaction was that 6 hours is not enough time to be certain that an opioid OD pt is stable and ready for discharge, but after reviewing the scant literature on the subject, I found articles like the one attached (NEJM) stating just that - administer naloxone, wait six hours, if oxygen sats and HR and BP are fine, then discharge. Of course, this presumes many things, predominantly that the pt has ODed on a short-half life opioid like diacetylmorphine (Heroin) and not a long-half-like one like methadone (which could explain the tragic consequences of last week). Conceivably, a pt could OD on a long-half-life opioid, be revived by naloxone, and then die of respiratory depression as bioavailability returned. Does anyone know of any newer (DOI: 10.1056/NEJMra1202561) and more nuanced protocols for the treatment of opioid ODs in the ED?
We have found within our community specialist PD team there are a small number of service users who present with exceptionally high risk clinical problems, complexity and comorbidity that they cannot be safely contained and supported in community settings. Their needs are complex, and often require more intensive and in-depth assessment, reformulation and stabilisation work which cannot be safely done within a community setting or whilst on an acute inpatient ward. Such service users, when in the stage of severe chaos, self-harm or suicidality may find an acute ward too stressful and over stimulating for them, which can lead to their attempts at coping to get worse, rather than better. The tendency to regress and lose skills and abilities whilst in an acute hospital setting has been well known clinically (e.g. Paris, 2004; Bateman and Krawitz, 2013).
Current research evidence and guidance on the use of hospital admission is mostly based on expert opinion and a little empirical research. Expert opinion and guidance suggest that admissions should be avoided as far as possible, but where needed, they should be used for acute crisis management rather than chronic risks and be as brief as possible (NICE, 2009; Paris, 2004; Krawitz and Watson, 2008; Fagin, 2004). There is some evidence that brief planned admissions are no more harmful than standard treatments (Van Kessel et al, 2002).
We are considering the development of a specialist unit where these focussed admissions may occur safely in order to stabilise service users so they are more abel to engage in evidence-based treatments in community settings.
I am looking for research that supports (or refutes) the effectiveness of inpatient psychiatric hospitalization.
Hi, our research team wants to do a pilot-study on psilocybin. Does anyone have any idea on how we can buy this substance? Can anyone help us on international laws on doing these kind of research in Iran?
Previous published researches on psylocibin haven't mentioned how they provided this substance. unfortunately we don't have necessary facilities to synthesis pcylocibin on our own.
thank you in advance.
I am looking for a scale to assess fatigue ("Müdigkeitssyndrom") in German. For example, a validated German version of the "Fatigue Assessment Instrument" (FAI) or the Chalder Fatigue Scale (CFL). We would like to assess fatigue in Hep C patients.
I am trying to find a validated Falls assessment tool for our psychiatric patient population. The Johns Hopkins tool we currently use places all of our patients on falls due to medications that place them at risk. I would like to use the Wilson-Sims Falls Risk Assessment tool. Does anyone use this tool? It appears to be validated in the literature. I'm trying to find out if it is free to use?
Recently I learned of the potent CYP1A2 induction effects of proton-pump inhibitors (ie. omeprazole etc). These medications can significantly reduce olanzapine and clozapine concentrations. Which medications are we overlooking when it comes to CYP1A2 induction?
Papakostas et al showed adjunctive LMF to be effective in treatment of mdd in 2012 with a NNT of 6 patients. The 2014 follow up article in J Clin Psych by Papakostas et al assessed biomarkers of LMF responders showing no statistically significant difference in HDRS-28 scores between MTHFR 677 CC (wild type) and MTHFR 677 TT (varient, reduced activity) patients.
Reduced or inactive MTHFR activity is not specific to depressive disorders.
Where does this leave us when depressed patients present with reduced or inactive MTHFR? I am thinking it should not lead towards LMF supplementation.
Just as uncertain that I am about the interest of this perspective in the scientific World I am just as convinced about it gains if conducted.
Upon moving to become Professor of Clinical Psychiatry at the University of Munich in 1903, Kraepelin increasingly wrote on social policy issues. He was a strong and influential proponent of eugenics and racial hygiene. His publications included a focus on alcoholism, crime, degeneration and hysteria. Kraepelin was convinced that such institutions as the education system and the welfare state, because of their trend to break the processes of natural selection, undermined the Germans’ biological "struggle for survival". He was concerned to preserve and enhance the German people, the Volk, in the sense of nation or race. He appears to have held Lamarckian concepts of evolution, such that cultural deterioration could be inherited. He was a strong ally and promoter of the work of fellow psychiatrist (and pupil and later successor as director of the clinic) Ernst Rudin to clarify the mechanisms of genetic inheritance as to make a so-called "empirical genetic prognosis".
Martin Brune has pointed out that Kraepelin and Rudin also appear to have been ardent advocates of a self-domestication theory, a version of social Darwinism which held that modern culture was not allowing people to be weeded out, resulting in more mental disorder and deterioration of the gene pool. Kraepelin saw a number of "symptoms" of this, such as "weakening of viability and resistance, decreasing fertility, proletarianisation, and moral damage due to "penning up people" [Zusammenpferchung]. He also wrote that "the number of idiots, epileptics, psychopaths, criminals, prostitutes, and tramps who descend from alcoholic and syphilitic parents, and who transfer their inferiority to their offspring, is incalculable". He felt that "the well-known example of the Jews, with their strong disposition towards nervous and mental disorders, teaches us that their extraordinarily advanced domestication may eventually imprint clear marks on the race". Brune states that Kraepelin's nosological system was "to a great deal, built on the degeneration paradigm".
I am aware there has not been much research on this subjects despite the Psychologist delivered reflective practice 's popularity within in-patient mental health services. Sometimes both services and staff feel drained when they have challenging patients within their care in-light of the need for care delivery to be in the best interest of the patient.
I am researching the impact on health professionals when a client commits suicide with a view to composing a hospital Trust policy and implementing improved organisational pathways and structures to ensure support for those affected.
I would welcome advice from anyone who has been involved in implementing robust support for professionals in these circumstances and/or composing organisational pathways and policies in this regard.
Is there a validated german translation of the "vestibular disorder activities of daily living scale" (VADL)? Thank you
a few days ago I talked to an occupational therapist about respiratory rates and patterns in children with ADHD. From her experience she is quite sure that children with ADHD usually show abnormal breathing patterns, which does make sense, but I can’t seem to find any reliable studies on it. There are lots of studies on the connection of ADHD and sleep apnea, but none on abnormal breathing in the state of being awake.
Does anyone of you know a study of that kind?
Thank you in advance and have a great day.
articles and books relevant to fear in psychiatric patients, especially if there is evidence that compares psychiatric patients and mentally healthy people about the feeling of fear.
I have been using techniques used in abreaction using IV diazepam to feed my patients with mental illnesses who present with food refusal for days. It has always produced instant feeding. I am of the opinion that it is a life-saving procedure. I have always wanted to produce a manual for it and try it in medical conditions as well. I need any recent developments in this abreaction procedure.
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?
In this study I have always been perceived that AIP was the main findings, however when looking at the results again I am not sure if there is an error in the findings or I have been blinded (most likely the latter) to think that AIP has been the main finding of this study but in actual fact PCTis, where his main finding as far as the results of the urine tests. In his results he states that 4 were positive PBG and 270 positive porphyrins, his final conclusion was that his study found 7 with AIP and 4 with PCT. I hope this makes sense. I am using this study in my thesis. I have enclosed a copy of the article. Thanks Karen
I am working with South Australian law but am interested in international law. Who are the carers?. What support do they receive? Have used deontological and utilitarian ethics, where does ethic of care come in? How can the needs of the patient be balanced with the needs of carers, families and communities? Stereotyping of the patients and their needs is a problem.
In last decade this is very important question and this issue should be discussed within each country, unfortunately only some countries have conducted this trials (U.K., U.S.). In many countries there are still no data on this topic. According to the some data available in the literature, patients with mental disorders are very often overtreated and especially antipsychotic polypharmacy is used in 1/3 cases without any evidence to support its use. In many cases appropriate treatment strategy with the use of advanced psychopharmacology and outcomes from the clinical trials can avoid the polypharmacy.
A patient came to my practice for ongoing and worsening anxiety attacks. No usual interventions were effective. Symptoms led back to time of Lasik surgery. Although he had 20/20 visual acuity, with haloes and starbursts, there was no relevant feedback about the post operative course. I am familiar with the condition in children and teenagers, but not with these moderating factors. It seems that vision therapy is indicated, but I'm wondering about correlational research with the three conditions.
Is there any evidence or personal clinical experience regarding the efficacy of antidepressants for depressive disorder and anxiety disorder in patients with carbon monoxide intoxication?
When a patient has previous history of depressive disorder and generalized anxiety disorder and later attempted suicide with subsequent carbon monoxide intoxication, is there any literature discussing the efficacy of antidepressants before or after the intoxication? Would the original antidepressant before the intoxication still be the best choice?
Would CO intoxication-induded Parkinsonism of the patient influence the choice of antidepressant?
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.
In your opinion, What are the five (5) most effective anti depression drugs with their generic and brand names having minimum adverse affects?
Has anyone ever seen a finding where people with schizophrenia perform more abnormally (on a cognitive or perceptual task) when stabilizing, compared to when they are acutely psychotic? I just completed a study where it looks like patients perform normally at hospital admission, abnormally at hospital discharge, and then normally again several months later. This doesn't seem to be an artifact (and it is replicated across multiple task conditions) but I have never seen a result like this before. The task is a visual perception task that involves integration of information and then an illusion effect. Any suggestions will be greatly appreciated! Thanks, Steve
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?
I'm working on a paper about reliability of subjective clinical prognosis (but evaluated with different tools than CGI) in patients with first episode schizophrenia, but I don't find any references. Moreover I can't neither find data about the reliability of subjective clinical prognosis in general in psychiatry. Any help would be more than welcomed!
Many thanks, Vali.
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 ...
Psychiatric patients usually take many different medications and often they have been already treated with beta-blockers. However, there are several cases in where You should add beta-blockers, because of newly recognized heart failure or even atrial fibrillation. Often psychiatric patients take medications, which included antipsychotics or even worse an antipsychotic polypharmacy or combinations with antidepressants. According to the survival studies We know that treatment with beta-blockers in patients with stable heart failure (EF less than 35 %) is necessary for better surviving.
The third group of cases consists the consequences of psychotropic medications adverse events (e. g. arrhythmias and clozapine or olanzapine) or prolonged QTc and supraventricular arrhythmias (e. g. amisulpride with clozapine combination or ziprasidone use and escitalopram together). In these cases a trial with beta blockers is usually a first step before drug discontinuation.
From EBM we know that combination of clozapine and amisulpride is benefitial in short term trials, however long term use should lead to several complications in this field.
To sum up, DDIs with psychotropics and beta-blockers should be calculated before prescribing beta-blockers. For example, atenolol is not appropriate with several antipsychotics and antidepressants (QTc prolongation). Also story with metoprolol is more or less the same, however metoprolol is very selective for B1 receptors, however there are cases of induced delirium with propranolol. Smart use included pindolol, especially in patients on antidepressants, because of add on efficacy, however we do not have long term trials. At the end I think cooperation between clinical pharmacist and psychiatrist and cardiologist is the best approach to deal with these patients.
Nitrofurantoin (NF)-induced adverse effects have been reported frequently, although NF seems to be a first line treatment for lower urinary infections according to the last E.U. and U.S. guidelines. However its use in psychiatric patients should be reviewed with a great caution. In these cases the use of penicillin is therefore sometimes more appropriate, although the total antibiotic consumption rises. Because of NF use, a dose adjustment because of its adverse events (hallucinations) is also possible and cooperation with clinical pharmacist is beneficial in these cases. What do you think?
Antipsychotic polypharmacy refers to the co-prescription of more than one antipsychotic drug for an individual patient. According to the many studies consumption of clozapine in patients with chronic schizophrenia is still low (about 25 %) and antipsychotic polypharmacy prevalence before clozapine use is very high, although the evidence usually does not support its use. How to manage patients with chronic schizophrenia with higher clozapine consumption?
It looks to me that the relationship between anxiety and dementia is much less strong than the one between depressive symptoms and dementia. And that anxiety could be confounded by depression (and vice-versa?).
Please, which are the most commonly used clinical cut-offs for considering depression in the following depression scales?
GDS- 15 items version
HADS- 7 items version (Depression sub-scale)
MDRS- 10 items version
thanks so much
I'm trying to understand if psuchiatric satisfaction scale for inpatient are commonly and routinely used in the acute psichiatric unit.
I have read studies that discuss mood and color in psychiatric settings, but often the study is of a person and the color which does not take into account the many other variables experienced by someone in the emergency department. There are studies of other rooms, such as used during therapy or in the general milieu.
I'm looking specifically for door color since our rooms are and will always be laboratory white. I'm thinking that a great study would be to have at least two rooms with different colored doors and see which one the person (in acute psychiatric distress) chooses indicating a perception of safety.
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.
In addition to environmental intervention, behavioral management, carer skills adjustments, what would be an effective medication for hypersexuality or inappropriate sexual behaviors in elderly patients with neurocognitive disorders?
Some research on the topic:
Inappropriate sexual behaviors in cognitively impaired older individuals. Am J Geriatr Pharmacother. 2008 Dec;6(5):269-88.
Hypersexual behavior in frontotemporal dementia: a comparison with early-onset Alzheimer's disease. Arch Sex Behav. 2013 Apr;42(3):501-9.
Rivastigmine in the treatment of hypersexuality in Alzheimer disease. Alzheimer Dis Assoc Disord. 2013 Jul-Sep;27(3):287-8.
Different classes of medication have been suggested to be effective, such as TCAs, SSRIs, antipsychotics, estrogens, anti-androgens, and LHRH agonists, etc. However, currently there is lack of consensus as to what would be the most effective pharmacotherapy. And there would be substantial individual differences between different patients. If anyone has the experience of treating hypersexuality or inappropriate sexual behavior, could you share the clinical experience and make some comments on its pharmacotherapy? Are there differences in terms of pharmacotherapy when treating male or female patients with hypersexuality?
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?
would someone like to share some articles about it?
- about the effectiveness of antidepressant (both prove and reject)
- about the side-effects of antidepressant
- qualitative research of the patient after taking antidepressant
- others articles you think is related to the question