What is Treatment-Resistant Depression?

Introduction

Treatment-resistant depression (TRD) is a term used in clinical psychiatry to describe a condition that affects people with major depressive disorder (MDD) who do not respond adequately to a course of appropriate antidepressant medication within a certain time.

Typical definitions of TRD vary, and they do not include a resistance to psychological therapies. Inadequate response has traditionally been defined as no clinical response whatsoever (e.g. no improvement in depressive symptoms). However, many clinicians consider a response inadequate if the person does not achieve full remission of symptoms. People with treatment-resistant depression who do not adequately respond to antidepressant treatment are sometimes referred to as pseudoresistant. Some factors that contribute to inadequate treatment are: early discontinuation of treatment, insufficient dosage of medication, patient noncompliance, misdiagnosis, and concurrent psychiatric disorders. Cases of treatment-resistant depression may also be referred to by which medications people with TRD are resistant to (e.g.: SSRI-resistant). In TRD adding further treatments such as psychotherapy, lithium, or aripiprazole is weakly supported as of 2019.

Refer to Atypical Depression and Masked Depression.

Risk Factors

Comorbid Psychiatric Disorders

Comorbid psychiatric disorders commonly go undetected in the treatment of depression. If left untreated, the symptoms of these disorders can interfere with both evaluation and treatment. Anxiety disorders are one of the most common disorder types associated with treatment-resistant depression. The two disorders commonly co-exist, and have some similar symptoms. Some studies have shown that patients with both MDD and panic disorder are the most likely to be nonresponsive to treatment. Substance abuse may also be a predictor of treatment-resistant depression. It may cause depressed patients to be noncompliant in their treatment, and the effects of certain substances can worsen the effects of depression. Other psychiatric disorders that may predict treatment-resistant depression include attention deficit hyperactivity disorder, personality disorders, obsessive compulsive disorder, and eating disorders.

Comorbid Medical Disorders

Some people who are diagnosed with treatment-resistant depression may have an underlying undiagnosed health condition that is causing or contributing to their depression. Endocrine disorders like hypothyroidism, Cushing’s disease, and Addison’s disease are among the most commonly identified as contributing to depression. Others include diabetes, coronary artery disease, cancer, HIV, and Parkinson’s disease. Another factor is that medications used to treat comorbid medical disorders may lessen the effectiveness of antidepressants or cause depression symptoms.

Features of Depression

People with depression who also display psychotic symptoms such as delusions or hallucinations are more likely to be treatment resistant. Another depressive feature that has been associated with poor response to treatment is longer duration of depressive episodes. Finally, people with more severe depression and those who are suicidal are more likely to be nonresponsive to antidepressant treatment.

Treatment

There are three basic categories of drug treatment that can be used when a medication course is found to be ineffective. One option is to switch the patient to a different medication. Another option is to add a medication to the patient’s current treatment. This can include combination therapy: the combination of two different types of antidepressants, or augmentation therapy: the addition of a non-antidepressant medication that may increase the effectiveness of the antidepressant.

Medication

Antidepressants

Dose Increase

Increasing the dosage of an antidepressant is a common strategy to treat depression that does not respond after adequate treatment duration. Practitioners who use this strategy will usually increase the dose until the person reports intolerable side effects, symptoms are eliminated, or the dose is increased to the limit of what is considered safe.

Switching Antidepressants

Studies have shown a wide variability in the effectiveness of switching antidepressants, with anywhere from 25-70% of people responding to a different antidepressant. There is support for the effectiveness of switching people to a different SSRI; 50% of people that were non-responsive after taking one SSRI were responsive after taking a second type. Switching people with TRD to a different class of antidepressants may also be effective. People who are non-responsive after taking an SSRI may respond to moclobemide or tricyclic antidepressant, bupropion or an MAOI.

However, the more antidepressants an individual had already tried, the less likely they were to benefit from a new antidepressant trial.

Some off label antidepressants are low dose ketamine and highly serotonergic catecholamines (including very controlled use of MDMA in the treatment of PTSD and crippling depression/anxiety). For lethargic syndromes, dysthymia, or caffeine-resistant amotivation, a dopaminergic stimulant such as methlyphenidate, or even 2.5 mg dextroamphetamine can be helpful.

Primarily dopaminergic or norepinephrine releasing stimulants, in low doses, have been used especially in the past, or in conjunction with a multidisciplinary therapy approach, although more targeted and “mild” agents, including modafinil and atomoxetine are considered first line for both childhood and adult lethargy and inattention disorders, due to their virtually non-existent abuse potential (limited to one or two cases per 10,000), and higher selectivity, safety, and thus slightly broader therapeutic index. When depression is related or co-morbid to an inattention disorder, often ADHD, then both can be carefully managed with the same first line stimulant medication, typically both methylphenidate and lisdexamphetamine.

Other Medications

Medications that have been shown to be effective in people with treatment-resistant depression include lithium, triiodothyronine, benzodiazepines, atypical antipsychotics, and stimulants. Adding lithium may be effective for people taking some types of antidepressants; it does not appear to be effective in patients taking SSRIs. Triiodothyroxine (T3) is a type of thyroid hormone and has been associated with improvement in mood and depression symptoms. Benzodiazepines may improve treatment-resistant depression by decreasing the adverse side effects caused by some antidepressants and therefore increasing patient compliance. Since the entry of olanzapine into psychopharmacology, anecdotal evidence suggests that many psychiatrists have been adding low dose olanzapine to antidepressants and other atypical antipsychotics such as aripiprazole and quetiapine. Eli Lilly, the company that sells both olanzapine and fluoxetine individually, has also released a combination formulation which contains olanzapine and fluoxetine in a single capsule. Some low to moderate quality evidence points to success in the short term (8-12 weeks) using mianserin (or antipsychotics cariprazine, olanzapine, quetiapine or ziprasidone) to augment antidepressant medications.

These have shown promise in treating refractory depression but come with serious side effects. Stimulants such as amphetamines and methylphenidate have also been tested with positive results but have potential for abuse. However, stimulants have been shown to be effective for the unyielding depressed combined lacking addictive personality traits or heart problems.

Ketamine has been tested as a rapid-acting antidepressant for treatment-resistant depression in bipolar disorder, and major depressive disorder.

Research

A 2016 placebo randomised controlled trial (RCT) evaluated the rapid antidepressant effects of the psychedelic ayahuasca in treatment-resistant depression with positive outcome.

Physical Psychiatric Treatments

Electroconvulsive Therapy

Electroconvulsive therapy is generally only considered as a treatment option in severe cases of treatment-resistant depression. It is used when medication has repeatedly failed to improve symptoms, and usually when the patient’s symptoms are so severe that they have been hospitalised. Electroconvulsive therapy has been found to reduce thoughts of suicide and relieve depressive symptoms. It is associated with an increase in glial cell line derived neurotrophic factor.

rTMS

rTMS (repetitive transcranial magnetic stimulation) is gradually becoming recognised as a valuable therapeutic option in treatment-resistant depression. A number of randomised placebo-controlled trials have compared real versus sham rTMS. These trials have consistently demonstrated the efficacy of this treatment against major depression. There have also been a number of meta-analyses of RCTs confirming the efficacy of rTMS in treatment-resistant major depression, as well as naturalistic studies showing its effectiveness in “real world” clinical settings.

dTMS

dTMS (deep transcranial magnetic stimulation) is a continuation of the same idea as rTMS, but with the hope that deeper stimulation of subcortical areas of the brain leads to increased effect. A 2015 systematic review and health technology assessment found lacking evidence in order to recommend the method over either ECT or rTMS because so few studies had been published.

Psychotherapy

There is sparse evidence on the effectiveness of psychotherapy in cases of treatment-resistant depression. However, a review of the literature suggests that it may be an effective treatment option. Psychotherapy may be effective in people with TRD because it can help relieve stress that may contribute to depressive symptoms.

A Cochrane systematic review has shown that psychological therapies (including cognitive behavioural therapy, dialectal behavioural therapy, interpersonal therapy and intensive short-term dynamic psychotherapy) added to usual care (with antidepressants) can be beneficial for depressive symptoms and for response and remission rates over the short term (up to six months) for patients with TRD. Medium‐ (7-12 months) and long‐term (longer than 12 months) effects seem similarly beneficial. Psychological therapies added to usual care (antidepressants) seem as acceptable as usual care alone.

Outcomes

Treatment-resistant depression is associated with more instances of relapse than depression that is responsive to treatment. One study showed that as many as 80% of people with TRD who needed more than one course of treatment relapsed within a year. Treatment-resistant depression has also been associated with lower long-term quality of life.

Another study saw just 8 of 124 patients in remission after two years of regular treatment with therapy and medicines.

Epidemiology

Treatment-resistance is relatively common in people with MDD. Rates of total remission following antidepressant treatment are only 50.4%. In cases of depression treated by a primary care physician, 32% of people partially responded to treatment and 45% did not respond at all.

What is Masked Depression?

Introduction

Masked depression (MD) was a proposed form of atypical depression in which somatic symptoms or behavioural disturbances dominate the clinical picture and disguise the underlying affective disorder.

The concept (as of March 2021) is not currently supported by the mental health profession.

Refer to Atypical Depression and Treatment-Resistant Depression.

Clinical Manifestations

Somatic manifestations of MD are distinguished by an extreme diversity and include headaches, back pain, abdominal pain etc. Pathological behaviour masking depression may take the form of compulsive gambling, compulsive work, changes in arousal or orgasmic function, decreased libido or, on the contrary, impulsive sexual behaviour, alcoholism, or drug addiction.

Dispute about the Concept

MD has been variously described as “depression sine (without) depression” (K. Schneider, 1925), “latent” depression (Lange J., 1928), “vegetative depression” (R. Lemke, 1949) “hidden” or “masked” depression (Lopez Ibor J.J. [es], 1972; Kielholz J.J., 1983; Pichot P.; Hasson J., 1973), “larvate” or “somatisation depression” (Gayral L., 1972), “depressive equivalents” etc. Most investigators, especially those in the German-speaking countries, assumed masked depression (German: die larvierte Depression) to be endogenous depression. The term was largely used in the 1970s and 1980s, but at the end of the 20th century there was a decline in interest in the study of masked depression. Today this diagnosis does not play a significant clinical or scientific role.

Epidemiology

MD is supposed to be a common clinical phenomenon. According to some authors, masked depression is as frequent as overt depression. Although masked depression can be found at any age, it has been observed more commonly after mid-life.

Making the diagnosis and the management of MD in clinical practice are complicated by the fact that the individual who has MD is unaware of their mental illness. Patients with MD are reluctant to associate their physical symptoms with an affective disorder and refuse mental health care. As a rule, these patients attribute their disturbances to physical illness, seek medical care for them, and report only somatic complaints to their medical professional, with the consequence that many of such depressions are not recognised or are misdiagnosed and mistreated Estimates of depressed patients who are correctly identified and treated range from 5% to 60%. Recent data show that about 10% of people who consult a medical professional for any reason originally suffer from affective disorders disguised by physical symptoms.

Official Diagnostic Status

Current classifications: ICD-10 and DSM-5 do not contain the term “masked depression”.

Some Ukrainian psychiatrists claim that MD is to be qualified as “depression with somatic symptoms” (F 3x.01), according to ICD-10. This means that those who struggle with masked depression often have more physical symptoms such as back pain, abdominal pain, headaches, and even pain during sexual activity or painful periods.

For those with more clinical depression, while they still may have physical symptoms, their symptoms are usually more mental or emotional. This includes feelings of helplessness, extreme and/or persisting sadness, numbness, tiredness, drowsiness, exhaustion, and even suicidal thoughts or feelings.

Diagnostic Criteria

Affective disorders in patients with MD can only be detected by means of a clinician-administered diagnostic interview. Organic exclusion rules and other criteria are used in making the diagnosis of MD. Some physical symptoms of masked depression include general aches, pains including headache, backache, musculoskeletal aches, and other nonpainful symptoms such as changes in appetite and libido, lack of energy, sleep disturbance, dizziness, palpitations, dyspnoea, and gastrointestinal tract disturbances.

What is Atypical Depression?

Introduction

Atypical depression as it has been known in the DSM IV, is depression that shares many of the typical symptoms of the psychiatric syndromes of major depression or dysthymia but is characterised by improved mood in response to positive events.

In contrast to atypical depression, people with melancholic depression generally do not experience an improved mood in response to normally pleasurable events. Atypical depression also features significant weight gain or an increased appetite, hypersomnia, a heavy sensation in the limbs, and interpersonal rejection sensitivity that results in significant social or occupational impairment.

Despite its name, “atypical” depression does not mean it is uncommon or unusual. The reason for its name is twofold: it was identified with its “unique” symptoms subsequent to the identification of melancholic depression and its responses to the two different classes of antidepressants that were available at the time were different from melancholic depression (i.e. monoamine oxidase inhibitors (MAOIs) had clinically significant benefits for atypical depression, while tricyclics did not).

Atypical depression is four times more common in females than in males. Individuals with atypical features tend to report an earlier age of onset (e.g. while in high school) of their depressive episodes, which also tend to be more chronic and only have partial remission between episodes. Younger individuals may be more likely to have atypical features, whereas older individuals may more often have episodes with melancholic features. Atypical depression has high comorbidity of anxiety disorders, carries more risk of suicidal behaviour, and has distinct personality psychopathology and biological traits.

Atypical depression is more common in individuals with bipolar I, bipolar II, cyclothymia and seasonal affective disorder. Depressive episodes in bipolar disorder tend to have atypical features, as does depression with seasonal patterns.

Refer to Masked Depression and Treatment-Resistant Depression.

Pathophysiology

Significant overlap between atypical and other forms of depression have been observed, though studies suggest there are differentiating factors within the various pathophysiological models of depression. In the endocrine model, evidence suggests the HPA axis is hyperactive in melancholic depression, and hypoactive in atypical depression. Atypical depression can be differentiated from melancholic depression via verbal fluency tests and psychomotor speed tests. Although both show impairment in several areas such as visuospatial memory and verbal fluency, melancholic patients tend to show more impairment than atypical depressed patients.

Furthermore, regarding the inflammatory theory of depression, inflammatory blood markers (cytokines) appear to be more elevated in atypical depression when compared to non-atypical depression.

Diagnosis

The diagnosis of atypical depression is based on the criteria stated in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). The DSM-5 defines atypical depression as a subtype of major depressive disorder that presents with “atypical features”, characterised by:

  • Mood reactivity (i.e., mood brightens in response to actual or potential positive events)
  • At least two of the following:
    • Significant weight gain or increase in appetite (hyperphagia);
    • Hypersomnia (sleeping too much, as opposed to the insomnia present in melancholic depression);
    • Leaden paralysis (i.e., heavy feeling resulting in difficulty moving the arms or legs);
    • Long-standing pattern of interpersonal rejection sensitivity (not limited to episodes of mood disturbance) that results in significant social or occupational impairment.

Criteria are not met for With Melancholic Features or With Catatonic Features during the same episode.

Treatment

Due to the differences in clinical presentation between atypical depression and melancholic depression, studies were conducted in the 1980s and 1990s to assess the therapeutic responsiveness of the available antidepressant pharmacotherapy in this subset of patients. Currently, antidepressants such as SSRIs, SNRIs, NRIs, and mirtazapine are considered the best medications to treat atypical depression due to efficacy and fewer side effects than previous treatments. Bupropion, a norepinephrine reuptake inhibitor, may be uniquely suited to treat the atypical depression symptoms of lethargy and increased appetite in adults. Modafinil is sometimes used successfully as an off-label treatment option.

Before the year 2000, monoamine oxidase inhibitors (MAOIs) were shown to be of superior efficacy compared to other antidepressants for the treatment of atypical depression, and were used as first-line treatment for this clinical presentation. This class of medication fell in popularity with the advent of the aforementioned selective agents, due to concerns of interaction with tyramine-rich foods (such as some aged cheese, certain types of wine, tap beer and fava beans) causing a hypertensive crisis and some – but not all – sympathomimetic drugs, as well as the risk of serotonin syndrome when concomitantly used with serotonin reuptake agents. Despite these concerns, they are still used in treatment-resistant cases, when other options have been exhausted, and usually show greater rates of remission compared to previous pharmacotherapies. They are also generally better tolerated by many patients. There are also newer selective and reversible MAOIs, such as moclobemide, which carry a much lower risk of tyramine potentiation and have fewer interactions with other drugs.

Tricyclic antidepressants (TCAs) were also used prior to the year 2000 for atypical depression, but were not as efficacious as MAOIs, and have fallen out of favour with prescribers due to the less tolerable side effects of TCAs and more adequate therapies being available.

Some evidence supports that psychotherapy such as cognitive behavioural therapy (CBT) has equal efficacy to MAOI. These are talk therapy sessions with psychiatrists to help the individual identify troubling thoughts or experiences that may have affected their mental state, and develop corresponding coping mechanisms for each identified issue.

No robust guidelines for the treatment of atypical depression currently exist.

Epidemiology

True prevalence of atypical depression is difficult to determine. Several studies conducted in patients diagnosed with a depressive disorder show that about 40% exhibit atypical symptoms, with four times more instances found in female patients. Research also supports that atypical depression tends to have an earlier onset, with teenagers and young adults more likely to exhibit atypical depression than older patients. Patients with atypical depression have shown to have higher rates of neglect and abuse in their childhood as well as alcohol and drug disorders in their family. Overall, rejection sensitivity is the most common symptom, and due to some studies forgoing this criterion, there is concern for underestimation of prevalence.

Research

In general, atypical depression tends to cause greater functional impairment than other forms of depression. Atypical depression is a chronic syndrome that tends to begin earlier in life than other forms of depression – usually beginning in the teenage years. Similarly, patients with atypical depression are more likely to suffer from personality disorders and anxiety disorders such as borderline personality disorder, avoidant personality disorder, generalised anxiety disorder, obsessive-compulsive disorder, and bipolar disorder.

Recent research suggests that young people are more likely to suffer from hypersomnia while older people are more likely to suffer from polyphagia.

Medication response differs between chronic atypical depression and acute melancholic depression. Some studies suggest that the older class of antidepressants, MAOIs, may be more effective at treating atypical depression. While the more modern SSRIs and SNRIs are usually quite effective in this illness, the tricyclic antidepressants typically are not. The wakefulness-promoting agent modafinil has shown considerable effect in combating atypical depression, maintaining this effect even after discontinuation of treatment. Antidepressant response can often be enhanced with supplemental medications, such as buspirone, bupropion, or aripiprazole. Psychotherapy, whether alone or in combination with medication, is also an effective treatment in individual and group settings.

Does Lack of a Consistent Definition Hinder Treatment for Clozapine-Resistant Schizophrenia Patients?

Research Paper Title

Characteristics and definitions of ultra-treatment-resistant schizophrenia – A systematic review and meta-analysis.

Background

The aim of this systematic review and meta-analysis was to characterise ultra-treatment-resistant Schizophrenia also known as clozapine-resistant schizophrenia (CRS) patients across clozapine combination and augmentation trials through demographic and clinical baseline data. Furthermore, the researchers investigated the variability and consistency in CRS definitions between studies.

Methods

Systematic searches of articles indexed in PubMed, EMBASE, the Cochrane Central Register of Controlled Trials (CENTRAL) and PsycINFO were conducted in March 2020. 1541 randomised and non-randomised clinical trials investigating pharmacological and non-pharmacological clozapine add-on strategies were screened and a total of 71 studies were included. The primary outcome was the overall symptom score at baseline, measured with Positive and Negative Syndrome Scale (PANSS) total or Brief Psychiatric Rating Scale (BPRS) total scores.

Results

Data from 2731 patients were extracted. Patients were overall moderately ill with a mean PANSS total score at baseline of 79.16 (±7.52), a mean duration of illness of 14.64 (±4.14) years with a mean clozapine dose of 436.94 (±87.47) mg/day. Illness severity data were relatively homogenous among patients independently of the augmentation strategy involved, although stark geographical differences were found. Overall, studies showed a large heterogeneity of CRS definitions and insufficient guidelines implementation.

Conclusions

This first meta-analysis characterising CRS patients and comparing CRS definitions revealed a lack of consistent implementation of a CRS definition from guidelines into clinical trials, compromising the replicability of the results and their applicability in clinical practice. The researchers offer a new score modelled on a best practice definition to help future trials increase their reliability.

Reference

Campana, M., Falkai, P., Siskind, D., Hasan, A. & Wagner, E. (2021) Characteristics and definitions of ultra-treatment-resistant schizophrenia – A systematic review and meta-analysis. Schizophrenia Research. 228, pp.218-226. doi: 10.1016/j.schres.2020.12.002. Online ahead of print.

Could Fake Poo & a Rubber Hand Treat OCD?

An illusion in which fake faeces are put on a rubber hand has been tested on people with obsessive compulsive disorder (OCD) (Jalal et al., 2020).

It may one day become a new treatment.

Therapies based on this illusion, designed to help people get more comfortable with germ exposure, could be less upsetting than existing therapies, says Baland Jalal at the University of Cambridge.

The original rubber hand illusion involves putting one hand out of sight and seeing a fake hand in its place. If someone else strokes both the fake and real hand, most people feel that the fake is their own.

Jalal and his colleagues tried a variant on people with hygiene-related OCD. They are usually treated with exposure therapy, but that would, for example, involve exposure on their actual hands. As a result, a quarter reject such therapy.

In the study, 29 people with OCD had fake faeces, made from foods and a fake odour, dabbed on the rubber hand, while their real, hidden hand was touched with a damp towel. While they knew the faeces were fake, they reported feeling disgusted and contaminated.

Jalal’s team plan to test the technique as a way of treating OCD.

References

Jalal, B., McNally, R.J., Elias, J.A., Potluri, S. & Ramanchandran, V.S. (2020) “Fake it till You Make it”! Contaminating Rubber Hands (“Multisensory Stimulation Therapy”) to Treat Obsessive-Compulsive Disorder. Frontiers in Human Neuroscience. 13:414. https://doi.org/10.3389/fnhum.2019.00414

Wilson, C. (2020) Rubber Hand Illusion and Fake Poo May be the may to Treat OCD. New Scientist. 18 January 2020, pp.17.

What is the Prevalence & Associated Factors of Depression among Patients with Schizophrenia?

Research Paper Title

The prevalence and associated factors of depression among patients with schizophrenia in Addis Ababa, Ethiopia, cross-sectional study.

Background

Depression is common among people with schizophrenia and associated with severe positive and negative symptoms, higher rates of disability, treatment resistance and mortality related to suicide, physical and drug-related causes.

However, to the researchers knowledge, no study has been conducted to report the magnitude of depression among people with schizophrenia in Ethiopia.

Therefore, this study aimed to determine the prevalence and associated factors of depression among people with schizophrenia.

Methods

A hospital-based cross-sectional study was conducted among 418 patients with schizophrenia selected by systematic sampling technique.

Patient Health Questionnaire 9 (PHQ-9) was used to measure depression among the study participants.

To identify the potential contributing factors, we performed binary and multi-variable logistic regression analysis adjusting the model for the potential confounding factors.

Odds ratios (OR) with the corresponding 95% confidence interval (95%CI)) was determined to evaluate the strength of association.

Results

The prevalence estimate of depression among people with schizophrenia was found to be 18.0% [95% confidence interval: 14.50-22.30].

The multi-variable analysis revealed that current substance use (AOR 2.28, 95%CI (1.27, 4.09), suicide attempt (AOR 5.24, 95%CI (2.56, 10.72), duration of illness between 6 and 10 years (AOR 2.09, 95%CI (1.08, 4.04) and poor quality of life (AOR 3.13, 95%CI (1.79, 5.76) were found to be the factors associated with depression among people with schizophrenia.

Conclusions

The current study revealed that co-morbid depression was high among people with schizophrenia and associated with current substance use, suicide attempt, and long duration of the illness as well as poor quality of life.

Attention needs to be given to address co-morbid depression among people with schizophrenia.

Reference

Fanta, T., Bekel, D. & Ayano, G. (2020) The prevalence and associated factors of depression among patients with schizophrenia in Addis Ababa, Ethiopia, cross-sectional study. BMC Pyschiatry. 20(1):3. doi: 10.1186/s12888-019-2419-6.

Electroconvulsive Therapy (ECT) in Treatment-Resistant Schizophrenia & Coexisting Myasthenia Gravis (MG)

Research Paper Title

Successful administration of electroconvulsive therapy in a patient with treatment-resistant schizophrenia and coexisting myasthenia gravis.

Background

Electroconvulsive therapy (ECT) is an efficacious treatment for resistant schizophrenia.

However, the presence of comorbid myasthenia gravis (MG) poses considerable challenge and concerns for administering anesthesia during ECT.

To the best of the researchers knowledge, till this date, there is only a solitary case reporting the use of ECT in schizophrenia with coexisting MG.

Hence, in this case report, they describe successful administration of modified ECT under anaesthesia in a patient with treatment-resistant schizophrenia with MG.

Reference

Sreeraj, V.S., Venkataramaiah, S., Sunka, A., Kamath, S. & Rao, N.P. (2019) Successful administration of electroconvulsive therapy in a patient with treatment-resistant schizophrenia and coexisting myasthenia gravis. Indian Journal of Psychiatry. 61(6), pp.653-654. Available from World Wide Web: http://www.indianjpsychiatry.org/text.asp?2019/61/6/653/270349. [Accessed: 16 February, 2020].

Examining the Role the Inflammatory Process & Immune System Play in Mental Disorder

Research Paper Title

Inflammatory Response and Treatment-Resistant Mental Disorders: Should Immunotherapy Be Added to Pharmacotherapy?

Abstract

Treatment resistance continues to challenge and frustrate mental health clinicians and provoke psychiatric researchers to seek additional explanatory theories for psychopathology.

Because the inflammatory process activates symptoms of depression, anxiety, and psychosis, it is a reasonable route to follow for primary and/or indirect contribution to mental disorders.

The current article reviews the research literature regarding the role the inflammatory process and immune system play in mental disorders as well as novel treatments under investigation for resistant depression, anxiety, substance use, and psychotic disorders.

Reference

Limandri, B.J. (2020) Inflammatory Response and Treatment-Resistant Mental Disorders: Should Immunotherapy Be Added to Pharmacotherapy? Journal of Psychosocial Nursing and Mental Health Services. 58(1), pp.11-16. doi: 10.3928/02793695-20191218-03.

Inflammatory Response & Treatment-Resistant Mental Disorders

Research Paper Title

Inflammatory Response and Treatment-Resistant Mental Disorders: Should Immunotherapy Be Added to Pharmacotherapy?

Abstract

Treatment resistance continues to challenge and frustrate mental health clinicians and provoke psychiatric researchers to seek additional explanatory theories for psychopathology.

Because the inflammatory process activates symptoms of depression, anxiety, and psychosis, it is a reasonable route to follow for primary and/or indirect contribution to mental disorders.

The current article reviews the research literature regarding the role the inflammatory process and immune system play in mental disorders as well as novel treatments under investigation for resistant depression, anxiety, substance use, and psychotic disorders.

Reference

Limandri, B.J. (2020) Inflammatory Response and Treatment-Resistant Mental Disorders: Should Immunotherapy Be Added to Pharmacotherapy? Journal of Psychosocial Nursing and Mental Health Services. 58(1), pp.11-16. doi: 10.3928/02793695-20191218-03.