Psychotic Depression: An Overview

Shelly John^*
*Correspondence: Shelly John, Department of Biotechnology, University of Arizona, USA, Email:

Commentary

Depressive psychosis, also known as psychotic depression, is a significant depressive episode followed by psychotic symptoms. It can happen as a side effect of bipolar disorder or serious depression. It's hard to tell the difference between it and schizoaffective illness, which needs the presence of psychotic symptoms for at least two weeks without any mood symptoms. The psychotic aspects of unipolar psychotic depression must only appear during episodes of major depression. Meeting the criteria for a severe depressive episode, as well as the requirements for "mood-congruent or mood-incongruent psychotic characteristics" specifier in the DSM-5, is required for diagnosis. Psychotic depression manifests itself as a significant depressive episode accompanied by one or more psychotic symptoms, such as delusions and/or hallucinations.

Mood congruent or incongruent delusions are classified according to whether or not the nature of the delusions corresponds to the individual's mood state. Guilt, persecution, retribution, personal inadequacy, and disease are all common themes in mood congruent delusions. More than one type of delusion affects half of the patients. In around half to two-thirds of people with psychotic depression, delusions occur without hallucinations. Hallucinations are congruent with delusional material and can be auditory, visual, olfactory (smell), or haptic (touch).

Affect isn't flat; it's sad. Symptoms include severe anhedonia, loss of interest, and psychomotor impairment. Psychotic symptoms are more likely to appear if a person has experienced numerous episodes of depression without psychosis. Psychotic symptoms, on the other hand, tend to return with each subsequent depressed episode. Psychotic depression does not have the same bad prognosis as schizoaffective disorders or basic psychotic disorders. Those who have had a depressive episode with psychotic symptoms, on the other hand, have a higher risk of relapse and suicide than those who haven't, and they have more prominent sleep irregularities. Psychotic depression and schizophrenia are more common in family members of persons who have had psychotic depression.

The majority of people with psychotic depression say their first episode happened between the ages of 20 and 40. Psychotic depression, like other depressive episodes, is episodic, with symptoms lasting a set amount of time before diminishing. While psychotic depression can be long-term (lasting more than two years), most depressive episodes are short-term (lasting less than a year). Kathleen S. Bingham discovered that people with psychotic depression who received appropriate treatment went into "remission." They reported having a similar quality of life to persons who did not have Parkinson's disease. A variety of biological characteristics may help to differentiate psychotic depression from non-psychotic depression. The presence of an anomaly in the hypothalamus pituitary adrenal axis may be the most significant distinction (HPA).

In psychotic depression, the HPA axis appears to be dysregulated, with dexamethasone suppression tests revealing increased cortisol levels after dexamethasone administration (i.e. lower cortisol suppression). Psychotic depression patients also have higher ventricular-brain ratios than non-psychotic depression patients. Psychotic symptoms are frequently overlooked in patients with psychotic depression, either because they do not believe their symptoms are odd or because they try to hide them from others. Psychotic depression, on the other hand, can be confused with schizoaffective illness. Dissociative illnesses are included in differential diagnosis due to overlapping symptoms. As a first-line treatment for unipolar psychotic depression, several treatment guidelines prescribe a combination of a second-generation antidepressant plus an atypical antipsychotic, tricyclic antidepressant monotherapy, or electroconvulsive therapy (ECT).

Some data suggests that antidepressant + antipsychotic combination therapy is more successful in treating psychotic depression than either antidepressant treatment alone or placebo. Tricyclic antidepressants, atypical antipsychotics, or a combination of an antidepressant from the newer, better tolerated SSRI or SNRI category plus an atypical antipsychotic are examples of pharmaceutical therapy. Although there is evidence that olanzapine is unsuccessful for depressive symptoms as a monotherapy and that olanzapine/ fluoxetine is more beneficial, olanzapine may be an effective monotherapy in psychotic depression. Quetiapine monotherapy may be especially beneficial in the treatment of psychotic depression because it has antidepressant and antipsychotic effects, as well as a tolerability profile that is comparable to other a typical antipsychotics.

Current drug-based treatments for psychotic depression are effective, but they can cause side effects such as nausea, headaches, dizziness, and weight gain. Tricyclic antidepressants are especially harmful since they can cause fatal heart arrhythmias if taken in excess. Electric current is used to generate a therapeutic clonic seizure in an anaesthetized, unconscious patient in modern ECT. ECT's exact mechanism of action is still unknown, despite much investigation. In addition to the cost of recurrent general anaesthetic exposures, ECT includes the risk of transitory cognitive abnormalities (e.g., disorientation, memory issues). Efforts are being made to find a treatment that tackles the underlying pathophysiology of psychotic depression, which has been proposed.

Mifepristone, a potential option, was supposed to repair an overactive HPA axis by competitively inhibiting particular neuro-receptors, making cortisol less able to operate directly on the brain. However, due to a lack of efficacy, a Phase III clinical research investigating the use of mifepristone in PMD was prematurely halted. In the treatment of depression, Transcranial Magnetic Stimulation (TMS) is being studied as an alternative to Electroconvulsive Therapy (ECT). TMS is a technique that uses a concentrated electromagnetic field to stimulate specific nerve pathways in the brain