The Truth About Anxiety Treatments: What Really Works 

In the first part of this series, we discussed anxiety and specifically generalized anxiety disorder (GAD) as a diagnosis. Now we are going to look at the research associated with the treatment of GAD and let the research inform our decision making about what works when a person presents with GAD. Some of these findings may surprise you. 

SSRIs 

Although the effect size of SSRIs in GAD is small, 0.33 they remain the recommended first line option for treatment. It’s also important to confirm that someone has had an adequate trial of SSRI treatment before assuming it’s not effective. The choice of which SSRI will depend on the side effect profile and other patient factors such as presence of insomnia, substance use, or pregnancy. Escitalopram is a good place to start, fluoxetine, or sertraline can be alternative options. Although paroxetine has the FDA approval for GAD it has more side effects like weight gain and sedation, along with several other factors that make this medication a poor first-line option. If the first medication trial is ineffective it’s reasonable to try a second SSRI or switch to the SNRI duloxetine. 

When SSRIs Don’t Work

The next step in many cases is to try a medication from a different class. Two SNRIs have been well studied in GAD, venlafaxine, and duloxetine. Venlafaxine is not considered a first line choice due to the side effect profile and the small increase in efficacy. From the meta-analysis on anxiety treatments the effect size is 0.36 slightly better than the SSRIs but it would likely be undetectable clinically. Duloxetine is slightly better with respect to side effects and can be a good choice if you chose to use an SNRI for anxiety treatment. It has the added benefit of lower risk for sexual side effects compared to venlafaxine and possibly improved cognition.

Bupropion in Anxiety Disorders

There is some evidence for the use of bupropion in GAD. In one study small study of 25 participants bupropion beat the SSRI escitalopram head-to-head. Other lines of evidence include more improvement in GAD when bupropion was added as a combination treatment with SSRIs compared to adding buspirone. For clarification the effect size of buspirone in GAD is 0.17 which would be unlikely to produce any observable clinical improvement in anxiety symptoms. I largely stay away from buspirone unless it’s used to treat sexual side effects of SSRIs. Bupropion may be good option for patients who do not want the side effect profile of an SSRI. Although we lack the large RCTs for bupropion in GAD there is some evidence to support its use. The negative studies indicating bupropion worsened symptoms of anxiety come from studies in panic disorder where bupropion was found to worsen panic symptoms. 

What About New Antidepressants?

Vortioxetine had a lot of hype when it first came out, and many believed it would work for GAD. Unfortunately, like many medications when we believe something should theoretically work based on the mechanism of action, we are sadly disappointed. This is one of those cases. The effect size was found to be 0.12 and it did not even cross into the small range. This medication performed worse than buspirone for GAD.  

Vilazodone also had one positive study published for GAD. Again, based on the MOA it should work just fine, it has typical SSRI like effects in addition to 5-HT1A effects like buspirone, you should get the best of both worlds theoretically. This one positive study was followed by two distinctly negative studies and a calculated effect size of 0.26 which is considered small. 

Both were not submitted for FDA approval for GAD based on the negative results. 

The Hydroxyzine Argument

Hydroxyzine is an antihistamine that’s been out for a long time. As I stated earlier it has approval for tension associated with psychoneurosis which is the old psychanalytic way of describing anxiety. It’s often seen as ineffective, but the effect size was higher than SSRIs and SNRIs for the treatment of GAD. Hydroxyzine had an effect size of 0.45, and we may want to reconsider the use of this medication. Some limitations are the size of the studies and duration of the studies, but this still provides a fair amount of evidence that hydroxyzine may perform better than we think. 

Quetiapine Surprised Me

Quetiapine is an antipsychotic medication usually not considered as a treatment option for anxiety disorders. However, the effect size was large with a range from 1.0 to 2.2. To put this in perspective this medication outperformed SSRIs, SNRIs, and benzodiazepines. Why did it not gain FDA approval? If you watched my other videos, you should know that the side effect profile is difficult to tolerate. Metabolic side effects and sedation are common, and the FDA does not view anxiety disorders as significant enough to warrant this degree of risk. One place where this medication may be very useful is in bipolar disorder with severe anxiety. We avoid antidepressants in this population at all costs, quetiapine offers a good option with strong evidence and strong antidepressant effects in bipolar depression. 

Where this fits in clinical practice for me is as a 3rd or 4th line option after all other avenues have been explored except for bipolar disorder as stated above. The antipsychotic medications have been known to have a positive effect on anxiety, but the limitation remains side effects. 

Anxiety as a less Severe Form of Psychiatric Illness

According to the FDA medications like aripiprazole and quetiapine are reasonable adjunctive therapies for patients with major depression that does not respond to first line treatment options. This is not their view for anxiety disorders that respond poorly to first line options. When we look at disability caused by depression and anxiety there isn’t much difference in the odds of being disabled for depression vs anxiety (3.5 Vs 3.1). For whatever reason we continue to view anxiety as less significant although DSM does not identify a clear diagnostic hierarchy. 

Things like psychotherapy are often recommended as first line options. In the 1980’s when GAD was first conceived, it was thought to be a mild disorder where psychotherapy is the most effective treatment. In fact, psychotherapy did well it had an effect size of 0.5 which is nearly the same as benzodiazepines. Psychotherapy is a good place to start for anyone presenting with an anxiety disorder. I’m also a big believer of combining psychotherapy and medication for anxiety disorders. 

What about Benzos?

Benzodiazepines can have all sorts of effects on the body. Largely we think of the benefits of benzodiazepines in anxiety disorders as having a major effect on the physical symptoms of anxiety and not so much on the chronic worry that characterizes the disorder. Many of the effects of benzodiazepines would not be measured by traditional anxiety rating scales based on the updated conception of GAD. Nevertheless, Benzodiazepines had an effect size of 0.4-0.5 which falls into the moderate range for GAD. 

A final Option to Consider

Silexan the proprietary extract of Lavender oil has good evidence and a large effect size when used to treat GAD. In Germany there is a respect for the power of natural products, and they are regulated and prescribed in the same manner as pharmaceutical drugs. When silexan was studied in GAD the effect size can range from 0.5 to 0.9. This is a large effect size and I have another video that covers Silexan in detail if you are interested. This can be added to most medication regimens without significant drug interactions and has even been shown to decrease the use of benzodiazepines in those who are using them for GAD. It can be purchased under the brand Name Calm Aid for around $30 per month, and if you are wondering I get no financial compensation for saying this I’m just presenting the evidence. 

Conclusion

We covered a lot here today and I think one of the most important points to stress is the importance of finding the underlying cause of anxiety symptoms. I believe anxiety is driven by other underlying factors as discussed at the beginning of the video. There are many reasons to be anxious and all require a different approach. Without this clarification the patient is likely to continue struggling. Another important point is theoretical mechanism of action that should work, do not always work as seen in the case of vilazodone. We also had some surprises, hydroxyzine, and silexan performed very well but traditional first line options such as SSRI and SNRIs were not so great. I hope this discussion was helpful and if you want more content on anxiety disorders, let me know below in the comments section. 

Does Everyone Have Autism or Is It Just Me? 

There is an ongoing fascination in the world of social media with regards to certain psychiatric diagnoses. It begins with the rise of self-diagnosing, which is rampant on social media these days and ends with a lot of individuals believing they have autism, tic disorder, or dissociative identity disorder (multiple personalities). I’ve also seen a rise in my patients suggesting they have autism as an explanation for symptoms clearly caused by other disorders. 

I can think of one specific example where an individual was convinced, they had autism. Later that day I observed the individual socializing with peers and staff making excellent eye contact, and all those symptoms they described in the diagnostic interview seemingly went away completely. It was clear at that point that autism was not the cause of this individual’s distress.

I feel like there is no better time to discuss autism spectrum disorders because we have a lot to clear up. 

Introduction

Autism spectrum disorder (ASD) was introduced in the diagnostic and statistical manual (DSM-5) to replace the category of pervasive developmental disorders (PDD) which previously included Asperger’s disorder, Autistic disorder, and PDD not otherwise specified (NOS). You might ask, why did they change the category in DSM-5 to just autism spectrum disorder? This was thought to improve the ability to make a diagnosis of ASD while maintaining the sensitivity of its criteria. In fact, research suggests that 91% of those who met the previous criteria would meet the new DSM-5 criteria. They also grandfathered in those with a previously well-established diagnosis of Asperger’s, autistic disorder, or PDD NOS. 

Epidemiology

In 2021, the CDC reported that approximately 1 in 44 children in the U.S. is diagnosed with ASD. The prevalence has been rising over the years, and this is largely thought to be related to better detection and awareness of the disorder not vaccinations or other environmental factors. ASD is 4.5 times more common in males than females. The median age when ASD is diagnosed in the U.S. is 50 months which is about 4 years of age. ASD can be found in all racial and ethnic groups although the prevalence does appear to be higher in Caucasian children. 

Clinical Features of ASD

The focus in DSM-5 was in two domains and not the three domains from the prior classification. These domains are social communication impairment and restricted/repetitive patterns of behavior, and an individual must have had these symptoms in early childhood. Specifiers were added to indicate the level of impairment, level 1: requiring support, level 2: requiring substantial support, and level 3: requiring very substantial support.

DSM-5 Criteria 

Persistent deficits in social communication and social interaction, as manifested by all 3 of the following:

-Deficits in social-emotional exchange: failure of back-and-forth communication, reduced sharing of interests, emotions, or affect, or failure to respond to social interactions. 

-Deficits in nonverbal communicative behaviors used for social interaction: difficulty understanding facial expressions, body language, or eye contact 

-Deficits in developing and maintaining relationships appropriate for the developmental level: difficulty adjusting behavior based on social context, difficult engaging in imaginative paly, or difficulty making friends 

These symptoms can be seen in other disorders in the adult population including social anxiety, OCD, schizoid personality disorder, schizotypal personality disorder, avoidant personality disorder, schizophrenia, bipolar disorder, and intellectual disability. Therefore, it’s important to establish that these deficits were present at an early age. 

Restricted, Repetitive Patterns of Behavior, Interests, or activities 

At least two of the following must be present:

  • Stereotyped or repetitive speech, motor movements, or use of objects (simple motor stereotypies, lining up toys, or repetitive use of objects). 
  • Insistence on sameness, inflexible adherence to routines, ritualized patterns of verbal or nonverbal behavior, or excessive resistance to change 
  • -Highly restricted, fixated interests that are abnormal in intensity or focus 
  • -Hyper-or hypo-reactivity to sensory input or unusual interest in sensory aspects of environment 

These individuals may have a rigid greeting ritual or struggle with small changes to normal activity. I had a case where the family took a different route to school one day and child became so upset that they jumped out of a moving car. This is the level of insistence on sameness and routine that we are talking about. 

Gender Impact on ASD

The prevalence of ASD is lower in females, but females are noted to have a greater impairment in social communication, lower cognitive abilities, and more difficulty externalizing problems than males. 

Causes of ASD

ASD is a complex neurodevelopmental disorder with both genetic and environmental factors. Family and genetic studies identified ASD as a highly heritable disorder. The heritability can range from 37% to more than 90% with only 15% of cases being attributed to a known genetic mutation. ASD is polygenic meaning there are multiple genes that contribute to the disease. Many inherited genetic variants contribute to a small additive risk of developing ASD. 

Neuroimaging research has found that ASD is often associated with atypical brain maturation. Children with autism usually have an excessive number of synapses in the cerebral cortex, this indicates abnormal pruning may be part of the etiology. Pruning occurs at a critical period in childhood where excess synapses are eliminated, it’s critical for proper cortical maturation. Other findings include abnormalities in neurotransmitter levels, immune dysfunction, and neuroinflammation. 

One of the greatest areas of controversy has focused on the impact on childhood vaccinations as a causative factor for ASD. The current evidence does not support this theory, and ASD is not associated with childhood vaccinations. 

Environmental factors including exposure to valproate, air pollution, low birth weight, and increased maternal and paternal age are all associated with increased risk for the development of ASD. 

Co-Morbidity

The most common co-morbid disorders in ASD include intellectual disability, ADHD, and seizure disorder. Approximately one-third of individuals with ASD meet criteria for intellectual disability. ADHD can be seen in 30% to 50% of individuals with ASD. Seizure disorders in these individuals can be difficult to treat, and often refractory to treatment. There is also increased risk of gastrointestinal disturbances such as constipation and restricted food intake.

Evaluating Someone with Suspected ASD

The assessment of ASD requires both an evaluation of the individual and collateral information from caregivers and teachers. ASD remains a clinical diagnosis, but there are several screening and diagnostic assessments that may help support the diagnosis. The most well-known is the ADOS autism diagnostic observation schedule, and the ADI-R autism diagnostic interview revised. 

A delay in spoken language is common first symptom that prompts referral in younger children for autism screening. The starting point is usually to check hearing and vision to be sure the individual is not suffering from deficit in either of these sensory domains. If there are dysmorphic characteristics, genetic testing for specific genetic disorders may also be completed prior to the evaluation. 

Treatment

There is no FDA approved medication for the treatment of ASD. The primary intervention is behavioral, and these interventions should be started as soon as possible. Applied behavioral analysis (ABA) is a type of therapy that focuses in developing specific behaviors such as social skills, communication, reading, and academics as well as fine motor dexterity, hygiene, grooming, domestic capabilities, and job competence. This should be the core of treatment and has good evidence to support its use. 

If medications are used, it’s important to note that they do change the underlying communication or social deficits seen in these children. They are used to target specific co-morbidities such as ADHD, or symptoms that include irritability and aggression. There are only two FDA approved medications for ASD-related symptoms. These medications are risperidone, and aripiprazole and they are approved to treat irritability in children. 

Conclusion

ASD is a complex disorder with multiple genetic and environmental factors contributing to the development of the disorder. Since it’s a neurodevelopmental disorder it’s often present at an early age and suspicion of ASD should be followed up with a proper diagnostic evaluation.  I think it’s important for people to avoid self-diagnosis and be careful what information they are consuming on social media. 

   Why It’s Important to Thrive and Not Just Survive

We Spend a significant amount of time as doctors monitoring for adverse outcomes. 

We use the absence of disease as an indicator of health. 

But the mere absence of disease is not enough to proclaim good health. 

If we only monitor for the absence of disease, we miss the things that are most important in our patients’ daily lives. 

The things I’ve found to be most important in my life, and often lacking in my patient’s lives are…

Being happy, having a sense of purpose and meaning, and having good relationships which are sometimes ignored if overt signs and symptoms of disease are not present. 

Being “well” is a state of complete mental, physical, and social wellbeing. 

Having a purpose in life is associated with reduced mortality risk, so is life satisfaction. Things like loneliness and social isolation are associated with increased mortality.

When these needs are met people not only live longer but they live with intention. 

Let’s Look beyond the absence disease 

Guide To Viewing My Content

If you are new to the blog and my social media content, we should start with a brief introduction. 

My name is Dr. Garrett Rossi, I’m a medical doctor who specializes in adult psychiatry. I’m board certified by the American Board of Psychiatry and Neurology. I’ve practiced in multiple settings including inpatient, outpatient, partial care, assertive community treatment teams, and I provide ECT services.

I make mental health content on multiple social media platforms and each one has a specific style and type of content. 

Shrinks In Sneakers YouTube Click Here

This is where you can find the deep dives on mental health topics including medication reviews, psychiatric diagnosis, and various other topics. Videos can range anywhere from 5-20 minutes and time stamps are available in the descriptions for longer content. 

Shrinks In Sneakers Instagram Click Here:

This is where you can find shorter videos and posts on mental health topics. The focus on Instagram is more on mental health advocacy, and myths about psychiatry and mental illness. The content here is shorter but still has a lot of educational value. 

Shrinks In Sneakers LinkedIn:

This is where you can find more information about my professional activities. I have information about my advocacy work, professional memberships, publications, and is another good place to follow my work. I make frequent posts here as well. 

Shrinks In Sneakers Twitter

Here I’m not very active and haven’t spent much time but I do update blog posts and other relevant information here as well. 

If you have a question or want to get in touch with me, I am most active on YouTube, LinkedIn, and Instagram. 

We are building a community where empathy is a central part of the content. The goal is to make psychiatry more accessible, provide education, and reduce stigma associated with mental health treatment. 

Diagnosis Depression: Sleep Dysregulation

One of the most common symptoms found in multiple psychiatric disorders is sleep disturbance. In fact, sleep disturbance is one of the criteria for the diagnosis of major depression. This post will offer an explanation of some of the changes observed in the sleep patterns of depressed patients.

Much of this information comes from sleep studies in patients who have a diagnosis of major depressive disorder. Without getting too technical there are two primary types of sleep, non-rapid eye movement sleep (NREM) and rapid eye movement sleep (REM). The NREM sleep can be broken down further but for the sake of simplicity we will consider these two categories. 

What we notice in sleep studies of patients who suffer from major depression is a much faster onset of REM sleep. The body usually cycles through these stages 4-6 times throughout the night, averaging 90 minutes in each stage. As the night progress NREM sleep decreases and REM sleep increases. A person with normal sleep architecture will enter REM after 90 minutes, in patients with depression this time period is shorter and can be observed on the sleep study results.

Other changes include decrease NREM sleep which can be thought of as restorative sleep. Increased REM density reduced total sleep time, and decreased sleep continuity are also present. 

Any single change in sleep architecture is not diagnostic of major depression. However, taken together decreased onset to REM, increased REM density, and decrease sleep efficiency can separate patients with major depression from a control group. 

Given all of this information, routine sleep studies are not diagnostic for major depression and are not routinely ordered unless you suspect another sleep disorder. 

Hopefully this provides a basis for why questions about sleep in depressed patients are important. The sleep changes also provide some objective evidence of altered sleeping patterns in patients with depression. 

Is Depression A Genetic Disorder?

Introduction:

This is a common and difficult question I get asked. Like everything in psychiatry, the answer is not clear.

When people think about genetic disorders, they tend to think about classic genetic diseases. Some examples would be sickle cell anemia or cystic fibrosis. There is a clear pattern of inheritance with a single gene involved in these diseases

The human genome project set out to sequence the entire human genome. While it accomplished the goal it did not offer the personalized medicine and targeted interventions initially promised. What it did reveal was a more complicated interplay of genetics and environmental factors. Depression is a multifactorial disease and does not have a single gene involved in the disorder. 

Let’s look at some the evidence supporting the genetic influence on the development of depression.

What Can Family studies tell us ?

The first place to look for a genetic link is family studies. This is one reason we obtain a family history in a psychiatric interview.

MDD is common in families. It’s found 2 to 3 times more often in first-degree biological relatives (e.g. mother or father) of individuals with the disorder than the general population. It’s important to note that the influence of genetics on the development of depression depends on the percent of the genome shared by the individuals. For example, first-degree relatives who share 50% of their genome will have a much greater influence than a second-degree relative who shares 25% of the genome.

What can twin studies tell us ?

The second area of evidence that supports the influence of genetics on depression comes from twin studies.

From the data we know for monozygotic twins (identical twins), there is a 50% chance that one twin will develop the trait (e.g. depression) if the other twin has depression. This number decreases to 20% for fraternal twins who only share 50% of their genome. One flaw in many of these studies is the twins were often raised together in the same environment. There is clearly something to be said for the influence of environment. Some researchers believe twins will influence each other’s behavior when raised together. Identical twins have been known to be treated more similar by their parents than fraternal twins. Taken at face value, when a twin with 100% of the same genetics (identical twins) develops depression the other twin is more likely to also develop depression. Keep in mind, they do not always develop depression even if they share 100% of the genome. 

What do adoption studies add?

Adoption studies make an attempt to differentiate the influence of genetics from environmental factors. These studies examine differences in rates of illness among biological relatives as opposed to adoptive relatives. The studies show higher rates of illness among biological parents rather than adoptive parents. This provides some additional evidence to support a genetic influence. 

Conclusion

There is clearly a genetic component to depression. However, it’s a complicated process that involves multiple genes interacting with the environment. This makes identifying a single causal gene difficult and likely impossible. There are people biologically predisposed to developing depression, but not everyone with biological predisposition will go on to develop depression. 

If you found this helpful please like, comment and share your thoughts for future posts on genetics.

Diagnosis Depression: Major Depressive Disorder (MDD) with Seasonal Pattern

With this specifier, the name provides most of the information. There has to be a clearly defined relationship between the onset and remission of depression with the changing of the seasons. For example, a patient becomes depressed in the late fall or winter and their depression remits once spring arrives. This is the most common pattern in clinical practice.

The relationship between the depressive episodes and season is present for at least the prior two years. Furthermore, the number of seasonal episodes is significantly more than nonseasonal episodes. Basically, what this means is there must be an established pattern related to the changing of the seasons for two years.

If the depressive episode is clearly related to another factor (e.g. start of school or change in work stats) the specifier does not apply. 

In the two-year period where the pattern is established there cannot be any nonseasonal episodes. 

For this specifier to apply, the person must clearly become depressed in the months where day light is reduced (possible mechanism for these episodes), and have remission of symptoms once the days become longer. (this is one example, there are others)

Like, Share, and leave a comment below if you ever felt depressed during the winter months

Diagnosis Depression: Major Depressive Disorder (MDD) with Melancholic Features

I wanted to finish the discussion on the various specifiers for major depressive disorder. In this post I will discuss melancholic features. 

The most distinct feature in MDD with melancholic features is profound loss of interest (anhedonia) in all or almost all activities. This is a common feature in MDD as well, but the loss of pleasure in activities is far more severe. There is also a complete lack of reactivity to anything that would usually be considered by the person as pleasurable. 

In addition, at least three of the following are required: 

  1. Depressed mood that is experienced as qualitatively different from the feeling experienced after a loss. 
  2. Depression that is worse in the morning. 
  3. Awakening at least two hours prior to the usual wake time 
  4. Marked psychomotor retardation (slow movement) or agitation 
  5. Significant anorexia or weight loss 
  6. Excessive or inappropriate guilt 

I think of this specifier as a more profound form of MDD. 

One thing we try to do with modern pharmacology is treat specific symptoms with classes of medication that match the neurotransmitter profile. The medication selection or augmentation strategy may change depending on the symptoms we want to target. For example, fatigue and concentration are largely regulated by norepinephrine and dopamine, so we may choose a medication that targets these neurotransmitters. In this example of melancholic depression sleep and appetite may be the primary issues, we may select a more sedating medication like mirtazapine. I will provide more details on the symptom-based selection of medication for depression in future posts. 

Diagnosis Depression: Major Depressive Disorder (MDD) With Atypical features

I like the DSM-5 and I think it provides us with a conceptual framework for evaluating patients. In clinical practice it’s rare to find patients that fit all diagnostic criteria perfectly. When that does occur it’s nice and makes life easy. 

Major depressive disorder with atypical features is one of those situations. Many patients have some of the symptoms but not enough to clearly make the distinction. Nonetheless, some of these symptoms are common and need to be discussed.

What makes this type of depression atypical?

I like to think of the symptoms as the opposite or reverse of major depression discussed in previous posts. 

A key distinction to look for is mood reactivity in response to positive events. In major depressive disorder nothing usually makes the patient feel happy. They may even present with a restricted, constricted or blunted affect. In the atypical case, these patients can react and show emotion when positive events occur. 

Along with mood reactivity, they must have two of the following features

  • Increased appetite or significant weight gain 
  • Hypersomnia (excessive sleep) 
  • Leaden paralysis often described as a heaviness of the arms and legs 
  • A longstanding pattern of sensitivity to interpersonal rejection 
  • It must be impairing social and occupational function 

When you look at the list above you see why we can think of these symptoms as the opposite of typical major depression.

Hope this post helps to clear up some question about atypical depression. Please like, share and comment. 

Diagnosis Depression: Major Depressive Disorder (MDD) With Psychotic features

In the last post we covered MDD and we introduced the specifiers. In this post I will talk about MDD with psychotic features. 

You may have guessed already, but what separates this disorder from MDD is the presence of delusions, and hallucinations along with symptoms of major depression. Fairly simple, right?

First, we need to define psychotic symptoms. 

In general, we can think about the following symptoms: 

  1. Delusions: which can be defined as fixed false beliefs. Something that the person believes despite evidence to the contrary. 
  2. Hallucinations: A hallucination is a sensory perception in the absence of external stimuli. There are several types including auditory (most common, consists of hearing a voice or several voices), visual, olfactory (smell), tactile (touch), and gustatory (taste). 
  3. Disorganized speech or behavior: This is an indication of the persons thought process. If the person is not thinking in a clear logical manner their though process may be difficult or impossible to follow for an outside observer.  

These psychotic symptoms can be congruent with the depressed mood (content is consistent with depressive thoughts) or mood incongruent (content is not consistent with typical depressive thoughts). Mood congruent psychotic symptoms will consist of depressive themes such as guilt, death, poor self-worth, and punishment. Mood incongruent symptoms include things such as delusions of control, thought broadcasting, or thought insertion. Both mood congruent and incongruent themes can occur in the same episode.  

Another key point is the psychotic symptoms only occur during a depressive episode. They are not present when the patient is not depressed. Once psychotic symptoms appear with an episode of depression, they tend to be present on subsequent episodes. 

In the next post we will cover atypical features of depression. Please like, comment, and share the content. Feel free to offer suggestions for future posts. 

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