In Partial / Full Remission

🧠 Overview — What Does “In Partial / Full Remission” Mean?

In the diagnostic system of DSM-5 and DSM-5-TR, when clinicians record a diagnosis such as Major Depressive Disorder (MDD) or other depressive disorders, they do not stop at simply stating whether the patient “has it or not.” They also add the specifiers
“In Partial Remission” or “In Full Remission” after the diagnosis to indicate the current phase of the illness and the degree of recovery at that point in time.

The term Remission refers to “a remitted phase” or “a period during which depressive symptoms have eased”, which is considered a critical stage in treatment. Even though the patient is doing better, clinicians still need to follow up closely to assess whether the symptoms will come back (relapse).

In general, DSM-5 divides this phase into two main forms:

🔹 In Partial Remission — Partially Remitted Phase
This means the patient has previously gone through a period of depression that fully met criteria (a major depressive episode), and now their symptoms have clearly decreased but have not fully resolved.
For example, they may still have low mood, fatigue, or intermittent insomnia, but the severity has decreased to the point where they no longer meet full criteria for a major depressive episode.

DSM-5 explains that “partial remission” covers two situations:

  • The patient still has some symptoms of MDD, but no longer meets the full diagnostic criteria for a current episode,

or

  • The patient is in a “between-episodes” interval where symptoms have improved, but the duration of having no significant symptoms has not yet reached a full 2 months after the previous episode.

This period is like “the upward slope of the recovery curve”, where the person has started to return to daily activities, but emotional regulation, concentration, and brain energy levels are not yet fully stable. Therefore, close monitoring is still necessary.

🔹 In Full Remission — Temporarily Fully Remitted Phase

This means the patient has no significant depressive symptoms remaining at all for at least 2 consecutive months.
For example, they are not sad, not anhedonic, have no prominent negative thoughts, and no physical or sleep-related symptoms that significantly interfere with daily functioning.

However, the word “Full” here does not mean a permanent cure — depression is still considered a condition with ongoing risk of recurrence, especially in those with a history of multiple episodes or who have previously discontinued treatment prematurely.

During full remission, the brain gradually restores the balance of neurotransmitters (such as serotonin, dopamine, and norepinephrine), and mood-related circuits return toward a more normal state. However, clinicians still recommend continuing treatment in the “maintenance phase” to reinforce biological stability and reduce the chance of recurrence.

🧾 In the ICD-10 / ICD-11 Coding System

This specifier is included in the diagnostic codes, for example:

  • F32.4 → Major depressive disorder, single episode, in partial remission
  • F32.5 / F33.42 → Major depressive disorder, single/recurrent episode, in full remission

These are used in medical documentation, insurance/benefit claims, and research to clearly distinguish patient groups by illness phase.

🔍 Why Is It Important to Specify “Partial” or “Full”?

Because it helps the treatment team to:

  • More accurately assess the risk of relapse
  • Adjust the treatment plan, such as modifying medication, adding psychotherapy, or extending follow-up duration
  • Monitor treatment outcome — whether the patient has reached the point of being “truly well” yet

In research, it has been found that patients in partial remission have a probability of relapse within the first 6 months as high as 40–60%, whereas those who have reached full remission have their risk reduced to around 15–20%.

🧩 Short Summary for Easy Recall

Type Characteristics Duration Relapse Risk
Partial Remission Symptoms have improved greatly, but some remain < 2 months after the last episode High
Full Remission No significant symptoms remaining ≥ 2 months Lower, but still requires monitoring

Put simply:

  • Partial = “Much better, but the episode isn’t over yet.”
  • Full = “This episode is over, but we’re still in a surveillance zone for possible return.”

If you post this on your website under “By Course & Outcome”, you can end with a nicely phrased closing line like:

💬 “Remission doesn’t mean the story is over — it means the mind is learning how to stand on its own again.”

🧩 Core Symptoms — What Does the Remission Phase Look Like?

After the fully acute phase of a major depressive episode has passed, the patient begins to enter a “recovery phase” or “remission phase.”
In reality, this phase is not black-and-white — it doesn’t mean the person is either fully well or still fully depressed. Instead, it’s a “middle zone” where the brain is “learning how to return to equilibrium.”

DSM-5 therefore distinguishes between:

  • Partial Remission = Partially remitted phase
  • Full Remission = Fully remitted phase (for the time being)

🧱 1) Symptom Profile in Partial Remission

Patients in this phase often “look much better” to the people around them — sometimes to the point that others think they’re completely fine. But internally, there are still “fragments of the illness” left.
These are called Residual Symptoms — and they are a crucial warning sign, because they often become the starting point for relapse if left unaddressed.

Common residual symptoms include:

  • Mood still somewhat low or a sense of emptiness on some days, without clear reasons
  • Fatigue or low energy despite adequate rest
  • Reduced concentration, slowed thinking, or a feeling that “my brain still hasn’t fully woken up”
  • Reduced interest or motivation in previously enjoyable activities
  • Sleep disturbances — shallow sleep, difficulty falling asleep, or frequent nocturnal awakenings
  • Changes in appetite — eating significantly more or less than usual
  • Persistent pockets of anxiety or guilt (psychic anxiety / guilt)
  • Feeling less self-confident or emotionally unstable
  • Mood swings — some days feeling bright, other days suddenly feeling sad without a clear cause
  • Being able to return to everyday life, yet still feeling “not quite like my old self”

The key feature of this phase is that the brain begins to function closer to normal, but has not fully recovered 100%.
Neurotransmitters (serotonin, norepinephrine, dopamine) are still not fully stabilized, and the prefrontal cortex is still not completely able to “brake” negative thinking.
This often presents as subthreshold depressive symptoms — not enough to qualify as a full episode, but collectively enough to keep quality of life below pre-illness levels.

Key insight from research:

People who still have residual symptoms — such as poor concentration, fatigue, or chronically poor sleep — have a 3–6 times higher risk of relapse than those who are completely symptom-free, because their brain remains in a “negative bias mode”, meaning it processes negative information too readily.

🌿 2) Symptom Profile in Full Remission

“Full Remission” refers to a period during which all depressive symptoms have resolved to the point that the person no longer meets DSM criteria for a Major Depressive Episode.
There must be no core symptoms such as depressed mood, loss of interest, or suicidal thoughts remaining for at least 2 consecutive months.

Typical features of patients in Full Remission:

  • Mood has returned to a neutral baseline or is appropriately bright according to circumstances
  • Interest in the surrounding world returns — e.g., reading, listening to music, exercising
  • Noticeable improvements in concentration, memory, and reasoning
  • Sleep, appetite, energy, and daily routines are close to normal
  • Relationships improve because the person can once again “emotionally connect” with others
  • No thoughts of death or overwhelming hopelessness
  • Self-confidence (self-efficacy) returns
  • Able to return to work or study at the same or near-pre-illness level

However, neurobiology research suggests that even when people in full remission “no longer feel depressed,” some parts of the brain still show signs of incomplete recovery, for example:

  • The prefrontal cortex and hippocampus still function more slowly than normal
  • The amygdala is still more reactive to negative stimuli than in people who never had depression
  • Levels of BDNF (Brain-Derived Neurotrophic Factor) have not fully returned to normal

This explains why some individuals, even though they are “clinically well,” still feel easily tired, mentally sluggish, or emotionally sensitive. These are not signs of weakness, but rather evidence of the brain’s adaptation during the healing process.

In summary:

  • Full Remission is the point at which clinical symptoms have resolved.
  • But neurobiological recovery — the brain’s physical and chemical healing — still requires several more months.

📋 Diagnostic Criteria — How Do Clinicians Decide Whether It’s Partial or Full?

Psychiatrists and other mental health professionals use structured criteria from DSM-5-TR and ICD-10 / ICD-11 to determine which stage of recovery a patient is in.
These criteria are not just “fancy wording” — they act as “decision points” to determine whether to:

  • Continue treatment or start tapering medication
  • Add more psychotherapy or not
  • Set the level of vigilance required for relapse monitoring

⚙️ 1) DSM-5 / DSM-5-TR Criteria

🔸 Partial Remission:

The patient must have previously experienced a full major depressive episode (meeting full criteria for MDD).
Now, symptoms have clearly decreased to the point that one of the following applies:

  • The patient still has some depressive symptoms, but not enough to meet full criteria for a Major Depressive Episode,

or

  • The patient is in a period where symptoms have partially or fully resolved, but the duration of being “without symptoms” has not yet reached a full 2 months since the previous episode ended.

A clinical example: A patient who previously had 8 out of the 9 MDD symptoms now only has 2–3 symptoms left — e.g., fatigue and insomnia, but no suicidal thoughts. This would be classified as “Partial Remission.”

🔸 Full Remission:

The patient has no symptoms at all that meet criteria for a major depressive episode for at least 2 consecutive months,
and they are able to function normally in daily life, with no signs of subclinical depression.

Key point: DSM emphasizes that full remission does not mean “recovery” in the sense of being completely cured for life. Depression still has a tendency to return, even years later.

🧮 2) Quantitative Criteria in Research

Researchers often use rating scales such as:

  • HAM-D (Hamilton Depression Rating Scale)
  • MADRS (Montgomery–Åsberg Depression Rating Scale)
  • PHQ-9 (Patient Health Questionnaire)

to determine which phase the patient is in.

Level Approximate Score Range Meaning
Remission (Full) HAM-D ≤ 7 / MADRS ≤ 10 / PHQ-9 ≤ 4 Fully well
Partial Remission HAM-D 8–13 / MADRS 11–19 / PHQ-9 5–9 Residual symptoms present
Active Episode HAM-D ≥ 14 / MADRS ≥ 20 / PHQ-9 ≥ 10 Ongoing depressive episode

In Thailand, the Clinical Practice Guideline (CPG) for Depression 2023 by the Department of Mental Health recommends that patients remain in a state of PHQ-9 < 7 continuously for at least 6 months before considering tapering medication, in order to prevent relapse.

🧭 3) Additional Clinical Decision Factors

Clinicians do not rely on scores alone; they also assess:

  • Functional status (ability to work and perform daily roles)
  • Sleep, appetite, and concentration patterns
  • Ability to regulate emotions and handle stress
  • Presence or absence of self-harm ideation

Sometimes, even if scores look good, if the patient still feels “empty, exhausted, or lacking inner motivation,” the clinician may still classify them as being in Partial Remission and choose to continue treatment for a while longer.

🩺 4) Documentation in Medical Records and Research

In medical records and ICD coding systems, this is documented as:

  • F32.4 — Major Depressive Disorder, Single Episode, In Partial Remission
  • F33.42 — Major Depressive Disorder, Recurrent Episode, In Full Remission

Using these codes helps researchers and insurers track the course of illness and the effectiveness of treatment over the long term.

📊 5) Clinical Meaning in Real Life

These criteria are not just for the sake of writing reports — they reflect the degree of recovery of the brain.

  • If the patient is in Partial Remission = the brain is still adjusting, neurotransmitters are not yet stable, continued care is required.
  • If the patient is in Full Remission = the brain has largely regained balance, but is still fragile and needs ongoing treatment to maintain that state.

Understanding the boundary between “Partial” and “Full” helps patients and clinicians co-create more precise treatment plans, preventing “stopping medication too early” or “mistakenly believing one is fully cured.”

Summary:

  • “Partial Remission means the body has started to heal, but the mind is still learning to come back.”
  • “Full Remission means the mind has returned, but the brain still needs time to rest.”

🧷 Subtypes or Specifiers — What Else Can Be Distinguished Within Remission?

Although “In Partial / Full Remission” is already a course specifier, in clinical practice and research, the concept is often elaborated further as follows:

1. Symptomatic vs Functional Remission

  • Symptomatic Remission
    • Core depressive symptoms have resolved or become minimal.
  • Functional Remission

    • The patient has returned to work, daily life, and relationship functioning to a level almost identical to before illness onset.

Very often, patients reach symptomatic improvement but functional recovery has not yet fully returned — this group is at high risk of relapse.

2. Partial Remission with Residual Symptoms

Within the partial remission group, researchers often further distinguish which type of residual symptoms predominate, for example: PMC+2Dove Medical Press+2

  • Residual emotional symptoms
    • Intermittent sadness, internal anxiety, feelings of worthlessness
  • Residual neurovegetative symptoms

    • Sleep disturbances, easy fatigue, poor appetite or overeating
  • Residual cognitive symptoms

    • Poor concentration, forgetfulness, slower cognitive processing
  • Residual painful physical symptoms

    • Chronic aches, back pain, headaches without a clear medical cause

In DSM, however, all of this is still grouped under “in partial remission”. It is mainly in academic literature that these subtypes are broken down to better study risk and tailor treatment strategies.

🧬 Brain & Neurobiology — Is the Brain Still Abnormal During Remission?

The answer is “yes,” absolutely — in people who have had depression, even when they appear to have recovered, the brain may not yet have returned to a fully normal state.
Multiple neurobiological studies over the past 20 years consistently show that remitted depression (a depressive disorder in the recovery phase) still involves dysregulation in various brain systems, both structurally and chemically.

🧩 1) Mood Regulation Circuits

The human brain regulates mood through interconnected networks of regions.
In depression — and even after clinical improvement — these circuits often retain “traces of imbalance,” for example:

Prefrontal Cortex (PFC)
This region is responsible for decision-making, inhibiting negative thoughts, and interpreting events rationally.
After a depressive episode, even when the patient’s mood appears normal, the PFC often remains underactive (hypoactivity), which makes the person more prone to negative thinking and emotionally sensitive to criticism.

Amygdala
The central hub for emotional processing, especially fear, sadness, and threat detection.
During remission, the amygdala often remains hyperreactive to negative stimuli — such as criticism, minor failures, or disapproval — making it easy for the person to slip back into sad or anxious states.

Hippocampus
This structure is involved in contextual memory and rational processing of emotional experiences.
Patients with depression often show reduced hippocampal volume due to chronic stress and elevated cortisol.
Even after clinical recovery, this volume only gradually restores, and typically requires 6–12 months to approach normal levels.

Anterior Cingulate Cortex (ACC)
This area is involved in perceiving “emotional pain” and monitoring internal conflict.
In remission, ACC often remains more sensitive to disappointment than usual, which is why some patients still feel “easily hurt” by events that others might consider trivial.

⚡ 2) The Habenula — A Trigger for Hopelessness

A small brain structure called the habenula functions as a kind of “chemical self-punishment center” when the brain predicts that outcomes will be bad.
In depression, the habenula fires excessively (hyperactive firing), reducing serotonin levels and contributing to feelings of hopelessness.

Even after entering remission, fMRI research shows that the habenula in people who have had depression remains highly responsive to “anticipated negative events,” such as:

  • Criticism
  • Minor failures
  • Or even the thought, “Something bad is going to happen again anyway.”

This is called anticipatory negative bias — the brain predicts negative outcomes before they occur, making it easy for worry and sadness to return.

🌪️ 3) HPA Axis — A Stress Circuit That Hasn’t Fully Reset

The HPA Axis (Hypothalamic–Pituitary–Adrenal axis) is the neuroendocrine system that controls the stress hormone cortisol.
In depression, this system is often overactive, producing persistently elevated cortisol — leading to sleep problems, mental fatigue, and emotional instability.

Even in remission, the HPA axis may still not have fully reset, especially in people who:

  • Have had chronic depression
  • Or remain under ongoing stress from work or environment

Fluctuating cortisol continues to slow recovery in the hippocampus and prefrontal cortex — becoming a risk factor for relapse.

🌱 4) BDNF and Neuronal Repair

BDNF (Brain-Derived Neurotrophic Factor) is a key protein that helps repair and generate new neurons.
During depression, BDNF levels usually drop markedly, especially in the hippocampus and prefrontal cortex.
Treatment with SSRIs / SNRIs and physical exercise can increase BDNF, but this takes time.

In patients who have just entered remission, BDNF levels have not yet fully returned to normal, which explains why the brain may still feel “foggy” or “less sharp than before the illness” even though the person is clinically well.

🧠 5) Serotonin, Dopamine, and Neuroplasticity Systems

Brain recovery after depression involves “rewiring” of neurotransmitter circuits:

  • Serotonin system → Stabilizes mood and sleep
  • Dopamine system → Restores motivation and capacity to feel pleasure
  • Norepinephrine system → Restores concentration and energy

This process is slow and relies on neuroplasticity, the brain’s ability to form new connections.
If patients stop medication too early, these circuits may not yet be “stably locked in,” making it easy to slide back into depression.

💡 Neurobiology Summary in the Remission Phase

Brain Region / System Status After Entering Remission Remaining Effects
Prefrontal Cortex Still underactive Incomplete inhibition of negative thoughts
Amygdala Hyperresponsive Oversensitivity to negative stimuli/stress
Hippocampus Reduced volume, slow recovery Temporary deficits in memory/concentration
ACC Hyperactive to conflict Increased emotional volatility
Habenula Overactive to negative expectations Increased relapse risk
HPA Axis Fluctuating cortisol Brain fatigue, sleep disturbances
BDNF Still below normal Slow neuronal repair

In short — even if a patient appears “well” emotionally, their brain is still in a fragile repair phase.
Therefore, continued treatment until a stable Full Remission is crucial for the brain to truly return to normal functioning.

⚠️ Causes & Risk Factors — Who Is More Likely to Remain “Stuck in Partial Remission”?

Not everyone who goes through a depressive episode reaches full remission easily.
Research suggests that roughly one-third of MDD patients remain in Partial Remission for many months or even years —
and this group has almost three times the relapse risk compared to those who are fully symptom-free.

Below are the main causes and key risk factors that lead to “incomplete recovery”:

🩸 1) Severity of the Initial Episode (Initial Episode Severity)

People who first present with severe depression (Severe MDD) or who have psychotic features or strong suicidal ideation usually recover more slowly.
Their brains tend to show more structural changes — for example, significant hippocampal atrophy — and their neurotransmitter systems require a longer time to readjust.
Even when symptoms improve, they are still at high risk of having multiple residual symptoms remaining.

🧠 2) Psychiatric Comorbidities

  • Anxiety Disorders — present in more than 50% of MDD patients, keeping the brain in a state of chronic hyperarousal
  • Personality Disorders — such as Borderline or Avoidant Personality Disorder, which complicate emotional regulation
  • Substance Use Disorders — alcohol, nicotine, or other drugs that suppress serotonin and decrease the effectiveness of antidepressants
  • ADHD or PTSD — add cognitive and emotional burden, making full remission harder to reach

🩺 3) Medical Comorbidities

Chronic conditions such as diabetes, hypertension, cardiovascular disease, or chronic pain affect inflammatory pathways and the HPA axis directly.
There is evidence that these patients have higher levels of CRP and cytokines (e.g., IL-6, TNF-α), causing slower antidepressant response and making remission more difficult to achieve.

⏱️ 4) Non-adherence or Premature Discontinuation of Treatment

This is one of the most common problems.
Patients often feel better after a few months of medication and stop taking it on their own — essentially “stopping halfway before the brain has truly recovered.”
Studies show that stopping medication within the first 6 months after improvement increases the risk of relapse by up to 70%.
Hence, global guidelines recommend continuing medication for at least 6–12 months after symptom improvement to consolidate biological stability in the brain.

💊 5) Poor Response to Medication or Psychotherapy (Partial Response)

Some people respond only partially to treatment, even at maximum medication doses.
Reasons may include genetic factors such as differences in CYP450 enzyme activity or inconsistent absorption/adherence.
Psychiatrists therefore often use augmentation strategies — e.g., adding lithium, bupropion, or low-dose antipsychotics — to push the patient into full remission.
At the same time, adding CBT or MBCT has been shown to significantly reduce residual symptoms.

💬 6) Psychological and Environmental Factors

  • Occupational/financial stress
  • Strained relationships
  • Lack of social support
  • Social isolation

These prevent the brain from entering a fully restorative state, as the HPA axis is being re-triggered daily.

🧩 7) Persistent Residual Symptoms

Some people only have mild leftover symptoms, such as:

  • Poor sleep
  • Distractibility
  • Irritability

But if these persist, they can become “drivers of relapse” because the brain has not yet escaped old negative patterns.

Patients with more than two residual symptoms have a 3–5 times higher chance of relapse within one year than those who are completely symptom-free.

🧬 8) Genetic and Biochemical Factors

Some people have genetic variants that reduce serotonin transporter (5-HTTLPR short allele) function or naturally low BDNF levels.
They tend to recover more slowly and require combined treatment (medication + psychotherapy + lifestyle changes) to reach full remission.

🌧️ 9) History of Multiple Episodes (Recurrent Episodes)

The more depressive episodes a person has, the more their brain “learns the pathway of sadness” (kindling effect).
With each new episode, the brain slips back into depression more quickly and more intensely.
Therefore, people with recurrent MDD typically require a longer maintenance treatment phase than first-episode patients.

📊 10) Socio-cultural Factors

In societies where depression is still highly stigmatized, patients may avoid continuous treatment or be unwilling to engage in psychotherapy.
Thus, even if physical symptoms appear to have resolved, internally they may still feel “stuck” and keep looping through the same negative thought patterns.

🧭 Summary: Who Is in the “High-Risk, Not Fully Recovered” Group?

Factor Impact on Recovery
Severe initial episode / psychotic features Structural brain changes, slow recovery
Psychiatric or medical comorbidities Hormonal–immune imbalance
Incomplete treatment / early discontinuation Brain not fully reset
Persistent stress / toxic environment HPA axis repeatedly activated
Residual symptoms remaining Brain still in depressive mode
Genetic vulnerabilities (low BDNF, 5-HTTLPR) Slower pharmacological response
History of multiple depressive episodes Faster and stronger relapse risk

Overall summary of these two major sections:

“Entering remission does not mean the brain instantly returns to its original state —
it is a slow, vulnerable phase of self-repair.
Those who understand this timing will see that continuing treatment a bit longer is actually long-term protection against the return of depression.”

💊 Treatment & Management — How Should the Remission Phase Be Managed?

This section is crucial, because the goal of modern depression treatment is no longer just:

  • To reduce depression scores,

but rather:

  • “To achieve full remission + restore functioning + reduce the risk of future episodes.”

❗ Important note: The content here is for understanding and educational/creative purposes only. It is not a substitute for professional medical advice. Anyone with symptoms should consult a doctor or qualified mental health professional.

1. During Partial Remission

Main goals:

  • To clear as many residual symptoms as possible
  • To prevent short-term relapse

Common combined approaches: Thai Depression+3PMC+3BMJ Mental Health+3

  • Adjusting / Optimizing pharmacotherapy
    • Adjusting antidepressant dosage
    • Switching medication or adding another agent (augmentation) when residual symptoms are treatment-resistant
  • Structured psychotherapy
    • CBT, MBCT, IPT, etc., to manage negative thinking and prevent relapse
  • Targeting specific residual symptom clusters

    • If sleep is poor → implement sleep hygiene programs / adjust medication
    • If functional capacity remains impaired → cognitive rehabilitation or occupational therapy

Continuation phase

  • Once symptoms improve, treatment should not be stopped; rather, medication should be continued for at least 6–12 months to reduce relapse risk.
2. During Full Remission
Main goals:

  • To prevent recurrence (a new episode) in the long term
  • To build a stronger buffer in both the brain and real life than before the illness

Typical strategies: Psychiatrist+1

    • Maintenance treatment
    • For those with multiple prior episodes or high-risk profiles
    • Clinicians may continue medication for years, then taper very slowly once true stability is achieved
  • Regular follow-up
    • Monitoring early warning signs (sleep disruption, energy drop, increased negative thoughts, etc.)
  • Lifestyle & psychoeducation
    • Adequate and regular sleep
    • Appropriate physical exercise
    • Reducing substances such as alcohol and drugs
    • Creating a balanced structure of work and rest
  • Role and function rehabilitation
    • Gradually increasing workload and social engagement
    • Starting with small life goals before moving toward bigger ones
  • Managing long-term stressors
    • Chronic issues such as job stress, family conflict, financial strain
    • If necessary, couple or family therapy, or altering aspects of the environment may be recommended

📝 Notes — Common Points of Confusion in Content Creation / Reading Medical Reports

  • “Response” vs “Remission”
    • Response = Symptoms improve by ≥50%, but significant symptoms still remain
    • Remission = Symptoms have decreased to a level considered “near-normal” or “normal” by diagnostic standards
  • “Remission” vs “Recovery”
    • Many frameworks use “recovery” when a person has remained in full remission for a sufficiently long time (e.g., 6–12 months or more).
  • Partial Remission is not just “a bit better.”
    • In many cases, when clinicians write “in partial remission,” it actually means:

    • The symptoms have reduced substantially, but residual symptoms remain that significantly increase the risk of plunging back into a full episode.
  • Residual Symptoms = Predictor of Relapse

    • Large-scale studies show that people with residual symptoms
      • Have a relapse risk about 3 times higher or more than those who are completely symptom-free. MDPI+1
  • For your writing/website
    • “In Partial / Full Remission” can absolutely be a dedicated sub-post, separate from severity (mild/moderate/severe) and “with psychotic features.”
    • A possible meta-structure:

      • Major Depressive Disorder — Course Specifier: In Partial / Full Remission
      • Then cross-link to posts on severity, psychotic features, and other course patterns (single episode / recurrent).

📚 References

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR). Washington, DC: APA Publishing; 2022.

World Health Organization. ICD-11 for Mortality and Morbidity Statistics. Geneva: WHO; 2021.

Paykel ES. “Partial remission, residual symptoms, and relapse in depression.” Dialogues in Clinical Neuroscience. 2008;10(4):431-437.

Israel JA. “The impact of residual symptoms in major depression.” Pharmaceuticals (Basel). 2010;3(8):2426-2440.

Tranter R, O'Donovan C, Chandarana P, Kennedy S. “Prevalence and outcome of partial remission in depression.” Journal of Psychiatry & Neuroscience. 2002;27(4):241-247.

Maletic V, Robinson M, Oakes T, et al. “Neurobiology of depression: An integrated view of key findings.” International Journal of Clinical Practice. 2007;61(12):2030-2040.

Drevets WC, Price JL, Furey ML. “Brain structural and functional abnormalities in mood disorders.” Brain Structure and Function. 2008;213:93-118.

Sheline YI et al. “Hippocampal atrophy in recurrent major depression.” Proceedings of the National Academy of Sciences USA. 1996;93(9):3908-3913.

Savitz J, Drevets WC. “Neuroreceptor imaging in depression.” Neurobiology of Disease. 2013;52:49-65.

Pariante CM, Lightman SL. “The HPA axis in major depression: classical theories and new developments.” Trends in Neurosciences. 2008;31(9):464-468.

Schüle C. “Neuroendocrinological mechanisms of actions of antidepressant drugs.” Journal of Neuroendocrinology. 2007;19(3):213-226.

Hasler G, Drevets WC, et al. “Cognitive and emotional disturbances in remitted depression.” Archives of General Psychiatry. 2004;61(8):785-794.

Pizzagalli DA. “The functional habenula and the pathophysiology of depression.” Nature Reviews Neuroscience. 2019;20:79-93.

Bains N, Abdijadid S. Major Depressive Disorder. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; Updated 2023.

Thai Psychiatric Association & Department of Mental Health. Clinical Practice Guideline for Major Depressive Disorder (Thailand CPG). 2022.

🔖 Hashtags

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