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Mood Disorder

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Last Update: May 8, 2023.

Continuing Education Activity

Mood is defined as a pervasive and sustained feeling tone that is endured internally and which impacts nearly all aspects of a person’s behavior in the external world. Mood disorders are described by marked disruptions in emotions (severe lows called depression or highs called hypomania or mania). These include bipolar disorder, cyclothymia, hypomania, major depressive disorder, disruptive mood dysregulation disorder, persistent depressive disorder, and premenstrual dysphoric disorder. These are common psychiatric disorders leading to an increase in morbidity and mortality. This activity reviews the role of the interprofessional team in the diagnosis and treatment of this disorder.


  • Identify the etiology of mood disorders.
  • Review the appropriate evaluation of mood disorders.
  • Outline the management options available for mood disorders.
  • Describe interprofessional team strategies for improving care coordination and communication to advance the delivery of care for patients affected by mood disorders and improve their outcome.
Access free multiple choice questions on this topic.


Mood is defined as a pervasive and sustained feeling tone that is endured internally, and that impacts nearly all aspects of a person’s behavior in the external world. Mood disorders or affective disorders are described by marked disruptions in emotions (severe lows called depression or highs called hypomania or mania). These are common psychiatric disorders leading to an increase in morbidity and mortality. 

According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), mood disorders have been broadly categorized as bipolar disorders and depressive disorders.[1] Bipolar disorders are further categorized as bipolar I, bipolar II, cyclothymic disorder, bipolar and related disorder to another medical condition, substance/medication-induced bipolar and related disorder, other specified bipolar and related disorder, and unspecified bipolar and related disorder. 

  • Bipolar I disorder is defined as a syndrome in which a complete set of mania symptoms (elevated mood with three or more of the following symptoms- increased goal-directed activity, grandiosity, a diminished need for sleep, distractibility, racing thoughts, increased/pressured speech, and reckless behaviors) has occurred lasting for at least one week or required hospitalization. If the mood is irritable instead of elevated, four or more of the aforementioned symptoms are needed to meet the criteria for a manic episode. 
  • Bipolar II disorder consists of current or past major depressive episodes interspersed with current or past hypomanic periods of at least four days duration.
  • Cyclothymia is defined as a subthreshold bipolar trait or temperament with low-grade affective manifestations of the sub-threshold major depression and mild hypomania. It is diagnosed in adults who experience at least 2 years of both hypomanic and depressive periods without ever meeting the criteria for mania, hypomania, or major depression. For a child or an adolescent to be diagnosed with cyclothymia, these episodes should last over 1 year. 
  • Hypomania is defined as a non-psychotic, milder, or subthreshold manic state of short duration lasting for at least four consecutive days and without marked social and occupational impairment. It requires elevated mood with (three or more symptoms) or irritable mood (with four or more of the following symptoms) - increased goal-directed activity, grandiosity, a diminished need for sleep, distractibility, racing thoughts, increased/pressured speech, and reckless behaviors. According to the International Classification of Diseases 11th Revision (ICD-11), cyclothymia and hypomania are considered as a prodrome of bipolar disorders, and per DSM 5, hypomania is a component of bipolar II disorder.[2]

Major depressive disorder is diagnosed by the presence of 5 out of the 9 symptoms of sad mood, insomnia, feelings of guilt, decreased energy levels, decreased concentration, decreased appetite, decrease in pleasurable activities (anhedonia), increased or decreased psychomotor activity, and recurrent suicidal ideation/acts of self-harm/suicide attempt existing over a period of 2 weeks.

Three new depressive disorders have been incorporated under mood disorders in DSM-5:

  1. Disruptive mood dysregulation disorder (DMDD) is seen in children and adolescents with frequent anger outbursts and irritability out of proportion to the situation
  2. Persistent depressive disorder (PDD) or dysthymia, which means a depressed mood that is not severe enough to meet the criteria for major depression. PDD is defined as the depressed mood for at least two years in adults and one year in children and adolescents
  3. The premenstrual dysphoric disorder (PMDD) is characterized by irritability, anxiety, depression, and emotional lability occurring in a week before the onset of menses followed by resolution of the symptoms after onset.[3] 

Major depression episodes may precede or occur concurrently with persistent depressive disorder, and this is known as double depression.

Other depressive disorders include depressive disorder due to another medical condition, substance or medication-induced depressive disorder, other specified depressive disorder, and unspecified depressive disorder.


The brain areas responsible for controlling our feelings and emotions are the amygdala and orbitofrontal cortex. Patients with mood disorders have shown to have an enlarged amygdala on brain imaging, which substantiates the certainty that abnormalities in these areas lead to mood disorders. Ventricular expansion results from repeated episodes of mood disorders.[4]

Biological Factors

Neurotransmitters that play an important function in mood disorders are serotonin and norepinephrine, which are decreased in episodes of depression. Serotonin is the neurotransmitter most commonly associated with depression. Dopamine has also been implicated in mood disorders with research showing that it may be decreased in depression and increased in mania. 

Medical conditions which lead to mood disorders include:

  • Brain tumors
  • CNS syphilis
  • Delirium
  • Encephalitis
  • Influenza
  • Metabolic changes associated with hemodialysis
  • Multiple sclerosis
  • Q fever
  • Cancer
  • AIDS
  • Hypothyroidism

There are certain drugs and medications, consumption of which lead to symptoms simulating a mood disorder. These are amphetamines, cocaine, procarbazine, and steroids.[5]

Genetic Factors

According to research based on twin studies, there are certain genes causing mood disorder.[6] Family and adoption studies have also indicated the heritability of mood disorders. People who have a strong positive family history of a mood disorder are more likely to develop mood disorders themselves. The parental mood disorder is a vital and constant risk factor for developing mood disorders in their children.[7]

Hormonal Factors

Increased HPA activity is associated with stress and depression. Increased TSH has been shown to be associated with depression.

Psychosocial Factors

Stressful life changes (death of significant other, parents, siblings, etc.) traumatic events and childhood abuse have been found to be major risk factors for the development of mood disorder later on in life, especially depressive disorder.[8] Personality traits or certain personality disorders like borderline and obsessive-compulsive disorder (OCD) are more frequently associated with depression. Attachment problems and early childhood adversity have been associated with depression.

Neuroimmunological Factors

Research shows that mood disorder leads to the altered release of neuroactive cytokines like IL-1beta, IL-6, and TNF-alpha.[9]

Recent research has found a crucial role of nitric oxide (NO) involved in causing the inflammatory process that leads to signs and symptoms of mood disorder. Altered levels of NO have also been found in patients suffering from mood disorders.[10]

Increased frequency of abnormal hyperintensities is seen in subcortical regions in depressive disorders and bipolar disorder.


Major depression has a lifetime prevalence of about 5% to 17%. Women have almost twice the prevalence rate vs. men.[11] The annual prevalence rate of depression is 7.1% in U.S. adults, while the annual prevalence rate for bipolar disorder is 2.8%. The median age of onset of major depressive disorder is 32 years.[12]

Mood disorders are commonly seen in children and adolescents with an estimated rate of 15% suffering from any mood disorder, and 12% have a mood disorder with severe impairment.[13] Depression is prominent in children and adolescents, with rates as high as 18% to 22% in girls and 7% to 10% in boys by the age of 17. Research shows the prevalence of disruptive mood dysregulation disorder ranges from 0.8% to 4.3% in children.[14] The lifetime prevalence of bipolar disorder subtypes is 0.6% for bipolar I, 0.4% for bipolar II, and 2.4% for bipolar spectrum disorder (BPS).[15]


Depression is a complex neuropsychiatric disorder represented by severe anhedonia (a substantial incapacity to enjoy pleasurable activities), sad mood, feelings of guilt, suicidality, and cognitive impairment. One of the primary risk factors for the development of depressive disorders is chronic stress. The pathophysiology of constant stress results from overactivation of the hypothalamic-pituitary-adrenal (HPA) axis, which results in glucocorticoid cortisol level increase.[16] Neuronal plasticity also plays a significant role in the pathophysiology of mood disorder. Patients with poor social support show signs of impaired neuronal plasticity, predisposing them to mood disorders. Mild to moderate impairment of neuronal plasticity causes depression, while severe impairment results in mania.[17] 

Other symptoms of mood disturbances are decreased sleep and appetite. There could be increased (agitation) or decreased psychomotor activity. Increased agitation can be life-threatening as it can lead to muscle breakdown, followed by kidney failure (due to increased creatinine). In severe cases, the patient may develop psychotic symptoms of delusions and hallucinations. Neurocognitive changes with deficits in attention and concentration, recent and remote memory, and executive functions have been detected in cases of mood disorders. These signs and symptoms are due to an interplay of factors such as genetic vulnerability, positive family history, and social support systems.[18]

History and Physical

The evaluation for mood disorders mandates comprehensive and detailed history taking. Patients with bipolar disorder are easily diagnosed when they present with episodes of mania characterized by inflated self-esteem, grandiosity, impulsivity, irritability, increased psychomotor activity, delusions, or hallucinations. When the patients exhibit symptoms of depression such as sad mood, decreased concentration, guilt, decreased interest in pleasurable activities, ideas of self-harm, and suicide, it is crucial to differentiate unipolar from bipolar depression. Clinical features suggestive of bipolar depression are early age of onset, acute onset, recurrent episodes of depression (more than 5 episodes), positive family history of bipolar disorder, antidepressant-induced hypomania, depression with psychotic symptoms before the age of 25, postpartum depression, and depressive mixed state.[19] During history taking patients often ignore past hypomanic or manic episodes, so clinicians must explore periods with mood dysregulation associated with decreased need for sleep and increased energy in the past. A careful assessment of the risk of suicide and homicide is essential. 

Once the patient is stabilized, a formal mental status examination is mandatory. Patients suffering from depression show poor/limited eye contact during the interview, have a flat or blunted affect with decreased speech and increased reaction time. They appear disheveled with unkempt hair and poor hygiene. Psychomotor activity is markedly decreased. On the other hand, patients with mania have increased psychomotor activity, are agitated, irritable, hyper talkative, have pressured speech, tangentiality, decreased reaction time, and are difficult to interrupt. Patients with mania can sometimes have hallucinations, delusions, and paranoia. Occasionally, major depression can have psychotic features. 


A detailed longitudinal and in-depth family history, followed by a thorough mental status examination, is crucial for early diagnosis of mood disorders. Mood disorders secondary to substance abuse require a urine drug test. Specific rating scales are also available for the evaluation of mood disorders. Hamilton Rating Scale for Depression (HAM-D) and the Montgomery-Asberg Depression Rating Scale (MADRS) are for depression, and the Young Mania Rating Scale (YMRS) is for mania.[20]

  • HAM-D is a 17 item depression rating scale administered by the clinician. It rates depressed mood, sleep difficulties, the ability to concentrate, guilt, suicidality, anxiety symptoms, and somatic symptoms on a 3 or 5 point scale. A score of 0 to 7 is considered normal, a score of more than 20 needs intervention.
  • MADRS is a questionnaire administered by the clinician for the diagnosis of depression. It assesses sadness, inner tension, appetite, sleep, thoughts of self-harm, and suicide on a scale of 0 to 60. Scores between 0 to 6 are considered normal, 7 to 19 as mild depression, 20 to 34 as moderate depression, and score more than 34 is categorized as severe depression.
  • YMRS is a clinician-administered scale for mania. It is an 11 item scale with 4 items (irritability, speech, thought content, and disruptive behavior) graded on a 0 to 8 scale and the remaining items (elevated mood, increase in motor activity, libido, sleep, appearance, and insight) are graded on a 0 to 4 scale. Scores less than 12 indicate remission, 13 to 25 as moderate, and 38 to 60 as severe mania.

Treatment / Management

Timely diagnosis and treatment of mood disorders can decrease the associated morbidity and mortality. The first step towards choosing an optimal treatment is a thorough assessment of the patient's safety and level of functioning. Distinct objectives of psychiatric management include solidifying and preserving a therapeutic alliance, educating the patient about signs and symptoms of mood disorders, reinforcing medication compliance, emphasizing the importance of regular sleep and appetite, foreseeing stressors, recognizing recurrences, and lessening social and functional impairment. 

Pharmacotherapy for Bipolar Disorder

  1. If presenting episode is a manic episode with severe symptoms or is a mixed episode: Start with a mood stabilizer (lithium or valproic acid), and an atypical antipsychotic (risperidone, olanzapine, quetiapine, ziprasidone, aripiprazole). 
  2. If the patient presents with a less severe episode: Monotherapy with lithium, an anticonvulsant, or an atypical antipsychotic. Alternatives to lithium or valproic acid are carbamazepine or oxcarbazepine. 
  3. If presenting episode is a depressive episode: Prescribe quetiapine or lurasidone or Lamotrigine or a combination of olanzapine and fluoxetine.
  • Lithium— It is the primary mood-stabilizer. The mechanism of action of lithium is to inhibit the hydrolysis of inositol 1 phosphate by inositol monophosphatase. As a result, the supply of free inositol for the regeneration of membrane phosphatidyl–inositides, which are the sources of inositol triphosphate and diacylglycerol, is reduced. It also inhibits enzyme glycogen synthase kinase, and the hyperactive neurons involved in manic states are preferentially affected because the supply of inositol from extracellular sources is compromised.

Dosage recommendation— In adults, the starting dose is 300 milligrams of the regular release formulation two-three times a day. In elderly persons with renal impairment, the starting dose is 300 milligrams once or twice daily. At a dose of 900 to 1200 milligrams, the plasma concentration of the drug is 0.6 - 1.0 milliequivalents/liter, which is effective in treating bipolar disorder. At a dose of 1200 to 1800 milligrams, the plasma concentration is 0.8 - 1.2 milliequivalent/liter.

Adverse effects—Gastrointestinal upset, fine tremors, polyuria, and polydipsia-reduction in urinary concentrating capacity leading to nephrogenic diabetes insipidus, hypothyroidism, hyperthyroidism, increased risk of hyperparathyroidism, and cognitive impairment. Check sodium, calcium, phosphorus, electrocardiogram, creatinine, urinalysis, complete blood count, thyroid function test, renal function test, and a pregnancy test. Lithium has a narrow therapeutic index; therefore, it requires monitoring of blood levels.

  • Sodium valproate— It blocks voltage-gated sodium channels and boosts the inhibitory transmission of gamma-aminobutyric acid (GABA).

Dosage recommendation—For patients having acute mania, oral loading is 20 to 30 milligram/kilogram/day. Therapeutic plasma concentration is attained on a dosage between 1,200 and 1,500 milligrams/day given in divided doses. Sodium valproate can also be given as an intravenous (IV) infusion to stabilize a patient who comes with agitated behavior rapidly.

Adverse effects— Weight gain, gastric irritation, hair loss, thrombocytopenia, leucopenia, red cell hypoplasia, tremor, menstrual irregularities, polycystic ovaries, hyperandrogenism, hirsutism, obesity, insulin resistance, fatal hepatotoxicity, pancreatitis, hyperammonemia-induced encephalopathy.

  • Carbamazepine, oxcarbazepine— These are anticonvulsant medications. These act by blockade of the sodium channels.

Dosage recommendation—The target dose for antimanic activity is 1,200 mg a day.

Adverse effects are dizziness, diplopia, drowsiness, ataxia, nausea and headache, dry mouth, edema, hyponatremia, and sexual dysfunction. Preliminary workup should include a CBC, liver function tests (LFTs), electrolytes, and ECG.

  • Lamotrigine— It acts by blockade of voltage-sensitive sodium channels, which in turn modulate the release of glutamate and aspartate and a slight effect on calcium channels.

Dosage recommendation— 50 to 200 milligrams per day is used for bipolar depression. It is usually started at 25 mg daily, and the dose is titrated upwards gradually to reduce the risk of Stevens-Johnson syndrome.

Adverse effects— Increased risk of rash (Stevens-Johnson syndrome /toxic epidermal necrolysis), which is associated with the speed of dose titration. The appearance of any kind of rash necessitates sudden discontinuation of the Lamotrigine regimen.

Other anticonvulsants which can be used as a mood stabilizer are riluzole, topiramate, zonisamide, gabapentin, pregabalin, and levetiracetam. Of these, topiramate is used most commonly and is associated with renal stones.

  • Benzodiazepines acting as anxiolytic, sedative-hypnotic, anticonvulsant is a valuable adjunctive to a mood stabilizer. These can be useful adjunctive treatment as anxiety and panic disorder is significantly comorbid with bipolar disorder.
  • Thyroid hormone: Triiodothyronine may stabilize mood in some bipolar patients. It is important to stabilize hypothyroidism with levothyroxine as thyroid abnormalities are associated with rapid-cycling bipolar disorder.

 Pharmacotherapy for Unipolar depression or dysthymia

  • Selective serotonin reuptake inhibitors (SSRIs): Sertraline, fluvoxamine, fluoxetine, citalopram, escitalopram, and paroxetine.

SSRIs are the first-line treatment option for depressive disorder, as they are tolerated better with lesser side effects. They normally take 4 to 5 weeks to display full effects. When on SSRI, it is important to monitor for suicidal thoughts, especially in young adults. The commonly seen adverse effects are nausea, vomiting, diarrhea, dizziness, loss of appetite, reduced sexual desire, anxiety, and insomnia.

  •  Serotonin-norepinephrine reuptake inhibitors (SNRI): venlafaxine, desvenlafaxine, duloxetine, milnacipran, and levomilnacipran

These are the next in line medication for the treatment of depression after SSRIs. This category of the medication has a dual-action and found to be beneficial in cases with comorbid pain. The common side effects include nausea, dry mouth, hypertension, fatigue, loss of appetite, insomnia, sweating, and anxiety.

  •  Atypical antidepressants: bupropion and mirtazapine. Agomelatine is another atypical antidepressant, but it is unavailable in the United States. 

Mirtazapine also acts as a second-line medication for depression. Side effects include somnolence, increased appetite, and weight gain. Bupropion lowers the seizure threshold and is contraindicated in cases with epilepsy, and in eating disorders.

  •  Tricyclic antidepressants (TCA): desipramine, nortriptyline, imipramine, and amitriptyline.

This category of medications can be effective, but no longer used as primary agents for depression due to the various side effects and toxicity due to overdose. Common side effects include weight gain, somnolence, orthostatic hypotension, increased heart rate, constipation, giddiness, and urinary retention.

  •  Serotonin modulators: nefazodone, trazodone, vilazodone, and vortioxetine. 

Serotonin modulators act as antagonists and agonists at postsynaptic serotonin receptors and inhibit the reuptake of postsynaptic serotonin. Nefazodone is contraindicated in liver disease. Priapism may be seen with trazodone. 

  •  Monoamine oxidase inhibitors (MAOIs):

These include tranylcypromine, phenelzine, and selegiline. These are scarcely used due to their particular dietary regulations to avoid the hypertensive crisis and serotonin syndrome. Commonly seen side effects include orthostatic hypotension and decreased sleep.

Phototherapy (bright light therapy) is used in the treatment of seasonal affective disorder (SAD).

  • Newer medications such as intravenous and intranasal ketamine (esketamine) have shown positive results in the treatment of mood disorders. Ketamine has also shown utility in rapidly reducing suicidal ideation though effects require repeat treatments and are not long-lasting. 
  • Somatic treatments like vagal nerve stimulation are used for patients with treatment-resistant depression.[11] 
  • Antipsychotics like aripiprazole can be used for the adjunctive treatment of depression.


Apart from pharmacotherapy, patients suffering from depression and other mood disorders benefit from several types of nonpharmacological therapies.

  1. Mindfulness-based cognitive therapy (MBCT) and acceptance and commitment therapy (ACT): These seem to be beneficial in ameliorating mood symptoms and in curbing relapse.
  2. Interpersonal psychotherapy: It recognizes interpersonal problems and role transitions.
  3. Cognitive-behavioral therapy: It improves dysfunctional cognitions and attitudes that are considered to sustain depression. Amongst psychotherapies, CBT is the most extensively studied therapy for depression.
  4. Dialectical behavioral therapy: It is a form of CBT that involves mindfulness, distress tolerance, and emotional regulation.

CBT, interpersonal therapy, and behavioral activation are considered important psychological treatments for depression. Behavioral activation involves encouraging depressed patients to be involved in activities that uplift mood like exercise, new skills, chores, etc.

 Brain Stimulation Therapy

  1. Repetitive transcranial magnetic stimulation (rTMS) has shown promising results in treating mood disorders. rTMS is a technique that utilizes a pulsed magnetic field to facilitate alteration in brain activity. Repeated cortical stimulation can enhance or lessen regional brain activity. rTMS procedure includes about 5 sessions delivered over a period of four to six weeks. The patient does not need a general anesthetic while undergoing rTMS, and it can be administered in the outpatient unit. Dissimilar to ECT, it does not cause cognitive side effects. The major adverse effects are headache and scalp discomfort at the site of administration.[21]
  2. Electroconvulsive therapy is used in treatment-resistant cases, in severe depression when patients refuse to eat/drink, in pregnancy, and highly suicidal patients. Side effects include headache, cognitive deficits, and memory( both anterograde and retrograde) impairment is of chief concern to the patients while undergoing ECT.[22]

 Healthy Lifestyles

  1. Diet and mental health: Research has demonstrated that following a 'healthy' diet routine is correlated with decreased risk of mood disorders.
  2. Exercise and yoga: Regular exercise and yoga are protective against the development of mood disorders. People who are physically inactive are at a greater risk for the development of depressive disorders. A likely mechanism behind this seems to be the effect of regular workouts on brain-derived neurotrophic factor (BDNF).
  3. Smoking: Smoking cessation is related to an increased optimistic mood and quality of life and fewer chances of getting anxious and depressed compared with regular smoking.
  4. Omega-3 fatty acids: The antidepressant effects of omega 3 fatty acids are due to the regulation of neurotransmitters (serotonin, dopamine), and its anti-inflammatory and antioxidant effects. 

Differential Diagnosis

Differential diagnosis: According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) following are the differential diagnosis of mood disorders.[18]

  • Generalized anxiety disorder, panic disorder, posttraumatic stress disorder (PTSD), or other anxiety disorders: A comprehensive history taking is required to distinguish generalized anxiety disorder from a mood disorder, as anxious ruminations can be misunderstood as racing thoughts. Actions to decrease anxiety may be comprehended as aggressive behavior seen in the manic episode. Likewise, signs and symptoms of PTSD, including anger and aggression, should be differentiated from bipolar disorder.
  • Substance/medication-induced mood disorder: Substance use disorders may present with symptoms suggestive of mania/ depression that needs to be differentiated. A primary diagnosis of a mood disorder must be ascertained based on symptoms that continue once the patient stops consuming the substance. Certain medications (steroids and alpha-interferon) can induce manic or depressive symptoms. Clinical judgment and a thorough history are required to distinguish these symptoms from mood disorders.
  • Attention-deficit/hyperactivity disorder (ADHD): Commonly seen in adolescents and children, this disorder can be mistaken for bipolar disorder. Symptoms such as increased psychomotor activity, difficulty to interrupt speech, distractibility, and decreased need for sleep overlap with symptoms in a manic episode. The episodic nature of bipolar disorder can be valuable in differentiating mania from ADHD.
  • Personality disorder: Symptoms of certain personality disorders like borderline personality disorder may have a significant overlap with bipolar disorders. Labile mood, impulsivity, delusions, and hallucinations are commonly seen in both disorders. These symptoms must appear in episodes with a marked increase over baseline, to be categorized as bipolar disorder.
  • Schizophrenia spectrum and other related psychotic disorders: Bipolar disorder and severe depression with psychotic symptoms must be differentiated from psychotic disorders. Schizophrenia and other related psychotic disorders are all defined by intervals of psychotic symptoms. Important criteria to distinguish these two are delusions, and hallucinations in psychotic disorders are seen in the absence of any mood symptoms. Other valuable considerations constitute the concurrent symptoms, the chronology of symptoms, and the longitudinal course.
  • Delirium, catatonia, and acute anxiety: It is crucial to distinguish symptoms of mania from hyperactive delirious symptoms, excited catatonia, and impulsivity/aggression associated with acute anxiety.


In the first year of follow-up, the patients who had a childhood-onset mood disorder, delay in the diagnosis, and longer duration of untreated illness exhibited quite considerable severity of the disorder, the larger number of episodes, additional days depressed, additional ultradian cycling, and limited days of euthymia.[23] About one-third of mood disorders recur, one-third of the patients develop psychotic disorders, and another one-third develop a lifetime anxiety disorder. Thoughts of dying (80.8%) and thoughts of suicide (69.5%) were continuous, and specific suicidal plans were more frequent in females during follow-up.[24] There are higher chances of comorbid lifelong anxiety, substance abuse disorder, absenteeism from work, and family discord leading to poor quality of life.[25] It is also associated with increased direct and indirect health care expenditures because of the longer duration of hospital stay.


Findings suggest a possible association between a longer duration of illness and a worse outcome in mood disorder, especially in terms of self-harm/suicide.[26] Mood disorders, especially bipolar disorders might be undiagnosed or misdiagnosed for as long as 10 years. A late diagnosis of bipolar disorder has serious outcomes. It leads to several forms of substance abuse. Anxiety disorder was amongst the most frequent lifetime comorbidity associated with mood disorders. Attention deficit-hyperactivity disorder, oppositional defiant disorder, and conduct disorders were also frequently seen. Mood disorders can cause serious functional impairment, for example, inability to work and problems in sustaining emotional relationships with family and friends.[27]

Deterrence and Patient Education

Mood disorders are common psychiatric disorders associated with high morbidity and mortality. Educating the patients regarding the symptoms and timely treatment is mandatory for recovery from mood disorders. Psychoeducation is important for treatment adherence to medications and psychotherapy and continued engagement in treatment and reduced risk of relapse. At the time of discharge from in-patient facilities, the patients and the caregivers should be taught about the early warning signs of mood disorder relapse. If the patients develop symptoms such as a decreased need for sleep, increased talkativeness, racing thoughts, and feeling more energetic, he/she should be immediately brought to the psychiatry office for treatment optimization. Recovery from mania and depression is very critical, and adherence to medication and therapy is important to recover fully. Regular follow-ups and compliance to treatment should be emphasized in every office visit.

Enhancing Healthcare Team Outcomes

The optimal treatment of patients with mood disorders requires the involvement of various health care professionals comprising of family physicians, nurses, psychiatrists, psychologists, and social workers with the strong cooperation of family and support groups. This formulates an integrated care team. Most of the time, the first contact of the patient is a family physician. Patients feel more comfortable discussing their personal matters with family physicians when confronted with a crisis and are unable to cope with the situation. Therefore, the family physician plays a key role in understanding the severity of the symptoms, formulating a diagnosis, and concluding whether a specialist psychiatry referral is required. Patients with moderate to severe mood symptoms with or without active suicidal ideation need a psychiatric referral. 

A mental health case manager (mental health care nurse) appointed by the mental health care team often in community mental health settings is important in cases of severe mood disorders to coordinate patient care. All health care providers involved in the management of the patient need to be notified of the current treatment plan regularly while the patient is admitted to an in-patient psychiatric unit in the event of a crisis. Outpatient treatment records must be sought from psychiatrists and outpatient providers and completed discharge summaries with a detailed plan of care during psychiatric admission. Psychiatric medications should be sent to outpatient providers prior to discharge from in-patient units.

The psychiatrist plays an important role in the decision making and treatment plan of the patient, but an overall effective response is seen when the different professionals involved in the patient care work as a collective team. Positive treatment response requires regular communication between the psychiatrists, family physicians, social workers, nurses, case managers, and pharmacists in both in-patient and outpatient settings.

Review Questions


Spijker J, Claes S. [Mood disorders in the DSM-5]. Tijdschr Psychiatr. 2014;56(3):173-6. [PubMed: 24643826]
Kurumaji A. [The trends of mood disorders in ICD-11: bipolar and depressive disorders]. Seishin Shinkeigaku Zasshi. 2013;115(1):60-8. [PubMed: 23691796]
Łojko D, Suwalska A, Rybakowski J. [Bipolar and related disorders and depressive disorders in DSM-5]. Psychiatr Pol. 2014 Mar-Apr;48(2):245-60. [PubMed: 25016763]
Kloiber S, Rosenblat JD, Husain MI, Ortiz A, Berk M, Quevedo J, Vieta E, Maes M, Birmaher B, Soares JC, Carvalho AF. Neurodevelopmental pathways in bipolar disorder. Neurosci Biobehav Rev. 2020 May;112:213-226. [PubMed: 32035092]
Bhangle SD, Kramer N, Rosenstein ED. Corticosteroid-induced neuropsychiatric disorders: review and contrast with neuropsychiatric lupus. Rheumatol Int. 2013 Aug;33(8):1923-32. [PubMed: 23588411]
Palma-Gudiel H, Córdova-Palomera A, Navarro V, Fañanás L. Twin study designs as a tool to identify new candidate genes for depression: A systematic review of DNA methylation studies. Neurosci Biobehav Rev. 2020 May;112:345-352. [PubMed: 32068032]
Kolaitis G. [Mood disorders in childhood and adolescence: continuities and discontinuities to adulthood]. Psychiatriki. 2012 Jun;23 Suppl 1:94-100. [PubMed: 22796978]
Juruena MF, Eror F, Cleare AJ, Young AH. The Role of Early Life Stress in HPA Axis and Anxiety. Adv Exp Med Biol. 2020;1191:141-153. [PubMed: 32002927]
Bhattacharya A, Derecki NC, Lovenberg TW, Drevets WC. Role of neuro-immunological factors in the pathophysiology of mood disorders. Psychopharmacology (Berl). 2016 May;233(9):1623-36. [PubMed: 26803500]
Ghasemi M, Claunch J, Niu K. Pathologic role of nitrergic neurotransmission in mood disorders. Prog Neurobiol. 2019 Feb;173:54-87. [PubMed: 29890213]
Rakofsky J, Rapaport M. Mood Disorders. Continuum (Minneap Minn). 2018 Jun;24(3, BEHAVIORAL NEUROLOGY AND PSYCHIATRY):804-827. [PubMed: 29851879]
Kessler RC, Berglund P, Demler O, Jin R, Merikangas KR, Walters EE. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2005 Jun;62(6):593-602. [PubMed: 15939837]
Merikangas KR, He JP, Burstein M, Swanson SA, Avenevoli S, Cui L, Benjet C, Georgiades K, Swendsen J. Lifetime prevalence of mental disorders in U.S. adolescents: results from the National Comorbidity Survey Replication--Adolescent Supplement (NCS-A). J Am Acad Child Adolesc Psychiatry. 2010 Oct;49(10):980-9. [PMC free article: PMC2946114] [PubMed: 20855043]
Tang MH, Pinsky EG. Mood and affect disorders. Pediatr Rev. 2015 Feb;36(2):52-60; quiz 61. [PubMed: 25646309]
Merikangas KR, Jin R, He JP, Kessler RC, Lee S, Sampson NA, Viana MC, Andrade LH, Hu C, Karam EG, Ladea M, Medina-Mora ME, Ono Y, Posada-Villa J, Sagar R, Wells JE, Zarkov Z. Prevalence and correlates of bipolar spectrum disorder in the world mental health survey initiative. Arch Gen Psychiatry. 2011 Mar;68(3):241-51. [PMC free article: PMC3486639] [PubMed: 21383262]
McGinn MA, Pahng AR. Pathophysiology of affective disorders: functional interaction of stress hormones and hippocampal excitation. J Neurophysiol. 2017 Feb 01;117(2):477-479. [PMC free article: PMC5288479] [PubMed: 27169510]
Omata N, Mizuno T, Mitsuya H, Wada Y. [Multiaxial evaluation of the pathophysiology of mood disorder and therapeutic mechanisms of clinical drugs by neuronal plasticity and neuronal load]. Nihon Shinkei Seishin Yakurigaku Zasshi. 2013 Nov;33(5-6):231-6. [PubMed: 25069263]
Jorge RE. Mood disorders. Handb Clin Neurol. 2015;128:613-31. [PubMed: 25701910]
Galvão F, Sportiche S, Lambert J, Amiez M, Musa C, Nieto I, Dubertret C, Lepine JP. Clinical differences between unipolar and bipolar depression: interest of BDRS (Bipolar Depression Rating Scale). Compr Psychiatry. 2013 Aug;54(6):605-10. [PubMed: 23375261]
Furukawa TA. Assessment of mood: guides for clinicians. J Psychosom Res. 2010 Jun;68(6):581-9. [PubMed: 20488276]
Phillips AL, Burr RL, Dunner DL. rTMS effects in patients with co-morbid somatic pain and depressive mood disorders. J Affect Disord. 2018 Dec 01;241:411-416. [PubMed: 30145511]
Kolar D. Current status of electroconvulsive therapy for mood disorders: a clinical review. Evid Based Ment Health. 2017 Feb;20(1):12-14. [PMC free article: PMC10688416] [PubMed: 28053184]
Post RM, Leverich GS, Kupka RW, Keck PE, McElroy SL, Altshuler LL, Frye MA, Luckenbaugh DA, Rowe M, Grunze H, Suppes T, Nolen WA. Early-onset bipolar disorder and treatment delay are risk factors for poor outcome in adulthood. J Clin Psychiatry. 2010 Jul;71(7):864-72. [PubMed: 20667291]
Kiss E, Baji I, Kellner A, Mayer L, Kapornai K. [Long-term follow-up of childhood-onset depression - comorbidity, suicidal behavior and prognosis in adulthood]. Psychiatr Hung. 2020;35(1):58-67. [PubMed: 31854323]
Cotrena C, Branco LD, Shansis FM, Fonseca RP. Predictors of quality of life in bipolar disorder: A path analytical study. Psychiatry Res. 2020 Feb 04;285:112846. [PubMed: 32066003]
Altamura AC, Dell'Osso B, Berlin HA, Buoli M, Bassetti R, Mundo E. Duration of untreated illness and suicide in bipolar disorder: a naturalistic study. Eur Arch Psychiatry Clin Neurosci. 2010 Aug;260(5):385-91. [PubMed: 19911248]
Lublóy Á, Keresztúri JL, Németh A, Mihalicza P. Exploring factors of diagnostic delay for patients with bipolar disorder: a population-based cohort study. BMC Psychiatry. 2020 Feb 19;20(1):75. [PMC free article: PMC7031950] [PubMed: 32075625]

Disclosure: Sandeep Sekhon declares no relevant financial relationships with ineligible companies.

Disclosure: Vikas Gupta declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK558911PMID: 32644337


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