Mood Disorders
Depression and mania look like opposite ends of one scale, and in a sense they are. But the clinical reasoning is not symmetrical, and one question dominates everything else.
Has this patient ever had a manic or hypomanic episode?
A patient presenting with depression who has had a previous manic episode does not have depression. They have bipolar disorder in a depressive phase, and that changes the diagnosis, the drug, the prognosis and the risk.
The reason this matters so much is practical. An antidepressant given alone to someone with undiagnosed bipolar disorder can precipitate mania or accelerate cycling, so the question must be asked of every depressed patient, and asked of relatives too, because patients rarely volunteer past elation as a problem.
A second idea organises severity and risk. Depression is not sadness. The features that distinguish clinical depression from unhappiness are the biological ones, and it is those that predict response to treatment.
1. Recognising Depression
The core symptoms are persistently low mood, loss of interest or pleasure, and reduced energy, present most of the day, nearly every day, for at least two weeks.
Anhedonia, the loss of capacity for pleasure, is the more specific of the first two. Sadness is universal; the inability to enjoy anything at all is not.
The biological symptoms
These carry the diagnostic and prognostic weight.
Early morning wakening, typically two or more hours before usual, with the mood worst on waking. Diurnal variation, with mornings worse than evenings. Loss of appetite and weight. Loss of libido. Psychomotor retardation or agitation.
Their presence indicates a depression likely to respond to biological treatment. Their absence in a patient with low mood raises the possibility of an adjustment reaction or a personality difficulty instead.
Cognitive features
Beck's cognitive triad describes negative views of the self, the world and the future.
Hopelessness about the future is the cognition most strongly associated with suicide, more so than the severity of low mood itself, which is why it is asked about directly.
Guilt in depression is characteristically excessive and inappropriate, and when it becomes delusional it indicates psychotic depression.
2. Depression That Does Not Look Like Depression
In older adults, depression presents as cognitive impairment. The resulting picture, sometimes called depressive pseudodementia, is distinguished from dementia by several features.
| Feature | Depressive pseudodementia | Dementia |
|---|---|---|
| Onset | Relatively rapid, datable | Insidious |
| Patient's account | Complains prominently of memory loss | Minimises or is unaware |
| Effort on testing | Frequent "I don't know" answers | Confabulation and near-misses |
| Mood | Depressed before cognitive change | Cognitive change first |
| Course | Improves with antidepressant treatment | Progressive |
The distinction matters because one is treatable, and because the two coexist: depression is common in early dementia and may be its first manifestation.
In children and adolescents, irritability may replace low mood, and in Indian practice adults frequently present with somatic complaints such as fatigue, headache or bodily pain rather than describing mood at all.
Masked depression behind physical illness is common and consequential. Depression after myocardial infarction, in cancer, in diabetes and after stroke worsens outcomes independently, and treating it improves function.
3. Mania and Bipolar Disorder
Mania is elevated, expansive or irritable mood with increased energy and activity, lasting at least a week or requiring hospitalisation.
The features are grandiosity, reduced need for sleep with no fatigue, pressured speech, flight of ideas, distractibility, increased goal-directed activity, and involvement in activities with painful consequences such as spending, sexual indiscretion or reckless investment.
Reduced need for sleep is the discriminator worth trusting. The patient sleeps two hours and feels rested, which differs entirely from insomnia, where the patient cannot sleep and feels exhausted.
Hypomania is the same phenomenology at lower intensity, lasting at least four days, without psychosis and without marked functional impairment or hospitalisation.
| Type | Requirement |
|---|---|
| Bipolar I | At least one manic episode; depression is common but not required |
| Bipolar II | At least one hypomanic and one major depressive episode, never mania |
| Cyclothymia | Chronic fluctuating subthreshold symptoms over two years |
Bipolar II is not milder than bipolar I. It carries a heavy depressive burden, and the depressive phases dominate the illness course and account for most of the disability and suicide risk.
Why bipolar disorder is missed
Patients seek help when depressed, not when hypomanic, because hypomania feels good and productive. The average delay between first symptoms and correct diagnosis is measured in years.
Features that should raise suspicion of bipolarity in a depressed patient are early age of onset, recurrent episodes, atypical features such as hypersomnia and increased appetite, psychotic features, a family history of bipolar disorder, poor or brief response to antidepressants, and any previous elevated period however brief.
4. Suicide Risk
Suicide is the outcome that mood disorders kill by, and assessment is a clinical skill rather than a checklist.
Asking about suicidal thoughts does not increase risk. This is the single most important thing to know, because reluctance to ask is the commonest barrier to detection.
Risk is raised by hopelessness, previous attempt, a clear plan or preparatory acts, access to means, male sex, older age, living alone, comorbid substance use, chronic pain and physical illness, and recent discharge from psychiatric care.
Two periods carry specific elevated risk. The first weeks of treatment, when psychomotor retardation lifts before mood does, giving the patient energy to act on unchanged despair. And the period immediately after discharge from hospital.
The Indian legal position
Section 115 of the Mental Healthcare Act 2017 effectively decriminalised attempted suicide. It presumes that a person who attempts suicide is under severe stress, so they are not tried or punished, and it places a duty on government to provide care and rehabilitation.
This reversed the position under Section 309 of the Indian Penal Code, and it changed practice directly: a patient presenting after self-harm is a patient requiring assessment and treatment, not a person requiring police involvement.
5. Treatment
Depression
Selective serotonin reuptake inhibitors are first-line for moderate to severe depression, with psychological therapy alone reasonable in mild illness.
Three practical points prevent most treatment failures.
Onset takes two to four weeks, and patients must be told this or they stop early. An adequate trial is four to six weeks at a therapeutic dose before declaring failure. Treatment is continued for at least six months after remission, because stopping at recovery produces high relapse rates.
Electroconvulsive therapy remains the most effective treatment for severe depression, and its specific indications are worth knowing: severe depression with high suicide risk requiring rapid response, depressive stupor, refusal of food and fluids, psychotic depression, and treatment resistance. It is also used in severe mania and in catatonia.
Bipolar disorder
Lithium remains the reference mood stabiliser and is the only agent with consistent evidence for reducing suicide risk.
Its narrow therapeutic index dominates its use. Levels are monitored, and toxicity is precipitated by dehydration, sodium depletion, non-steroidal anti-inflammatory drugs, thiazide diuretics and angiotensin-converting enzyme inhibitors.
Lithium toxicity presents with coarse tremor, vomiting, diarrhoea, ataxia, dysarthria, confusion and eventually seizures, which is distinct from the fine tremor of therapeutic use.
Long-term monitoring covers renal and thyroid function, since lithium causes hypothyroidism and nephrogenic diabetes insipidus.
Valproate must not be used in women of childbearing potential unless there is no alternative and pregnancy prevention is assured, because it is both teratogenic, causing neural tube defects, and associated with impaired neurodevelopment in exposed children.
Antidepressant monotherapy is avoided in bipolar depression because of the risk of switching to mania and of accelerating cycling. Treatment uses a mood stabiliser or an appropriate antipsychotic, with lamotrigine particularly useful for the depressive pole.
When the first antidepressant fails
Before calling a depression treatment-resistant, four things are checked, and the first two account for most apparent failures.
Was the dose adequate and the duration long enough? Four to six weeks at a therapeutic dose is the minimum, and many patients are switched at two weeks on a starting dose.
Was the drug actually taken? Adherence falls sharply once early side effects appear and before benefit arrives, which is precisely the window the patient must be warned about.
Is the diagnosis right? Undiagnosed bipolar disorder, comorbid substance use, hypothyroidism and untreated anxiety all produce apparent antidepressant failure.
Is something maintaining it? Ongoing abuse, chronic pain, poverty and social isolation are not treated by any drug.
Only then does genuine treatment resistance apply, and the options are switching within or between classes, augmentation with lithium or an atypical antipsychotic, and electroconvulsive therapy where the illness is severe.
Persistent depressive disorder
Chronic low-grade depression lasting two years or more, formerly called dysthymia, is easily missed because patients and clinicians treat it as personality rather than illness.
It causes cumulative disability greater than that of many discrete depressive episodes, precisely because it is continuous, and it responds to the same treatments. Double depression, a major depressive episode superimposed on persistent depressive disorder, carries a worse prognosis than either alone.
6. Mood Disorders in Specific Settings
The perinatal period
Three conditions are separated by timing and severity, and confusing them has consequences.
Postpartum blues affects a majority of women, begins around day three to five, involves tearfulness and lability, and resolves within two weeks without treatment.
Postnatal depression begins within weeks to months, meets criteria for a depressive episode, and requires treatment. It is frequently missed because low mood is attributed to fatigue and adjustment, and because women fear being judged as inadequate mothers.
Puerperal psychosis is a psychiatric emergency. It typically begins abruptly within the first two weeks, often with a rapidly fluctuating picture of confusion, mood disturbance and psychotic symptoms, and it carries real risk of suicide and of harm to the infant. It requires admission, ideally with the baby, and urgent treatment.
A personal or family history of bipolar disorder is the strongest risk factor for puerperal psychosis, which is why the question is asked in antenatal care rather than after delivery.
Seasonal and atypical patterns
Atypical depression reverses the usual biological symptoms: hypersomnia rather than early wakening, increased appetite and weight gain rather than loss, leaden heaviness of the limbs, and mood that lifts temporarily in response to positive events, which is called mood reactivity. Rejection sensitivity is characteristic.
Recognising it matters because atypical features are among the pointers toward underlying bipolarity in a patient presenting with depression.
Grief and depression
Normal grief and depression overlap, and the distinction is one of pattern rather than intensity.
Grief characteristically comes in waves, preserves self-esteem, and permits moments of pleasure and connection. Depression is pervasive rather than wave-like, and carries global worthlessness rather than sadness focused on the loss.
Features that suggest depression rather than grief include persistent guilt unrelated to the deceased, psychomotor retardation, worthlessness, and suicidal thoughts driven by hopelessness rather than by a wish to rejoin the person who died.
7. Worked Examples
Example 1. A 26-year-old presents with a third episode of depression. She is started on an SSRI. Two weeks later she is elated, sleeping three hours, spending heavily and speaking rapidly. What has happened and what should have been asked?
An antidepressant-precipitated manic switch, revealing underlying bipolar disorder. What should have been asked, of her and of a relative, is whether she had ever had a period of elevated mood, reduced need for sleep with preserved energy, or unusual productivity and spending.
Several features in her history should also have raised suspicion before prescribing: onset in her twenties, and a third recurrence at a young age. Atypical features, psychotic symptoms, family history of bipolar disorder and brief or poor previous antidepressant response would have added further weight.
Management now is to stop the antidepressant and treat the manic episode, with a mood stabiliser or antipsychotic, and to reconsider long-term treatment as bipolar disorder rather than recurrent depression.
Example 2. A 72-year-old man is brought with six months of memory complaints. He answers many questions with "I don't know", his family date the onset to a specific month, and his sleep and appetite have been poor since his wife died. How would you approach this?
The picture suggests depressive pseudodementia rather than a primary dementia. Several features point that way: relatively rapid, datable onset; prominent complaint of memory loss by the patient himself rather than minimisation; frequent "I don't know" answers indicating reduced effort rather than the near-misses and confabulation of dementia; and biological depressive symptoms with a clear precipitant.
The distinction matters because this is treatable. A trial of antidepressant treatment with reassessment of cognition after response is appropriate, alongside standard investigation for reversible causes.
Two cautions are necessary. Depression and dementia frequently coexist, and depression can be the first manifestation of an early dementia, so improvement in mood without improvement in cognition requires ongoing follow-up rather than reassurance.
Example 3. A severely depressed patient starts an SSRI. Ten days later the ward reports he is more active and getting out of bed, and the family are pleased. What is the specific concern?
This is the period of highest suicide risk in the treatment course. Psychomotor retardation typically improves before mood and hopelessness do, so the patient regains the energy and initiative to act while the despair that motivates the act is unchanged.
The apparent improvement is therefore not reassuring on its own and must be interrogated directly: has his mood actually lifted, or only his activity? Hopelessness about the future should be asked about explicitly, since it is more strongly associated with suicide than the severity of low mood.
Practical management is increased observation rather than relaxed observation during this window, direct enquiry about suicidal thoughts, which does not increase risk, and attention to access to means.
Example 4. A 24-year-old woman with bipolar disorder is stable on valproate and plans to marry. What must be discussed?
Valproate must not be continued in a woman of childbearing potential unless there is genuinely no alternative and pregnancy prevention is assured. It is teratogenic, causing neural tube defects, and it is associated with impaired neurodevelopment and reduced IQ in children exposed in utero, with the neurodevelopmental risk being the less widely known and arguably more important of the two.
The discussion covers the specific risks, the need for effective contraception if valproate continues, and, preferably, a planned switch to an alternative before conception rather than after a pregnancy is discovered, since neural tube closure is complete before most pregnancies are recognised.
Alternatives include lithium, with its own pregnancy considerations, or an appropriate antipsychotic, and lamotrigine where the depressive pole dominates. High-dose folic acid supplementation is advised but does not remove the risk.
Example 5. A patient on lithium develops vomiting and diarrhoea from gastroenteritis, then becomes ataxic and confused with a coarse tremor. Explain the sequence.
This is lithium toxicity precipitated by volume depletion. Lithium is handled by the kidney like sodium, being freely filtered and substantially reabsorbed in the proximal tubule. When the patient becomes dehydrated and sodium-depleted through vomiting and diarrhoea, proximal sodium reabsorption increases and lithium is reabsorbed along with it, so the serum level rises even though the dose has not changed.
The clinical features distinguish toxicity from therapeutic effect. A fine tremor is expected at therapeutic levels, whereas a coarse tremor with ataxia, dysarthria, confusion and eventually seizures indicates toxicity.
Management is to stop lithium, rehydrate with saline, check the level and renal function, and consider haemodialysis in severe toxicity. The same mechanism explains why thiazide diuretics, non-steroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors raise lithium levels, and why any intercurrent illness with fluid loss is a reason to check.
Summary
Ask every depressed patient whether they have ever had a manic or hypomanic episode.
An antidepressant alone in undiagnosed bipolar disorder can precipitate mania.
Anhedonia is more specific than sadness.
The biological symptoms carry the diagnostic and prognostic weight.
Hopelessness predicts suicide more strongly than severity of low mood.
Depression in older adults can present as cognitive impairment and is treatable.
In pseudodementia the patient complains of memory loss; in dementia they minimise it.
Reduced need for sleep with preserved energy distinguishes mania from insomnia.
Bipolar II is not milder; the depressive burden dominates its course.
Bipolar disorder is missed because patients seek help when depressed, not when hypomanic.
Asking about suicidal thoughts does not increase risk.
Risk peaks in the first weeks of treatment and after discharge.
Section 115 of the Mental Healthcare Act 2017 decriminalised attempted suicide.
SSRIs take two to four weeks to work and need a four to six week trial.
Continue antidepressants at least six months after remission.
Electroconvulsive therapy is the most effective treatment for severe depression.
Lithium is the only mood stabiliser with consistent evidence for reducing suicide.
Lithium toxicity gives coarse tremor, ataxia, dysarthria and confusion.
Dehydration, NSAIDs, thiazides and ACE inhibitors raise lithium levels.
Valproate is avoided in women of childbearing potential for teratogenic and neurodevelopmental reasons.
