Abstract
Mania is a state of abnormally and persistently elevated, expansive, or irritable mood accompanied by increased energy and goal-directed activity, which cognitive psychology and clinical neuroscience study as the defining episode of bipolar disorder and the clearest natural experiment in pathological mood elevation. A manic episode raises not only mood but the tempo of thought, speech, and action: ideas race, speech is pressured, the need for sleep falls, and judgment loosens into grandiosity and risk. This article sets out what distinguishes mania from ordinary elation, the criteria and rating scales that make it measurable, its place on the continuum from hypomania to psychotic mania, and the prefrontal-limbic dysregulation that underlies it, together with its primary and secondary forms, and closes with three interactive demonstrations.
Keywords: mania, bipolar disorder, affect
Mania is one of the most striking states in all of psychopathology, because it is an illness of excess rather than deficit. Where most psychiatric syndromes subtract — dimming mood, narrowing thought, slowing action — mania adds: it floods the mind with energy, speeds its tempo, and inflates its estimate of what is possible. The manic person often feels, at least at first, extraordinarily well, which is precisely what makes the state so dangerous and so hard to treat. Understanding mania means understanding how the ordinary regulation of mood, drive, and judgment can fail not downward into apathy but upward into a self-amplifying surplus of activity.
Key Takeaways
- Mania is pathological mood elevation, not mere happiness. It is a distinct period of abnormally elevated, expansive, or irritable mood plus increased energy and activity, lasting at least a week, that impairs functioning or requires hospitalization (American Psychiatric Association, 2013). - It became measurable through rating scales. The Young Mania Rating Scale turns the manic syndrome into an eleven-item score, so that severity and change can be tracked reproducibly rather than impressionistically (Young et al., 1978). - Mania sits on a spectrum. From the milder, non-impairing elevation of hypomania through full mania to mania with psychotic features, the bipolar spectrum arranges mood elevation by degree rather than by kind (Angst, 2007). - Its neurobiology is a regulation failure. The consensus model locates mania in dysregulated ventral prefrontal-limbic circuits, where weakened prefrontal control over limbic and striatal structures releases the heightened drive and reward-seeking of the manic state (Strakowski et al., 2012). - Mania has primary and secondary forms. It is the defining episode of bipolar disorder, but the same syndrome can be produced by drugs, medications, or physical illness — a distinction that changes both explanation and treatment (Krauthammer & Klerman, 1978).
What Mania Is
Mania is a syndrome of elevated mood and activity. At its core is a change in affect — the mood becomes abnormally elevated, expansive, or, as often, irritable — but the state is far more than a mood: it is a whole-system acceleration. Thought speeds up and jumps between loosely connected ideas (flight of ideas); speech becomes rapid, loud, and hard to interrupt (pressured speech); the need for sleep falls sharply without a corresponding sense of tiredness; self-esteem inflates, sometimes into frank grandiosity; attention scatters; and activity multiplies into a pursuit of goals, pleasures, and risks that the person would ordinarily avoid (American Psychiatric Association, 2013; Goodwin & Jamison, 2007).
The defining feature that separates a manic episode from ordinary high spirits is that this elevation is sustained, autonomous, and impairing. A happy person is elevated by circumstance and returns to baseline when the circumstance passes; the manic person is elevated regardless of circumstance, cannot be argued or cheered down, and the elevation damages their judgment, relationships, and safety. Diagnostic convention fixes this with a duration criterion — a distinct period lasting at least one week, or any duration if hospitalization is needed — and a functional criterion: the disturbance is severe enough to impair work and social life or to require hospitalization, or it is accompanied by psychotic features (American Psychiatric Association, 2013).
MeSH classifies Mania as a neurobehavioral manifestation — an observable behavioural sign of nervous-system function — which reflects the term's clinical use: mania is a syndrome an observer recognizes and grades, a surface pattern of mood, speech, and action that signals what has happened to the systems regulating drive and affect underneath.
The Shape of a Manic Episode
Mania is not a single symptom but a cluster, and the diagnostic criteria capture this by pairing the mood change with a defined set of additional symptoms. Beyond the elevated or irritable mood and the increased energy that are required, the manic syndrome draws on a short list of further features, of which several must be present. These are often remembered by clinicians through the mnemonic DIGFAST, and together they describe the characteristic acceleration of a mind in the manic state (American Psychiatric Association, 2013).
Table 1
The core additional symptoms of a manic episode
| Symptom | How it appears |
|---|---|
| Distractibility | Attention drawn too easily to irrelevant external stimuli; difficulty holding a train of thought. |
| Indiscretion / risk | Excessive involvement in activities with a high potential for painful consequences — spending, sex, ventures. |
| Grandiosity | Inflated self-esteem, from unrealistic confidence to grandiose delusions of special powers or identity. |
| Flight of ideas | Racing thoughts that leap between loosely connected topics faster than they can be expressed. |
| Activity increase | A surge in goal-directed activity or purposeless restlessness; the overlap with psychomotor agitation. |
| Sleep need reduced | Feeling rested after little sleep — a decreased need for sleep, not insomnia with fatigue. |
| Talkativeness | Pressured speech: rapid, loud, and difficult to interrupt. |
Note. The seven features follow the DSM-5 Criterion B list for a manic episode (American Psychiatric Association, 2013), arranged here by the DIGFAST mnemonic. A diagnosis requires the sustained mood-and-energy change plus at least three of these (four if the mood is only irritable).
Score a manic episode on the Young Mania Rating Scale
The YMRS turns a clinical picture into a number. Seven items are scored 0 to 4 and four (irritability, speech, thought content, disruptive behaviour) are weighted 0 to 8, so the total runs from 0 to 60. The sliders start at the article’s worked example (total 32). Move them and watch the total cross the bands that separate remission, the hypomanic range, and mania.
YMRS total: 32 / 60 — Moderate-to-severe mania.
A falling total is the standard endpoint in trials of antimanic treatment; the score grades severity, it does not make the diagnosis (after Young et al., 1978).
The demonstration assembles a manic presentation from its component symptoms and scores it on the standard clinician's instrument, showing how a qualitative picture becomes a quantitative severity. It makes concrete that mania is a graded syndrome: adjust the severity of each feature and watch the total move across the thresholds that separate euthymia, hypomania, and full mania.
Hypomania, Mania, and the Bipolar Spectrum
Mania is the severe pole of a continuum, not an isolated state. Its milder relative is hypomania — the same qualitative syndrome of elevated mood and increased energy, but below the threshold of marked impairment, lasting as little as four days, and without psychotic features or the need for hospitalization. The distinction is one of degree and consequence rather than of kind: hypomania can even raise productivity and sociability, which is why it so often goes unreported, while mania disrupts the life it inhabits (American Psychiatric Association, 2013).
This graded view is the heart of the bipolar spectrum concept, which arranges mood elevation along a dimension from normal variation through hypomania to full and then psychotic mania, and which reframes the bipolar disorders as a family defined by where and how far mood departs from baseline (Angst, 2007). The spectrum also has a lateral dimension: at the severe end, elevation can coexist with depressive features in a mixed state, where racing, driven activity carries a dysphoric or despairing mood rather than an elated one — a combination captured in the factor structure of manic symptoms, which separates an elated-grandiose dimension from a dysphoric one (Cassidy et al., 1998).
Figure 1
Slide along the bipolar spectrum
Mania is the severe pole of a continuum, not an isolated state. Move the single control — the degree of mood elevation — and watch the state it names change, and the functional impairment rise. Note that impairment stays low through the hypomanic range and climbs steeply only once the manic threshold is crossed: there is no sharp line, only a graded departure from baseline.
Hypomania — elevated mood and energy; function intact or enhanced; no psychosis. Modelled impairment: 7 / 100.
Mood elevation and impairment rise together only past the hypomanic range; the curve is schematic, not an empirical fit (after Angst, 2007).
The demonstration lets the reader move a single control — the degree of mood elevation — along the spectrum and watch the state it names change from euthymia through hypomania to mania and psychotic mania, with the associated impairment and the defining clinical features updating at each step. It makes the spectrum concept tangible: there is no sharp line between the states, only a graded departure of mood from baseline (Angst, 2007).
Assessing Mania
For most of its history mania could only be described, which made its severity a matter of clinical impression. The instrument that changed this is the Young Mania Rating Scale (YMRS), an eleven-item clinician-rated scale that scores the cardinal features of mania — elevated mood, increased motor activity and energy, sexual interest, sleep, irritability, speech, language and thought disorder, thought content, disruptive or aggressive behaviour, appearance, and insight — and sums them into a single severity figure. Seven items are scored from 0 to 4 and four items (irritability, speech, thought content, and disruptive behaviour) are weighted from 0 to 8, so that the total runs from 0 to 60 (Young et al., 1978).
The scale's value is that it fixes severity to explicit, anchored descriptions and so makes change measurable: a falling YMRS total is the standard endpoint in trials of antimanic treatment, and conventional bands place a score below about 12 in the euthymic or remitted range, the low twenties at the threshold of clinically significant mania, and the high thirties and above in the severe range. The YMRS does for mania what ordinal arousal scales do for lethargy: it converts a vivid but slippery clinical picture into a reproducible number (Young et al., 1978).
Worked Example
How does the YMRS turn a presentation into a severity? Consider a patient brought in by family after a week of sleeping two hours a night, talking without pause, and committing to three new business ventures. The clinician rates the eleven items. On the seven items scored 0 to 4, suppose the ratings are: elevated mood 3, increased activity and energy 3, sexual interest 2, sleep 3, language and thought disorder 2, appearance 1, and insight 2 — a subtotal of 3 + 3 + 2 + 3 + 2 + 1 + 2 = 16.
On the four items weighted 0 to 8, suppose the ratings are: irritability 4, speech 6, thought content 4, and disruptive or aggressive behaviour 2 — a subtotal of 4 + 6 + 4 + 2 = 16.
The total YMRS score is therefore 16 + 16 = 32 out of a maximum of 60, which is 32 / 60 ≈ 0.53, or 53% of the scale's range. Where does 32 fall? It is well above the ~12 remission ceiling and above the low-twenties threshold for clinically significant mania, placing the patient squarely in the moderate-to-severe band. The number does not make the diagnosis — the clinical criteria do that — but it anchors it: it says how manic, converts floridly manic into a value that can be re-measured next week, and gives treatment a target to move.
What Happens in the Brain
Why should mood regulation fail upward? The leading neurobiological account frames mania as a failure of regulation rather than a simple excess of mood. In the consensus functional-neuroanatomy model, mood and drive are normally governed by an anterior limbic network: ventral and medial prefrontal regions exert top-down control over limbic and striatal structures — notably the amygdala and the ventral striatum — that generate emotional responses and reward-driven motivation. Mania arises when that prefrontal control is weakened and the limbic and striatal structures it normally modulates become disinhibited, releasing the heightened drive, reward-seeking, and emotional reactivity characteristic of the manic state (Strakowski et al., 2012).
Weaken prefrontal control and release the limbic drive
The consensus model frames mania as a failure of regulation. Ventral and medial prefrontal regions normally hold top-down control over the limbic and striatal structures that generate emotion and reward-driven motivation. Lower the prefrontal control and those structures are disinhibited — the released drive is the modelled substrate of the manic state.
Disinhibiting — control weakening, drive rising. Limbic drive 52, modelled manic severity 56 (both / 100).
The same weakened regulation that releases mood also releases the inhibitory control on which judgment depends (after Strakowski et al., 2012).
This model does useful explanatory work. It accounts for why mania so often combines elevated mood with impulsivity and poor judgment — the same weakened prefrontal regulation that releases mood also releases the inhibitory control on which judgment depends. It fits the triggering role of sleep loss, which further taxes prefrontal function, and the overlap of mania with the driven, goal-insensitive activity of psychomotor agitation. And it situates the broader illness: the same circuits, dysregulated in the other direction, are implicated in the depressive pole of bipolar disorder, so that mania and depression can be read as opposite failures of one regulatory system (Strakowski et al., 2012; Vieta et al., 2018). The demonstration above lets the reader weaken prefrontal control and watch limbic drive rise and the modelled manic severity climb with it.
Primary and Secondary Mania
A manic episode is not always a sign of bipolar disorder. The same syndrome can be produced by an identifiable external cause — a drug of abuse such as a stimulant, a prescribed medication such as a corticosteroid or an antidepressant, or a physical illness affecting the brain — in which case it is termed secondary mania. The distinction, drawn sharply in the classic account, is that primary mania arises as part of a mood disorder with no such antecedent, whereas secondary mania is caused by a demonstrable organic or pharmacological factor (Krauthammer & Klerman, 1978).
The distinction matters because it changes both explanation and action. A secondary mania points to its cause: the first task is to identify and remove the offending drug or treat the underlying illness, after which the mania often resolves. A primary mania points to the mood disorder itself and calls for the pharmacological treatment of the acute episode, where mood stabilizers and antipsychotics are the mainstays and their comparative efficacy has been established by network meta-analysis (Cipriani et al., 2011). That mania can be summoned by so many different routes — a stimulant, a steroid, a stroke, or a mood disorder — is itself informative: it suggests that the manic syndrome is a final common pathway, a characteristic way the regulatory system fails when pushed, rather than the signature of any single cause.
Discussion
Mania repays close attention because it inverts the usual shape of psychopathology and, in doing so, exposes the machinery of mood regulation. Most disorders of affect are disorders of too little; mania is a disorder of too much, and the fact that mood, energy, thought, and judgment all rise together tells us that they are governed by a common system rather than independently. The manic state is, in this sense, a natural experiment: it shows what happens when the regulation of drive and affect fails upward, and the symptoms that result — the racing thought, the pressured speech, the inflated confidence, the collapse of the need for sleep — map the functions that regulation normally holds in check (Goodwin & Jamison, 2007).
The history of mania as a scientific object is, like that of many clinical syndromes, a history of measurement and of unification. Kraepelin's insight was to unify mania and melancholia into a single relapsing illness, making the manic episode one phase of a lifelong condition rather than a disease in itself; the rating scales that followed made its severity reproducible; and the spectrum concept extended it downward into the subtler elevations of hypomania (Angst, 2007; Young et al., 1978). The parallel advance on the mechanistic side has been the move from describing mania to locating it, in the dysregulated prefrontal-limbic circuitry that the consensus model specifies (Strakowski et al., 2012).
The open problems follow from this. On the clinical side, the challenge is recognition: hypomania is underreported and mixed states are easily mistaken for agitated depression, so the boundaries of the spectrum remain hard to draw reliably. On the mechanistic side, the challenge is to connect the circuit-level account to the molecular and genetic findings of contemporary bipolar research, and to explain why the system fails in one direction in some episodes and the other direction in others (Vieta et al., 2018; McIntyre et al., 2020).
Cognitive and Psychological Implications
Mania makes vivid a dependency that cognitive psychology often studies only at its lower end: that coherent thought and action depend on a regulated level of drive, not merely an adequate one. Too little arousal yields the sluggish, unreliable cognition of lethargy; too much, as in mania, yields a different failure — thought so fast and so poorly gated that it loses its thread, attention so readily captured that it cannot be sustained, and judgment so inflated that risk is systematically underweighted. The manic mind is not slow but ungoverned, and the result is a degradation of performance that comes from excess rather than shortfall (American Psychiatric Association, 2013).
The state also illuminates the relationship between mood and cognition. In mania the elevated affect does not sit alongside the cognitive changes but drives them: the grandiosity biases reasoning toward optimism, the heightened reward sensitivity reshapes decision-making toward immediate gain, and the pressured flow of ideas reflects a mood-driven loosening of the normal constraints on association. This makes mania an instructive counterpart to the mood-congruent biases studied in depression, and a reminder that affect is not merely coloured by cognition but can commandeer it (Goodwin & Jamison, 2007).
Finally, mania belongs among the whole-system disturbances of organized behaviour that cognitive psychology studies alongside the single-faculty deficits. It is the hyperactive, mood-driven counterpart to the arousal failures of lethargy and the motor derangements of catatonia, and its depressive opposite — including the loss of pleasure in anhedonia — completes the picture of a single regulatory system that can fail toward either pole (Vieta et al., 2018).
Current Directions
Three threads mark the recent work on mania. The first is cognition between episodes: the recognition that cognitive impairment often persists beyond the resolution of acute mania has turned residual deficits in attention, memory, and executive function into a treatment target in their own right, with task-force recommendations now guiding how they are assessed and addressed (Miskowiak et al., 2018). The second is staging and mechanism: contemporary syntheses of bipolar disorder increasingly frame the illness in terms of its progression and its neurobiological substrates, seeking to connect the circuit-level account of mania to molecular, genetic, and inflammatory findings and to the staged treatment they imply (Vieta et al., 2018; McIntyre et al., 2020). The third is refining the boundaries: the spectrum concept continues to drive work on where hypomania ends and ordinary variation begins, and on how mixed states — manic activity with depressive mood — should be classified and treated, since they are common, dangerous, and easily missed (Angst, 2007; Cassidy et al., 1998). Across all three, the unifying aim is the one this article has traced: to convert mania from a state that can only be recognized into one that can be measured, located, and acted on.
Common Misconceptions
- Mania is just being very happy or energetic.
- It is a pathological state, not an intensified good mood. Manic elevation is sustained regardless of circumstance, cannot be reasoned down, and impairs judgment, relationships, and safety; the mood is often irritable rather than euphoric, and the episode is defined in part by the harm it causes (American Psychiatric Association, 2013).
- Mania and hypomania are the same thing.
- They are the same syndrome at different severities. Hypomania is milder, briefer, non-psychotic, and by definition does not cause marked impairment or require hospitalization, whereas mania does; the distinction is clinically decisive, not a matter of wording (Angst, 2007).
- A manic episode always means bipolar disorder.
- Not necessarily. The same syndrome can be caused by stimulants, corticosteroids, antidepressants, or physical illness affecting the brain — secondary mania — in which case the cause, not a primary mood disorder, is the target of treatment (Krauthammer & Klerman, 1978).
- A manic person is simply out of touch with reality.
- Psychotic features occur only at the severe end of the spectrum. Many manic episodes involve no delusions or hallucinations at all, and milder elevations can leave insight partly intact — which is part of why the spectrum is graded rather than all-or-none (American Psychiatric Association, 2013).
Glossary
- Affect.
- The experienced and expressed state of feeling; in mania the affect is abnormally elevated, expansive, or irritable.
- Anterior limbic network.
- The prefrontal, limbic, and striatal circuit that regulates mood and drive; its dysregulation is the proposed neural substrate of mania.
- Bipolar disorder.
- The mood disorder defined by episodes of mania or hypomania, typically alternating with depression, of which a manic episode is the hallmark.
- Distractibility.
- The too-easy capture of attention by irrelevant stimuli; one of the core additional symptoms of a manic episode.
- Flight of ideas.
- A near-continuous flow of accelerated thought that leaps between loosely connected topics; the thought-tempo sign of mania.
- Grandiosity.
- Inflated self-esteem ranging from unrealistic confidence to grandiose delusions of special powers, wealth, or identity.
- Hypomania.
- The milder form of the manic syndrome — elevated mood and energy without marked impairment, psychosis, or the need for hospitalization — lasting at least four days.
- Manic episode.
- A distinct period, at least a week long, of abnormally elevated or irritable mood plus increased energy and activity, severe enough to impair functioning or require hospitalization.
- Mixed features.
- The co-occurrence of manic activity with depressive mood within an episode; the dysphoric, rather than elated, face of mania.
- Mood stabilizer.
- A class of medication used to treat and prevent manic episodes; with antipsychotics, a mainstay of acute antimanic treatment.
- Pressured speech.
- Rapid, loud, and hard-to-interrupt speech driven by the accelerated thought of mania.
- Primary mania.
- A manic episode arising as part of a mood disorder, with no identifiable external or organic cause.
- Psychomotor agitation.
- Excessive, often purposeless motor activity driven by inner tension; a frequent component of the increased activity of mania.
- Reduced need for sleep.
- Feeling rested after much less sleep than usual, without daytime fatigue; a near-universal and often early sign of mania, distinct from insomnia.
- Secondary mania.
- A manic syndrome produced by a drug, medication, or physical illness rather than a primary mood disorder; treating the cause often resolves it.
- Young Mania Rating Scale (YMRS).
- An eleven-item clinician-rated scale, scored 0 to 60, that quantifies the severity of a manic episode and tracks its change with treatment.
Key Researchers
Jules Angst
(1926-2026). Swiss psychiatrist and Emeritus Professor at the University of Zurich whose long-term cohort studies defined the bipolar spectrum and the concept of hypomania, broadening mania from a categorical state to a dimension of mood elevation. Wikipedia - Wikidata
Kay Redfield Jamison
(b. 1946). Dalio Professor in Mood Disorders and Professor of Psychiatry at the Johns Hopkins University School of Medicine; co-author of the standard reference Manic-Depressive Illness and among the most influential modern authorities on the phenomenology and lived experience of mania. Wikipedia - Wikidata - Faculty
Emil Kraepelin
(1856-1926). German psychiatrist at the University of Munich and founder of modern psychiatric nosology, who unified mania and melancholia into a single relapsing-remitting illness, manic-depressive insanity — the conceptual ancestor of today's bipolar disorder. Wikipedia - Wikidata
Stephen M. Strakowski
(contemporary). American psychiatrist at the Dell Medical School, University of Texas at Austin, whose neuroimaging work produced the consensus functional-neuroanatomy model of bipolar disorder, locating mania in dysregulated ventral prefrontal-limbic circuits. Faculty
Eduard Vieta
(contemporary). Professor and Head of Psychiatry at the Hospital Clinic, University of Barcelona; a leading contemporary researcher on bipolar disorder, the staging of manic episodes, and cognitive impairment in mood disorders. ORCID - Wikipedia - Wikidata - Faculty
Frequently Asked Questions
What is mania in psychology and psychiatry?
Mania is a state of abnormally and persistently elevated, expansive, or irritable mood together with increased energy and activity, lasting at least a week. It accelerates thought, speech, and action, reduces the need for sleep, and inflates self-esteem and risk-taking. It is defined as a pathological episode because it is sustained regardless of circumstance and impairs a person's functioning or safety (American Psychiatric Association, 2013).
How is mania different from just being happy or energetic?
Ordinary happiness is a response to circumstance and fades when the circumstance passes, and it leaves judgment intact. Mania is a sustained, autonomous elevation that cannot be reasoned or cheered down and that damages judgment, relationships, and safety. The mood in mania is also frequently irritable rather than euphoric, and the episode is defined in part by the impairment it causes (American Psychiatric Association, 2013).
What is the difference between mania and hypomania?
They are the same syndrome at different severities. Hypomania is milder and briefer, involves no psychotic features, and by definition does not cause marked impairment or require hospitalization, so it can even raise sociability and productivity. Mania is more severe, lasts longer, can include psychosis, and disrupts the life it inhabits. The distinction sits at the heart of the bipolar spectrum (Angst, 2007).
How is the severity of mania measured?
The standard instrument is the Young Mania Rating Scale, an eleven-item clinician-rated scale scored from 0 to 60. It rates features such as elevated mood, activity, sleep, irritability, speech, and thought content, with four items weighted more heavily. A falling score is the usual measure of response to treatment, and conventional bands separate remission, clinically significant mania, and severe mania (Young et al., 1978).
What causes mania in the brain?
The leading account frames mania as a failure of regulation. Ventral and medial prefrontal regions normally exert top-down control over limbic and striatal structures that generate emotion and reward-driven motivation; when that prefrontal control weakens, those structures are disinhibited, releasing the heightened drive, reward-seeking, and emotional reactivity of the manic state (Strakowski et al., 2012).
Does a manic episode always mean someone has bipolar disorder?
No. Mania is the defining episode of bipolar disorder, but the same syndrome can be caused by stimulant drugs, medications such as corticosteroids or antidepressants, or physical illness affecting the brain. This is called secondary mania, and the priority is to identify and treat the cause, after which the mania often resolves (Krauthammer & Klerman, 1978).
What is a mixed state in mania?
A mixed state is an episode in which the driven, accelerated activity of mania coincides with a depressive or dysphoric mood rather than an elated one. Factor-analytic studies of manic symptoms separate an elated-grandiose dimension from a dysphoric dimension, which is what allows the two to combine. Mixed states are common, dangerous, and easily mistaken for agitated depression (Cassidy et al., 1998).
How is acute mania treated?
Acute mania is treated pharmacologically, with mood stabilizers and antipsychotics as the mainstays, and their comparative efficacy and tolerability have been established by network meta-analysis. In secondary mania, the first step is to remove the offending drug or treat the underlying illness. Recognizing residual cognitive impairment after the acute episode has also become part of comprehensive care (Cipriani et al., 2011).
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