Some manic episodes develop with amazing swiftness, although onset may be gradual, lasting for months. Individuals being treated for depression may evolve quickly into mania and mania may sharply switch back to depression. The DSM requires euphoria and/or irritability to be present for there to be a diagnosis of mania. During an episode of mood disturbance, there are some listed symptoms and signs and three of them must be present to a significant degree to make a diagnosis [7].

• There is a decreased need for sleep. In mania, unlike other disorders, there is no resultant fatigue and patients feel well rested after 3 hours sleep.
• There is also increased activity as patients with mania are almost always up and about at night. This has to be apparent to others apart from the patient for it to be considered a symptom.
• There will also be racing thoughts which can be elicited during the history taking. Flight of ideas is seen commonly.
• Patients also have a short attention span and lack the ability to concentrate for a period of time. This may be attributed to the racing thoughts.
• Pressured speech is also present and patients speak rapidly and expressively.
• Delusions of grandeur may range from modest overestimation of talents to grandiose delusions where the individual has global or supernatural importance. They are often complicated by persecutory delusions.
• There is extreme involvement in pleasurable but reckless behavior. The patients, due to grandiose delusions have a false sense of invulnerability and optimism that causes this behavior. This is responsible for much of the morbidity associated with mania.

Patient should be screened for alcohol and substance abuse. Laboratory investigations like liver and renal function are also important to establish a baseline. MRI could also be done. Although its role remains unclear, some have reported that there is hyperintensity in the temporal lobes of patients with mania [8].

ECG is also required to establish a baseline as some drugs used in management have cardiovascular effects. EEG should also be done for baseline assessment before interventions like electroconvulsive therapy.

There are two goals of treatment. The first is rapid control of hyperactivity, sleeplessness, irritability and psychotic features. The second is selection of mood stabilizers.

Many patients initially refuse oral medication so parenteral antipsychotics should be used. Intramuscular zisparodone can be used. Haloperidol, the most popular of the atypical psychotics can also be used. When typical psychotics are used, their increased risk of extrapyramidal symptoms should be considered and a low dose anticholinergic agent should be given along with it to reduce this risk.

Patients on rapidly increasing doses of high potency neuroleptics should be closely monitored as there is an increased risk of neuroleptic malignant syndrome.

When patients can tolerate orally, atypical antipsychotics are preferable because their acute side effects are less problematic. Although no one drug has a clear benefit over another, rapidly dissolving form of olanzapine may be preferable to increase compliance and reducing the incidence of ‘cheeking’ of drugs [9].

The preferred and most popular mood stabilizer is lithium. Several trials have shown its prophylactic efficacy. Mood stabilizers should be introduced as soon as patient is willing to accept oral medication. Valproate is another mood stabilizer that has proven efficacy [10].

Single manic episodes usually resolve over time with or without treatment, but these single occurrences are rare. It is also rare for individuals to experience only manic episodes as many manic patients usually experience depressive phases. Most bipolar patients have more morbidity from depression than from mania [5].

There is no evidence to show a variation in course or outcome relative to age or sex. Mania developed in childhood is indicative of more long term morbidity than that developed later in life. Patients who experience discrete episodes of mania or depression have shorter, less frequent episodes than those who switch directly from one pole to the other [6].

Lastly, the presence of psychotic features portend a more long-term morbidity.

The exact cause or biochemical pathway by which mania occurs is unknown. It is a psychiatric disease but a lot of factors have been implicated in its etiology. These factors could be genetic as there is an increased risk in individuals who have first degree relatives with the condition. It could also be biochemical caused by therapeutic and recreational drugs. Other factors could be neurophysiologic, psychodynamic and environmental [2].

A manic episode differentiates bipolar 1 disorder which is said to have a lifetime prevalence of 1.6% in the US. Unlike many other mood disorders that affects more women than men, this condition affects male and female individuals equally. First age of onset is usually in the 20s. First occurrence of a manic episode in an older individual should be properly screened for underlying diseases [3].

The pathophysiology behind mania is still unclear. The mechanism of action of antimanic agents and the behavior of patients experiencing a manic episode has been used to arrive at some postulates. One of the theorems is overactivity of dopamine D2 receptors. There is also overactivity of Glycogen synthase kinase 3 as well as Protein kinase C and Inositol monophosphate. There is also increased arachnoid acid turnover and increased cytokine synthesis. Imaging studies have shown that the left amygdala is more active in women who have mania than the orbitofrontal cortex [4].

There is no known way to prevent the primary episode but prevention of secondary manic episodes requires absolute drug compliance.

It is a symptom for many different psychiatric and organic disorders, mania is often a manifestation of an underlying disease or condition. It is usually a part of the more expansive bipolar affective disorder where it alternates with depression. Mania is often analyzed collectively, whether as a single entity or part of an entity, like one end of the bipolar spectrum [1].

Definition: Mania is defined as a period of persistently and abnormally elevated, irritable or expansive mood lasting at least one week or requiring hospitalization.It hardly occurs alone and is most times followed by depression in what is known as manic depressive episodes.

Causes: There are several factors that could contribute to this condition. It could be familial as there is an increased risk if first relatives suffer from it. It could also be cause by drugs, either legal or illegal drugs. Environmental factors as well as psychological and brain lesions could cause it.

Symptoms: These includes excitement, irritability, reduced sleep time, increased activity, short attention span, elevated self-esteem, pressured speech and reckless behavior.

Diagnosis: This is done clinically and is based on the history and physical examination. Patients must fit a diagnostic criteria to be said to have mania.

Treatment: This involves the use of medications, first to control the hyperactivity, irritability and sleeplessness and then to stabilize the patient’s mood. It is important that these drugs are taken religiously to avoid a relapse.

1. Goldberg JF, Harrow M, Grossman LS. Recurrent affective syndromes in bipolar and unipolar mood disorders at follow-up. Br J Psychiatry 1995; 166:382.
2. Greenwood TA, Badner JA, Byerley W, et al. Heritability and linkage analysis of personality in bipolar disorder. J Affect Disord 2013; 151:748.
3. Duax JM, Youngstrom EA, Calabrese JR, Findling RL. Sex differences in pediatric bipolar disorder. J Clin Psychiatry. Oct 2007;68(10):1565-73.
4. Garrett A, Chang K. The role of the amygdala in bipolar disorder development. Dev Psychopathol. Fall 2008;20(4):1285-96.
5. Harrow M, Goldberg JF, Grossman LS, Meltzer HY. Outcome in manic disorders. A naturalistic follow-up study. Arch Gen Psychiatry 1990; 47:665.
6. Faraone SV, Biederman J, Wozniak J, Mundy E, Mennin D, O'Donnell D. Is comorbidity with ADHD a marker for juvenile-onset mania?. J Am Acad Child Adolesc Psychiatry. Aug 1997;36(8):1046-55. 
7. Skjelstad DV, Malt UF, Holte A. Symptoms and signs of the initial prodrome of bipolar disorder: a systematic review. J Affect Disord 2010; 126:1.
8. Arnone D, Cavanagh J, Gerber D, et al. Magnetic resonance imaging studies in bipolar disorder and schizophrenia: meta-analysis. Br J Psychiatry 2009; 195:194.
9. Singh MK, Ketter TA, Chang KD. Atypical antipsychotics for acute manic and mixed episodes in children and adolescents with bipolar disorder: efficacy and tolerability. Drugs. Mar 5 2010;70(4):433-42.
10. Bowden CL, Brugger AM, Swann AC, et al. Efficacy of divalproex vs lithium and placebo in the treatment of mania. The Depakote Mania Study Group. JAMA 1994; 271:918.