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Postpartum bipolar disease belongs to the bipolar spectrum, whose disorders exist in two contrasting forms – mania and depression. They are highly heritable,<ref>Bertelsen A, Harvald B, Hauge M (1977) A Danish twin study of manic-depressive disorders. British Journal of Psychiatry 130: 330-351.</ref> and affected individuals (less than 1% of the population <ref>Ferrari A J, Stockings E, Khoo J P, Erskine H E, Degenhardt L, Vos T, Whiteford H A (2016) The prevalence and burden of bipolar disorder: findings from the Global Burden of Disease Study 2013. Bipolar Disorders 18: 440-450.</ref>) have a lifelong tendency (diathesis) to develop psychotic episodes in certain circumstances. The 'triggers' include a number of pharmaceutical agents, surgical operations, adrenal corticosteroids, seasonal changes, menstruation and childbearing. Research into puerperal mania is, therefore, not the study of a 'disease-in-its-own right', but an investigation into the childbearing triggers of bipolar disorder.
Postpartum bipolar disease belongs to the bipolar spectrum, whose disorders exist in two contrasting forms – mania and depression. They are highly heritable,<ref name="pmid558030">{{cite journal | vauthors = Bertelsen A, Harvald B, Hauge M | title = A Danish twin study of manic-depressive disorders | journal = The British Journal of Psychiatry : the Journal of Mental Science | volume = 130 | issue = | pages = 330–51 | date = April 1977 | pmid = 558030 | doi = 10.1192/bjp.130.4.330 }}</ref> and affected individuals (less than 1% of the population<ref name="pmid27566286">{{cite journal | vauthors = Ferrari AJ, Stockings E, Khoo JP, Erskine HE, Degenhardt L, Vos T, Whiteford HA | title = The prevalence and burden of bipolar disorder: findings from the Global Burden of Disease Study 2013 | journal = Bipolar Disorders | volume = 18 | issue = 5 | pages = 440–50 | date = August 2016 | pmid = 27566286 | doi = 10.1111/bdi.12423 }}</ref>) have a lifelong tendency (diathesis) to develop psychotic episodes in certain circumstances. The 'triggers' include a number of pharmaceutical agents, surgical operations, adrenal corticosteroids, seasonal changes, menstruation and childbearing. Research into puerperal mania is, therefore, not the study of a 'disease-in-its-own right', but an investigation into the childbearing triggers of bipolar disorder.


Psychoses triggered in the first two weeks after the birth – between the first postpartum day (or even during parturition<ref name = "Brockington_2017" />{{rp|115-116}} until about the 15th day – complicate approximately 1/1,000 pregnancies.<ref name="Kendell R E 1987">Kendell R E, Chalmers J C, Platz C (1987) Epidemiology of puerperal psychoses. British Journal of Psychiatry 150: 662-673.</ref> The impression is sometimes given that this is the only trigger associated with childbearing. But there is evidence of four other triggers – late postpartum,<ref name="Brockington_2017" />{{rp|200-204}} prepartum,<ref name="Brockington_2017" />{{rp|190-195}} post-abortion<ref name="Brockington_2017" />{{rp|184-190}} and weaning.<ref name="Brockington_2017" />{{rp|204-206}} Marcé, widely considered an authority on puerperal psychoses,<ref>Marcé L V (1858) Traité de la Folie des Femmes Enceintes, des Nouvelles Accouchées et des Nourrices, et Considérations Médico-légales qui se rattachent à ce sujet. Paris, Baillière.</ref> claimed that they could be divided into early and late forms; the late form begins about six weeks after childbirth, associated with the return of the menses.<ref>Marcé L V (1862) Traité Pratique des Maladies Mentales, Paris, Baillière, pages 143-147.</ref> His view is supported by the large number of cases in the literature with onset 4–13 weeks after the birth, mothers with serial 4-13 week onsets and some survey evidence.<ref>Munk-Olsen T, Lauren T M, Petersen C B, Mors O, Mortensen P B (2006) New parents and mental disorders: a population-based study. Journal of the American Medical Association 296: 2582-2589.</ref> The evidence for a trigger acting in pregnancy is also based on the large number of reported cases, and particularly on the frequency of mothers experiencing two or more prepartum episodes. There is evidence, especially from surveys,<ref>Reardon D C, Cougle J R, Rue V M, Shuping M W, Coleman P K, Ney P G (2003) Psychiatric admissions of low-income women following abortion and childbirth. Canadian Medical Association Journal 168: 1253-1256.</ref> of bipolar episodes triggered by abortion (miscarriage or termination). The evidence for a weaning trigger rests on 32 cases in the literature, of which 14 were recurrent. The relative frequency of these five triggers is given by the number of cases in the literature – just over half early postpartum onset, 20% each late postpartum and prepartum onset, and the rest post-abortion and weaning onset.
Psychoses triggered in the first two weeks after the birth – between the first postpartum day (or even during parturition<ref name = "Brockington_2017" />{{rp|115-116}} until about the 15th day – complicate approximately 1/1,000 pregnancies.<ref name="Kendell_1987">{{cite journal | vauthors = Kendell RE, Chalmers JC, Platz C | title = Epidemiology of puerperal psychoses | journal = The British Journal of Psychiatry : the Journal of Mental Science | volume = 150 | issue = | pages = 662–73 | date = May 1987 | pmid = 3651704 | doi = 10.1192/bjp.150.5.662 }}</ref> The impression is sometimes given that this is the only trigger associated with childbearing. But there is evidence of four other triggers – late postpartum,<ref name="Brockington_2017" />{{rp|200-204}} prepartum,<ref name="Brockington_2017" />{{rp|190-195}} post-abortion<ref name="Brockington_2017" />{{rp|184-190}} and weaning.<ref name="Brockington_2017" />{{rp|204-206}} Marcé, widely considered an authority on puerperal psychoses,<ref>{{cite book | vauthors = Marcé LV | date = 1858 | title = Traité de la Folie des Femmes Enceintes, des Nouvelles Accouchées et des Nourrices, et Considérations Médico-légales qui se rattachent à ce sujet. | location = Paris | publisher = Baillière }}</ref> claimed that they could be divided into early and late forms; the late form begins about six weeks after childbirth, associated with the return of the menses.<ref>{{cite book | vauthors = Marcé LV | date = 1862 | title = Traité Pratique des Maladies Mentales | location = Paris | publisher = Baillière | pages = 143-147 }}</ref> His view is supported by the large number of cases in the literature with onset 4–13 weeks after the birth, mothers with serial 4-13 week onsets and some survey evidence.<ref name="pmid17148723">{{cite journal | vauthors = Munk-Olsen T, Laursen TM, Pedersen CB, Mors O, Mortensen PB | title = New parents and mental disorders: a population-based register study | journal = Jama | volume = 296 | issue = 21 | pages = 2582–9 | date = December 2006 | pmid = 17148723 | doi = 10.1001/jama.296.21.2582 }}</ref> The evidence for a trigger acting in pregnancy is also based on the large number of reported cases, and particularly on the frequency of mothers experiencing two or more prepartum episodes. There is evidence, especially from surveys,<ref name="pmid12743066">{{cite journal | vauthors = Reardon DC, Cougle JR, Rue VM, Shuping MW, Coleman PK, Ney PG | title = Psychiatric admissions of low-income women following abortion and childbirth | journal = CMAJ : Canadian Medical Association Journal = Journal De l'Association Medicale Canadienne | volume = 168 | issue = 10 | pages = 1253–6 | date = May 2003 | pmid = 12743066 | pmc = 154179 | doi = }}</ref> of bipolar episodes triggered by abortion (miscarriage or termination). The evidence for a weaning trigger rests on 32 cases in the literature, of which 14 were recurrent. The relative frequency of these five triggers is given by the number of cases in the literature – just over half early postpartum onset, 20% each late postpartum and prepartum onset, and the rest post-abortion and weaning onset.


In addition, episodes starting after childbirth may be triggered by adrenal corticosteroids, surgical operations (such as Caesarean section) or bromocriptine as an alternative to, or in addition to, the postpartum trigger.<ref>Brockington I F (2017) Non-reproductive triggers of postpartum psychosis. Archives of Women's Mental Health 20: 55-59.</ref>
In addition, episodes starting after childbirth may be triggered by adrenal corticosteroids, surgical operations (such as Caesarean section) or bromocriptine as an alternative to, or in addition to, the postpartum trigger.<ref name="pmid27722949">{{cite journal | vauthors = Brockington I | title = Non-reproductive triggers of postpartum psychosis | journal = Archives of Women's Mental Health | volume = 20 | issue = 1 | pages = 55–59 | date = February 2017 | pmid = 27722949 | pmc = 5237449 | doi = 10.1007/s00737-016-0674-9 }}</ref>


===Course of the illness===
===Course of the illness===

Revision as of 21:20, 20 January 2023

Postpartum psychosis
Other namespuerperal psychosis
Rates of psychoses among Swedish first-time mothers
SpecialtyPsychiatry Edit this on Wikidata
SymptomsHallucinations, delusions, mood swings, confusion, restlessness, personality changes[1]
CausesGenetic and environmental
Risk factorsFamily history, bipolar disorder, schizophrenia, difficult pregnancy[1]
TreatmentAnti-psychotics, mood stabilizers , anti-depressants

Postpartum psychosis (PPP), also known as puerperal psychosis or peripartum psychosis, involves the abrupt onset of psychotic symptoms shortly following childbirth, typically within two weeks of delivery but less than 4 weeks postpartum.[2] PPP is a condition currently represented under "Brief Psychotic Disorder" in the Diagnostic and Statistical Manual of Mental Disorders, Volume V (DSM-V).[3] Symptoms may include delusions, hallucinations, disorganized speech (e.g, incoherent speech), and/or abnormal motor behavior (e.g., catatonia).[3] Other symptoms frequently associated with PPP include confusion, disorganized thought, severe difficulty sleeping, variations of mood disorders (including depression, agitation, mania, or a combination of the above), as well as cognitive features such as consciousness that comes and goes (waxing and waning) or disorientation.[2][4]

The cause of PPP is currently unknown, though growing evidence for the broad category of postpartum psychiatric disorders (e.g., postpartum depression) suggests hormonal and immune changes as potential factors contributing to their onset,[5] as well as genetics and circadian rhythm disruption.[6] There is no agreement in the evidence about risk factors, though a number of studies have suggested that sleep loss, first pregnancies (primiparity), and previous episodes of PPP may play a role.[2] More recent reviews have added to growing evidence that prior psychiatric diagnoses, especially bipolar disorder, in the individual or their families may raise the risk of a new-onset psychosis triggered by childbirth.[2][6][7][8] There are currently no screening or assessment tools available to diagnose PPP; a diagnosis must be made by the attending physician based on the patient's presenting symptoms, guided by diagnostic criteria in the DSM-V (see Diagnosis).[2][6]

While PPP is only seen in every 1 to 2 of 1000 childbirths,[2][4] the rapid development of psychotic symptoms, particularly those that include delusions of misidentification or paranoia,[9] raise concerns for the safety of the patient and the infant; thus, PPP is considered a psychiatric emergency, usually requiring urgent hospitalization.[2][4][6] Treatment may include medications such as benzodiazepines, lithium, and antipsychotics, as well as procedures such as electroconvulsive therapy (ECT).[2][4][6] In some cases where pregnant persons have a known history of bipolar disorder or previous episodes of PPP, prophylactic use of medication (especially lithium) either throughout or immediately after delivery has been demonstrated to reduce the incidence of psychotic or bipolar episodes in the postpartum period.[2][4][6]

PPP is not an independently recognized diagnosis in the DSM-V; instead, the specifier "with peripartum onset" is used for both "Brief psychotic disorder" and "Unspecified bipolar and related disorders."[3] Recent literature suggests that, more frequently, this syndrome occurs in the context of known or new-onset bipolar illness (see Postpartum Bipolar Disorder).[6]

Clinical Presentation

By diagnostic definition (Brief psychotic disorder with peripartum onset), PPP occurs either during pregnancy or within 4 weeks of delivering the infant.[3] Generally, PPP symptoms have been observed within 3-10 days of childbirth, though individuals with a past history of bipolar disorder may experience symptoms even sooner.[2][6] The persistence of symptoms varies; while the average reported length of an episode may last weeks to several months,[6] there is currently no strong literature documenting the course of individual episodes. Recurrence rates for psychotic episodes, on the other hand, have stronger supporting studies and are covered in more detail below (see Prognosis and Outcomes).

Depression, as well as other mood symptoms like mania and irritability, is a relatively common feature of postpartum psychosis.

Diagnostic criteria per the DSM-V requires the presence of at least one psychotic symptom, defined as delusions, hallucinations, bizarre or incoherent speech (disorganized speech), or abnormal movements (psychomotor behavior), such as catatonia.[3] Delusions, particularly about the infant, are the most commonly reported psychotic symptom associated with PPP.[4][6][8] Paranoid delusions are a frequently noted theme in cases of PPP,[4][10] but a small review noted infrequent cases of delusional misidentification syndromes, such as Capgras syndrome (the belief that someone or something familiar has been replaced with an imposter), Fregoli syndrome (the belief that a stranger is actually a known person in disguise), and others.[9] The latter types of delusions may have a significant negative impact on the bond between a mother and child, raising concerns for the safety of both (see Prognosis and Outcomes).[9][11] Both postpartum obsessive-compulsive disorder (OCD) and PPP may present with concerning thoughts about the infant: typically, the thoughts associated with OCD are unwanted and distressing to the individual (who does not wish to act on their thoughts) where persons with PPP are often not as distressed by their beliefs and may even feel the need to act on their beliefs.[2][4][12] Delusions associated with PPP tend to be less bizarre than those more frequently seen in patients with schizophrenia, and hallucinations, when present, tend to be more visual than auditory (compared to schizophrenia which is often associated with auditory hallucinations).[6] The sensation of being outside one's body or feeling that your surroundings are unreal (i.e., derealization) has also been described in cases of PPP.[2]

Additional distinctions in PPP compared to classical schizophrenia include the presence of mood and cognitive (or neurological) symptoms.[2][6] Rapid mood changes or the presence of abnormal moods such as depression or mania (increased energy, decreased need for sleep, etc.) tend to be seen in a large percentage of patients experiencing PPP.[2][4][6] Irritability, anxiety, and general difficulties with sleep may also be present.[6] Confusion or disorientation, disorganized thoughts, incoherent speech, or abrupt changes in a person's mental capacity may also be seen in individuals experiencing PPP,[4][6] though one small study observed these neurological symptoms in only one-quarter of PPP cases.[6][13] Like delirium, these symptoms may come and go in unpredictable patterns.[6]

Thoughts of committing suicide or harming one's infant or children have also been reported as common occurrences in PPP, with as many as half of PPP cases exhibiting these features.[2][6] In many cases where harmful thoughts exist, the person experiencing these thoughts does not consider their intended action to be harmful; rather, they believe that their actions are in the best interest of the child.[4][6]

In addition to the rapid onset of symptoms (less than two weeks) with the presence of a psychotic symptom, further diagnostic criteria defined by the DSM-V for "brief psychotic disorder with peripartum onset" includes that the symptomatic episode ends within one month and involves a return to the individual's previous functional ability, as well as confidence that the episode is not a different psychiatric illness (e.g., depressive or bipolar disorder with psychotic features) or the result of substance-induced psychosis.[3]

Risk Factors

Childbirth is the leading cause of PPP, while other causes and risk factors remain largely under investigation.[6]

The largest reported risks for the occurrence of PPP include a prior history of having a postpartum psychotic episode, as well as having a known history of bipolar disorder (whether personally or within one's family history).[2][6] A significant number of PPP cases, however, represent the first time an individual may experience any psychotic episode in their life;[6][14] therefore, an individual may have no risk factors prior to developing PPP (though some may consider a first-time pregnancy to be the associated risk factor).[2][4][6] A review of pregnancy-related complications demonstrated some association between emergency caesarean sections (C-sections), excess bleeding, uterine rupture, and stillbirth (amongst other complications) and the subsequent development of PPP; however, several of the reviewed studies were contradictory and thus no consensus can confirm the relationship between problems related to pregnancy and PPP.[6][7]

Lifestyle and psychological factors, such as previous trauma or single parenthood, have likewise been inconclusive as factors contributing to PPP,[8] though reports from several of the patients who suffered from PPP suggest a perception that social and pregnancy-related challenges were the cause of their episodes.[8][15]

Pathophysiology

Currently, the pathophysiology of PPP is not well understood and remains an open field of ongoing research. The leading theories under investigation involve areas of genetics, hormones, immunology, and sleep disturbance processes.[6]

Genetics

The majority of research devoted to genetic understanding of PPP has evaluated patients who have known bipolar disorder, therefore findings uncovering variation in serotonin transporter genes and signaling or changes at specific chromosomes (e.g., 16p13 or METTL13) are not necessarily precise to PPP generally.[6][10][16][17][18][19]

Hormones

Despite significant hormone changes that occur around pregnancy and childbirth, there is little evidence supporting hormonal causes behind PPP.[6][10] Changes in corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH), as well as rapid changes in estrogen and progesterone, are known effects associated with delivering a child, and they are present in both those affected and unaffected by PPP; therefore, the relationship between hormonal change and the onset of psychosis is not well-supported,[6][10] though some researchers continue to explore potential differences in sensitivity to rapid hormone change as it relates to postpartum disorders such as postpartum depression.[20] Estrogen has known impacts on various neurotransmitters (e.g., glutamate, GABA, serotonin and dopamine), including the increase of dopamine synthesis along with its receptors.[21] The predominant theories surrounding psychosis include dysfunction in serotonin and/or dopamine systems,[22] thus strong interest was placed in the association between estrogen changes and PPP onset; however, investigations of estrogen concentrations, dopamine receptor sensitivity, and trials of estrogen replacement following birth currently do not lend support for this theory.[10]

Immune System Alteration

The theory between immune system changes and associated PPP onset has been largely spurred by higher than average occurrences of PPP in individuals also experiencing immunologic complications, such as anti-N-methyl-D-aspartate (NMDA) receptor encephalitis and autoimmune thyroid disorders,[5][6] as well as the onset of PPP occurring at the same time the body is experiencing higher immune responses (a natural process associated with the period immediately following childbirth).[6][23] There is some evidence connecting PPP with changes to levels of peripheral immune cells (e.g., lymphocytes and NK or natural killer cells) traveling in the bloodstream, but more research is required to identify the specific mechanisms and cell types involved which might be related to PPP onset.[5] No direct evidence has shown a link between cytokine levels and PPP.[5]

Sleep Disturbance

The link between sleep difficulty and PPP is not strongly supported by current evidence; however, some studies have demonstrated an increased risk for postpartum psychosis in women with bipolar disorder who have had manic episodes triggered by sleep disturbance.[6][24]

Diagnosis and Screening

Diagnosis

There are no tests designed to diagnose postpartum psychosis. A complete blood count, pictured above, may be part of the initial work-up to rule out other organic causes of psychotic symptoms.

Not recognized as its own distinct disorder, PPP is instead classified by the DSM-V as a "Brief Psychotic Disorder with peripartum onset."[3][6] Clinical requirements for the diagnosis of a brief psychotic disorder require the presence of at least one of the following psychotic symptoms: delusions, hallucinations, disorganized speech, and/or grossly disorganized or catatonic behavior.[3] Additional requirements include that the psychotic symptom lasts between one day and one month, eventually resulting in the person recovering their previous level of functional ability, and that the symptoms are not better related to a different psychiatric illness (including the result of ingesting substances such as alcohol or drugs).[3] The specifier, "with peripartum onset," requires the development of the above within 4 weeks of delivering a child.[3]

There are no laboratory or imaging tools available to diagnose PPP, though a work-up of different laboratory analyses and imaging of the brain may be conducted to ensure other potential confounding diagnoses (e.g., vascular disorders, infective delirium, etc.) are not the cause of the patient's presentation (see Differential, Other non-organic postpartum psychoses, and Organic postpartum psychoses).[6] These may include, but are not limited to, a complete blood count, comprehensive metabolic panel, urinalysis and urine drug screen, and tests for thyroid functioning; further workup in the setting of classically neurological symptoms (such as delirium-like confusion) may include magnetic resonance imaging (MRI), a test of cerebrospinal fluid (CSF), or electroencephalogram (EEG).[6]

Screening

Currently, no screening tools exist to evaluate for PPP, though providers may choose to use standard screens for postpartum depression and mania to evaluate the presence of these particular symptoms.[6]

Due to the presence of several symptoms that are classically associated with other postpartum conditions, such as postpartum blues or depression, and often benign changes that accompany new parenthood (anxiety, irritability, poor sleep), recognition of postpartum psychosis may be difficult for providers and family-members to identify[4][6]; thus, it is recommended that providers directly address thoughts of harm for both the patient and child.[2]

Differential

The presentation of PPP includes a large differential overlapping neurological and psychiatric diseases and syndromes. Neurological, or cognitive, symptoms like disorientation and confusion raise concerns for conditions that organically affect the brain: this may include autoimmune processes resulting in various forms of encephalitis, embolism (and other vascular disorders), and infectious processes.[3][6] Physical causes as a result of chronic hormonal disease (e.g., thyroid diseases, hyperparathyroidism) or complications resulting from childbirth, such as Sheehan's syndrome or other complications resulting from excess blood loss, should also be evaluated.[4][6] Other psychiatric conditions must also be considered: postpartum blues, postpartum depression, anxiety disorders, and postpartum OCD may have many overlapping symptoms with PPP.[6] Finally, psychosis as a result of various substances (including medications such as steroids), should be ruled out.[6] If this is a first-onset episode of psychosis, new-onset bipolar disorder and schizophrenia cannot be ruled out; the diagnosis of these disorders is based on time and recurrence of episodes.[3]

Prognosis and Outcomes

Symptoms may last for a variable length of time (up to one year in 25% of cases) despite adequate treatment.[6] Despite most individuals (50-80%) experiencing a relapse episode and development of chronic psychiatric disorders (such as bipolar spectrum disorder), these same individuals are expected to be able to resume normal activities of their daily life with the same level of function as previously experienced.[6][25] Of the minority of persons who experience PPP and choose to have another pregnancy, evidence has shown that about 33% will have a repeat psychotic episode.[6][14] Other factors that contribute to poorer prognosis include an experience of PPP that's limited to the postpartum period (rather than a diagnosis of bipolar disorder, for example), longer initial psychotic episodes, and a higher severity in the initial episode.[6][14]

Infanticide (or filicide) is thought to occur in 1 to 4% of PPP cases,[2][4][6][26] and some evidence suggests that these incidents are more commonly related to PPP episodes that feature more depressive symptoms.[26]

Postpartum bipolar disorder

Signs and symptoms

Almost every symptom known to psychiatry occurs in these mothers – every kind of delusion including the rare delusional parasitosis,[27] delusional misidentification syndrome,[28] Cotard delusion,[29] erotomania,[30] the changeling delusion,[31] denial of pregnancy or birth,[32] command hallucinations,[33] disorders of the will and self,[34] catalepsy and other symptoms of catatonia,[35] self-mutilation[36] and all the severe disturbances of mood. In addition, literature from the 18th century also describes symptoms not generally recognized, such as rhyming speech,[37] enhanced intellect,[38] and enhanced perception.[39]

As for collections of symptoms (syndromes), about 40% have puerperal mania,[40][41]: 217  with increased vitality and sociability, reduced need for sleep, rapid thinking and pressured speech, euphoria and irritability, loss of inhibition, violence, recklessness and grandiosity (including religious and expansive delusions); puerperal mania is considered to be particularly severe, with highly disorganized speech, extreme excitement and eroticism.[41]: 212–213 

Another 25% have an acute polymorphic (cycloid) syndrome. This is a changing clinical state, with transient delusions, fragments of other syndromes, extreme fear or ecstasy, perplexity, confusion, and motility disturbances. In the past, some experts regarded this as pathognomonic (specific) for puerperal psychosis, but this syndrome is found in other settings, not just the reproductive process, and in men. These psychoses are placed in the World Health Organization's ICD-10 under the rubric of acute and transient psychotic disorders.[42] In general psychiatry, manic and cycloid syndromes are regarded as distinct, but, studied long-term among childbearing women, the bipolar and cycloid variants are intermingled in a bewildering variety of combinations, and, in this context, it seems best to regard them as members of the same 'bipolar/cycloid' group. Together, the manic and cycloid variants make up about two thirds of childbearing psychoses.[43]: 177 

Diagnosis

Postpartum bipolar disorders must be distinguished from a long list of organic psychoses that can present in the puerperium, and from other non-organic psychoses; both of these groups are described below. It is also necessary to distinguish them from other psychiatric disorders associated with childbirth, such as anxiety disorders, depression, post-traumatic stress disorder, complaining disorders and bonding disorders (emotional rejection of the infant), which occasionally cause diagnostic difficulties.

Clinical assessment requires obtaining the history from the mother herself and, because she is often severely ill, lacking in insight and unable to give a clear account of events, from at least one close relative. A social work report and, in mothers admitted to hospital, nursing observations are information sources of great value. A physical examination and laboratory investigations may disclose somatic illness complicating the obstetric events, which sometimes provokes psychosis. It is important to obtain the case records of previous episodes of mental illness, and, in patients with multiple episodes, to construct a summary of the whole course of her psychiatric history in relation to her life.

In the 10th edition of the International Classification of Diseases, published in 1992, the recommendation is to classify these cases by the form of the illness, without highlighting the postpartum state. There is, however, a category F53.1, entitled 'severe mental and behavioural disorders associated with the puerperium', which can be used when it is not possible to diagnose some variety of affective disorder or schizophrenia. The American Psychiatric Association's Diagnostic and Statistical Manual, whose 5th edition was published in May 2013, allows the use of a 'peripartum onset specifier' in episodes of mania, hypomania or major depression if the symptoms occur during pregnancy or the first four weeks of the puerperium. The failure to recognize postpartum psychosis, and its complexity, is unhelpful to clinicians, epidemiologists, and other researchers.[43]Template:Rp 166

Onset groups

Postpartum bipolar disease belongs to the bipolar spectrum, whose disorders exist in two contrasting forms – mania and depression. They are highly heritable,[44] and affected individuals (less than 1% of the population[45]) have a lifelong tendency (diathesis) to develop psychotic episodes in certain circumstances. The 'triggers' include a number of pharmaceutical agents, surgical operations, adrenal corticosteroids, seasonal changes, menstruation and childbearing. Research into puerperal mania is, therefore, not the study of a 'disease-in-its-own right', but an investigation into the childbearing triggers of bipolar disorder.

Psychoses triggered in the first two weeks after the birth – between the first postpartum day (or even during parturition[43]: 115–116  until about the 15th day – complicate approximately 1/1,000 pregnancies.[46] The impression is sometimes given that this is the only trigger associated with childbearing. But there is evidence of four other triggers – late postpartum,[43]: 200–204  prepartum,[43]: 190–195  post-abortion[43]: 184–190  and weaning.[43]: 204–206  Marcé, widely considered an authority on puerperal psychoses,[47] claimed that they could be divided into early and late forms; the late form begins about six weeks after childbirth, associated with the return of the menses.[48] His view is supported by the large number of cases in the literature with onset 4–13 weeks after the birth, mothers with serial 4-13 week onsets and some survey evidence.[49] The evidence for a trigger acting in pregnancy is also based on the large number of reported cases, and particularly on the frequency of mothers experiencing two or more prepartum episodes. There is evidence, especially from surveys,[50] of bipolar episodes triggered by abortion (miscarriage or termination). The evidence for a weaning trigger rests on 32 cases in the literature, of which 14 were recurrent. The relative frequency of these five triggers is given by the number of cases in the literature – just over half early postpartum onset, 20% each late postpartum and prepartum onset, and the rest post-abortion and weaning onset.

In addition, episodes starting after childbirth may be triggered by adrenal corticosteroids, surgical operations (such as Caesarean section) or bromocriptine as an alternative to, or in addition to, the postpartum trigger.[51]

Course of the illness

With modern treatment, a full recovery can be expected within 6–10 weeks.[52]: 38 [43]: 214  After recovery from the psychosis, some mothers have depression, which can last for weeks or months. About one third have a relapse, with a return of psychotic symptoms a few weeks after recovery; these relapses are not due to a failure to comply with medication, because they were often described [53] before pharmaceutical treatment was discovered.[54] A minority have a series of periodic relapses related to the menstrual cycle.[43]: 214  Complete recovery, with a resumption of normal life and a normal mother-infant relationship is the rule.[52]: 23 

Many of these mothers experience other bipolar episodes, on the average about one every six years. Although suicide is almost unknown in an acute puerperal manic or cycloid episode, depressive episodes later in life carry an increased risk,[55][56] and it is wise for mothers to maintain contact with psychiatric services in the long term.

In the event of a further pregnancy, the recurrence rate is high – in the largest series, about three quarters had a recurrence, but not always in the early puerperium; the recurrence could occur during pregnancy, or later in the postpartum period.[43]: 214–215  This suggests a link between early onset and other onset groups.

Management, treatment and prevention

Pre-conception counselling

It is known that women with a personal or family history[57][58][59] of puerperal psychosis or bipolar disorder are at risk of a puerperal episode. The highest risk of all (82%) is a combination of a previous postpartum episode and at least one earlier non-puerperal episode.[43]: 274  There is a need to counsel women at high risk before they embark on pregnancy, especially those on prophylactic treatment. The issues include the teratogenic risk, the frequency of recurrence and the risks and benefit of various treatments during pregnancy and breast-feeding; a personal analysis should be made for each individual,[60] and is best shared with close family members. The teratogenic risks of antipsychotic agents are small,[61] but are higher with lithium[43]: 231–232  and anti-convulsant agents. Carbamazepine, when taken in early pregnancy, has some teratogenic effects,[62] but valproate is associated with spina bifida and other major malformations, and a foetal valproate syndrome;[63] it is contra-indicated in women who may become pregnant. Given late in pregnancy, antipsychotic agents and lithium[43]: 230–232  can have adverse effects on the infant. Stopping mood-stabilisers has a high risk of recurrence during pregnancy.[64]

Pre-birth planning

If a woman at high risk becomes pregnant, it is essential to convene a planning meeting. This is urgent because the diagnosis of pregnancy may be late, and the birth may be premature. The meeting should be attended by primary care, obstetric and psychiatric staff, together (if possible) with the expectant mother and her family and (if appropriate) a social worker. There are many issues – pharmaceutical treatment, antenatal care, early signs of a recurrence, the management of the puerperium, and the care and safety of the infant. It is important that the psychiatric team is notified as soon as the infant is born.

Home treatment and hospitalization

It has been recognized since the 19th century[65] that it is optimal for a woman with puerperal psychosis to be treated at home, where she can maintain her role as homemaker and mother to her other children, and develop her relationship with the new-born. But there are many risks,[66] and it is essential that she is monitored by a competent adult round the clock, and visited frequently by professional staff. Home treatment is a counsel of perfection and most women will be admitted to a psychiatric hospital, many as an emergency, and usually without their babies. In a few countries, especially Australia, Belgium, France, India, the Netherlands, Switzerland and the United Kingdom, special units allow the admission of both woman and infant. Conjoint admission has many advantages, but the risks to the infant of admission to a ward full of severely ill mothers should not be understated,[67][41]: 556–558  and the high ratio of nursing staff, required to safeguard the infants, make these among the most expensive psychiatric units.

Treatment of the acute episode

These mothers require sedation with anti-psychotic (neuroleptic) agents, but are liable to extrapyramidal symptoms,[43]: 228  including the neuroleptic malignant syndrome.[68] Since the link with bipolar disorder was recognized (about 1970), treatment with mood-stabilizing agents, such as lithium[52]: 20–23  and anti-convulsant drugs, has been employed with success. Electroconvulsive therapy has the reputation of efficacy in this disorder,[69] and it can be given during pregnancy (avoiding the risk of pharmaceutical treatment), with due precautions.[70] But there have been no trials, and Dutch experience has shown that almost all mothers recover quickly without it.[52]: 22  After recovery the mother may need antidepressant treatment and/or prophylactic mood stabilizers; she will need counselling about the risk of recurrence and will often appreciate psychotherapeutic support.[60]

Prevention

There is much evidence that lithium can at least partly prevent episodes in mothers at high risk.[52]: 45–59  It is dangerous during parturition, when pressure in the pelvis can obstruct the ureters and raise blood levels.[43]: 233–234  Started after the birth its adverse effects are minimal, even in breast-fed infants.[71]


Causes

The cause of postpartum bipolar disorder breaks down into two parts – the nature of the brain anomalies that predispose to manic and depressive symptoms, and the triggers that provoke these symptoms in those with the bipolar diathesis. The genetic, anatomical and neurochemical basis of bipolar disorder is at present unknown, and is one of the most important projects in psychiatry; but is not the main concern here. The challenge and opportunity presented by the childbearing psychoses is to identify the triggers of early postpartum onset and other onset groups.

Considering that these psychoses have been known for centuries, little effort has so far been made to understand the underlying biology.[72] Research has lagged far behind other areas of medicine and psychiatry.[73] There is a dearth of knowledge and of theories. There is a much evidence of heritability, both from family studies[69][55][57] and molecular genetics.[74] Early onset cases occur more frequently in first time mothers,[75] but this is not true of late postpartum or pregnancy onset. There are not many other predictors. Sleep deprivation has been suggested.[76] Inhibition of steroid sulphatase caused behavioural abnormalities in mice.[77] A recent hypothesis,[52]: 75–82  supported by collateral studies, invokes the re-awakening of auto-immunity after its suppression during pregnancy, on the model of multiple sclerosis or autoimmune thyroiditis; a related hypothesis has proposed that abnormal immune system processes (regulatory T cell biology) and consequent changes in myelinogenesis may increase postpartum psychosis risk.[78] Aberrant steroid hormone–dependent regulation of neuronal calcium influx via extracellular matrix proteins and membrane receptors involved in responding to the cell's microenvironment might be important in conferring biological risk.[79] Another promising lead is based on the similarity of bipolar-cycloid puerperal and menstrual psychosis; many women have had both. Late-onset puerperal psychoses, and relapses may be linked to menstruation. Since almost all reproductive onsets occur when the menstrual cycle is released from a long period of inhibition, this may be a common factor, but it can hardly explain episodes starting in the 2nd and 3rd trimesters of pregnancy.[43]: 320–330 

History

Between the 16th and 18th centuries about 50 brief reports were published; among them is the observation that these psychoses could recur,[80] and that they occur both in breast-feeding and non-lactating women.[81] In 1797, Osiander,[82] an obstetrician from Tübingen, reported two cases at length – masterly descriptions which are among the treasures of medical literature. In 1819, Esquirol [83] conducted a survey of cases admitted to the Salpêtrière, and pioneered long-term studies. From that time, puerperal psychosis became widely known to the medical profession. In the next 200 years over 2,500 theses, articles and books were published. Among the outstanding contributions were Delay's unique investigation using serial curettage [84] and Kendell's record-linkage study comparing 8 trimesters before and 8 trimesters after the birth.[75] In the last few years, two monographs[85][43]: 1–278 Cite error: A <ref> tag is missing the closing </ref> (see the help page). The psychotic symptom is usually a delusion. Over 50 cases have been described, but usually in unusual circumstances, such as abortion[86] or adoption,[87] or in fathers at the time of the birth of one of their children.[88] They are occasionally seen after normal childbirth.[43]: 169–171 

Paranoid and schizophrenic psychoses

These are so uncommon in the puerperium that it seems reasonable to regard them as sporadic events, not puerperal complications.

Early postpartum stupor

Brief states of stupor have rarely been described in the first few hours or days after the birth.[43]: 119–122 Cite error: A <ref> tag is missing the closing </ref> (see the help page). and 2010,[89] and it is quite likely that others will be described. Organic psychoses, especially those due to infection, may be more common in nations with high parturient morbidity.[90]

Infective delirium

The most common organic postpartum psychosis is infective delirium. This was mentioned by Hippocrates:[91] there are 8 cases of puerperal or post-abortion sepsis among the 17 women in the 1st and 3rd books of epidemics, all complicated by delirium. In Europe and North America the foundation of the metropolitan maternity hospitals, together with instrumental deliveries and the practice of attending necropsies, led to epidemics of streptococcal puerperal fever, resulting in maternal mortality rates up to 10%. The peak was about 1870, after which antisepsis and asepsis gradually brought them under control. These severe infections were often complicated by delirium, but it was not until the nosological advances of Chaslin[92] and Bonhöffer[93] that they could be distinguished from other causes of postpartum psychosis. Infective delirium hardly ever starts during pregnancy, and usually begins in the first postpartum week. The onset of sepsis and delirium are closely related, and the course parallels the infection, although about 20% of patients continue to have chronic confusional states after recovery from the infection. Recurrences after another pregnancy are rare. Their frequency began to decline at the end of the 19th century,[94] and fell steeply after the discovery of the sulphonamides. Puerperal sepsis is still common in Bangladesh,[95] Nigeria[96] and Zambia.[97] Even in the United Kingdom, cases are still occasionally seen.[43]: 27  It would be a mistake to forget this cause of puerperal psychosis.

Eclamptic and Donkin psychoses

Eclampsia is the sudden eruption of convulsions in a pregnant woman, usually around the time of delivery. It is the late complication of pre-eclamptic toxaemia (gestosis). Although its frequency in nations with excellent obstetric services has fallen below 1/500 pregnancies, it is still common in many other countries. The primary pathology is in the placenta, which secretes an anti-angiogenic factor in response to ischaemia, leading to endothelial dysfunction.[98][99] In fatal cases, there are arterial lesions in many organs including the brain. This is the second most frequent organic psychosis, and the second to be described.[100] Psychoses occur in about 5% of cases, and about 240 detailed cases have been reported.[43]: 28–35  It particularly affects first time mothers. Seizures may begin before, during or after labour, but the onset of psychosis is almost always postpartum. These mothers usually experience delirium but some have manic features. The duration is remarkably short, with a median duration of 8 days. This, together with the absence of a family history and of recurrences, contrasts with puerperal bipolar/cycloid psychoses. After recovery, amnesia and sometimes retrograde memory loss may occur, as well as other permanent cerebral lesions such as dysphasia, hemiplegia or blindness.

A variant was described by Donkin .[101] He had been trained by Simpson (one of those who first recognized the importance of albuminuria) in Edinburgh, and recognized that some cases of eclamptic psychosis occurred without seizures; this explains the interval between seizures (or coma) and psychosis, a gap that has occasionally exceeded 4 days: seizures and psychosis are two different consequences of severe gestosis. Donkin psychosis may not be rare: a British series included 13 possible cases;[43]: 35  but clarifying its distinction from postpartum bipolar disorder requires prospective investigations in collaboration with obstetricians.

Wernicke-Korsakoff psychosis

This was described by Wernicke[102] and Korsakoff.[103] The pathology is damage to the core of the brain including the thalamus and mamillary bodies. Its most striking clinical feature is loss of memory, which can be permanent. It is usually found in severe alcoholics, but can also result from pernicious vomiting of pregnancy (hyperemesis gravidarum), because the requirement for thiamine is much increased in pregnancy; nearly 200 cases have been reported.[43]: 36–41  The cause is vitamin B1 (thiamine) deficiency. This has been available for treatment and prevention since 1936,[104] so the occurrence of this syndrome in pregnancy should be extinct. But these cases continue to be reported – more than 50 in this century – from all over the world, including some from countries with advanced medical services;[105] most are due to rehydration without vitamin supplements. A pregnant woman who presents in a dehydrated state due to pernicious vomiting urgently needs thiamine, as well as intravenous fluids.

Vascular disorders

Various vascular disorders occasionally cause psychosis, especially cerebral venous thrombosis. Puerperal women are liable to thrombosis, especially thrombophlebitis of the leg and pelvic veins; aseptic thrombi can also form in the dural venous sinuses and the cerebral veins draining into them. Most patients present with headache, vomiting, seizures and focal signs such as hemiplegia or dysphasia, but a minority of cases have a psychiatric presentation.[106] The incidence is about 1 in 1,000 births in Europe and North America,[107] but much higher in India, where large series have been collected.[108] Psychosis is occasionally associated with other arterial or venous lesions: epidural anaesthesia can, if the dura is punctured, lead to leakage of cerebrospinal fluid and subdural haematoma.[109] Arterial occlusion may be due to thrombi, amniotic fragments or air embolism. Postpartum cerebral angiopathy is a transitory arterial spasm of medium caliber cerebral arteries; it was first described in cocaine and amphetamine addicts, but can also complicate ergot and bromocriptine prescribed to inhibit lactation. Subarachnoid haemorrhage can occur after miscarriage or childbirth. All these usually present with neurological symptoms, and occasionally with delirium.

Epilepsy

Women with a lifelong epileptic history are liable to psychoses during pregnancy, labour and the puerperium. Women occasionally develop epilepsy for the first time in relation to their first pregnancy, and psychotic episodes have been described. There are over 30 cases in the literature.[43]: 56–58 

Hypopituitarism

Pituitary necrosis following postpartum haemorrhage (Sheehan's syndrome) leads to failure and atrophy of the gonads, adrenal and thyroid. Chronic psychoses can supervene many years later, based on myxoedema, hypoglycaemia or Addisonian crisis. But these patients can also develop acute and recurrent psychoses, even as early as the puerperium.[110][43]: 59–62 

Water intoxication

Hyponatraemia (which leads to delirium) can complicate oxytocin treatment, usually when given to induce an abortion. By 1975, 29 cases had been reported, of which three were severe or fatal.[111]

Urea cycle disorders

Inborn errors of the Krebs-Henseleit urea cycle lead to hyperammonaemia. In carriers and heterozygotes, encephalopathy can develop in pregnancy or the puerperium. Cases have been described in carbamoyl phosphate synthetase 1, argino-succinate synthetase and ornithine carbamoyltransferase deficiency.[43]: 63–65 

Anti-NMDA receptor encephalitis

The most recent form of organic childbearing psychosis to be described is encephalitis associated with antibodies to the NMDA receptor; these women often have ovarian teratomas. A Japanese review found ten reported during pregnancy and five after delivery.[112]

Other organic psychoses with a specific link to childbearing

Sydenham's chorea, of which chorea gravidarum is a severe variant, has a number of psychiatric complications, which include psychosis. This usually develops during pregnancy, and occasionally after the birth or abortion. Its symptoms include severe hypnagogic hallucinations (hypnagogia),[113][114] possibly the result of the extreme sleep disorder. This form of chorea was caused by streptococcal infections, which at present respond to antibiotics; it still occurs as a result of systemic lupus or anti-phospholipid syndromes. Only about 50 chorea psychoses have been reported, and only one this century; but it could return if the streptococcus escapes control. Alcohol withdrawal states (delirium tremens) occur in addicts whose intake has been interrupted by trauma or surgery; this can happen after childbirth. Postpartum confusional states have also been reported during withdrawal from opium[115] and barbiturates.[116] One would expect acquired immunodeficiency syndrome (HIV/AIDS) encephalitis to present in pregnancy or the puerperium, because it is a venereal disease that can progress rapidly; one case of AIDS encephalitis, presenting in the 28th week of gestation, has been reported from Haiti,[117] and there may be others in countries where AIDS is rife. Anaemia is common in pregnancy and the puerperium, and folate deficiency has been linked to psychosis.[118]

Incidental organic psychoses

The psychoses, mentioned above, all had a recognized connection with childbearing. But medical disorders with no specific link have presented with psychotic symptoms in the puerperium; in them the association seems to be fortuitous.[43]: 6–73  They include neurosyphilis, encephalitis including von Economo's, meningitis, cerebral tumours, thyroid disease and ischaemic heart disease.

Society and culture

Support

In the UK, a series of workshops called "Unravelling Eve" were held in 2011, where women who had experienced postpartum depression shared their stories.[119]

Notable cases in history and fiction

Harriet Sarah, Lady Mordaunt (1848–1906), formerly Harriet Moncreiffe, was the Scottish wife of an English baronet and Member of Parliament, Sir Charles Mordaunt.[citation needed] She was the defendant in a sensational divorce case in which the Prince of Wales (later King Edward VII) was embroiled; after a controversial trial lasting seven days, the jury determined that Lady Mordaunt had "puerperal mania" and her husband's petition for divorce was dismissed, while Lady Mordaunt was committed to an asylum.[120]

Andrea Yates had depression and, four months after the birth of her fifth child, relapsed, with psychotic features. Several weeks later she drowned all five children. Under the law in Texas, she was sentenced to life imprisonment, but, after a retrial, was committed to a mental hospital.

Guy de Maupassant, in his novel Mont-Oriol (1887) described a brief postpartum psychotic episode.

Charlotte Perkins Gilman, in her short story The Yellow Wallpaper (1892) described severe depression with psychotic features starting after childbirth, perhaps similar to that experienced by the author herself.

Stacey Slater, a fictional character in the long-running BBC soap-opera EastEnders had postpartum psychosis in 2016, and was one of the show's biggest storylines that year.[citation needed]

In the House, M.D. episode Forever, House takes the case of a mother with postpartum psychosis.

Legal status

Postpartum psychosis, especially when there is a marked component of depression, has a small risk of filicide. In acute manic or cycloid cases, this risk is about 1%.[43]: 240–246  Most of these incidents have occurred before the mother came under treatment, and some have been accidental. Several nations including Canada, United Kingdom, Australia, and Italy recognize postpartum mental illness as a mitigating factor in cases where mothers kill their children.[121] In the United States, such a legal distinction was not made as of 2009,[121] and an insanity defense is not available in all states.[122]

The United Kingdom has had the Infanticide Act since 1922.

Books written about postpartum psychosis and postpartum bipolar disorder

Apart from the two monographs mentioned in the text (references 1 and 86), the following books have been published about these psychoses:

  • Ripping, Dr (1877) Die Geistesstörungen der Schwangeren, Wöchnerinnen und Säugenden. Stuttgart, Enke.
  • Knauer O (1897) Über Puerperale Psychose für practische Ärzte. Berlin, Karger.
  • Twomey T (2009) Understanding Postpartum Psychosis: A Temporary Madness. Westport, Praeger.
  • Harwood D (2017) Birth of a New Brain - Healing from Postpartum Bipolar Disorder. Brentwood, Post Hill Press.

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