The emphasis of the treatment of bipolar disorder is on effective management of the long-term course of the illness, which can involve treatment of emergent symptoms. Treatment methods include pharmacological and psychological techniques.
Bipolar disorder is a serious and debilitating mental health disorder, which causes patients to experience extreme highs and lows, such as mania and major depression.[1]
Principles
editThe primary treatment for bipolar disorder consists of medications called mood stabilizers, which are used to prevent or control episodes of mania or depression. Medications from several classes have mood stabilizing activity. Many individuals may require a combination of medication to achieve full remission of symptoms.[2] As it is impossible to predict which medication will work best for a particular individual, it may take some trial and error to find the best medication or combination for a specific patient. Psychotherapy also has a role in the treatment of bipolar disorder. The goal of treatment is not to cure the disorder but rather to control the symptoms and the course of the disorder. Generally speaking, maintenance treatment of bipolar disorder continues long after symptom control has been achieved.
Following diagnostic evaluation, the treating clinician must determine the optimal treatment setting in order to ensure the patient's safety. Assessment of suicide risk is key, as the rate of suicide completion among those with bipolar disorder may be as high as 10–15%.[3] Hospitalization should be considered in patients whose judgment is significantly impaired by their illness, and those who have not responded to outpatient treatment; this may need to be done on an involuntary basis.[3] Treatment setting should regularly be re-evaluated to ensure that it is optimal for the patient's needs.
Treatment | NNT for depressive relapse | NNT for manic relapse | Efficacy in Acute Mania | Efficacy in Acute Depression | Common Side Effects | Serious Side Effects | Safety during pregnancy | Routes of Administration |
---|---|---|---|---|---|---|---|---|
Aripiprazole monotherapy | 50 | 6.2 | ++ | - | Weight gain, nausea, vomiting, constipation, akathisia, dizziness, extrapyramidal symptoms, headache, insomnia, sedation, tremor, blurred vision, anxiety, restlessness, fatigue | Seizure (0.1-0.3%), suicidal behaviour, blood clots (<1%), agranulocytosis, leukopenia (<1%), neutropenia(<1%), pancreatitis (<0.1%), metabolic syndrome, neuroleptic malignant syndrome, tardive dyskinesia, angioedema (<1%), rhabdomyolysis | Pregnancy Category: B3 (Au) C (US) |
Oral, Intramuscular |
Aripiprazole adjunct to lithium/valproate | 33.3 | 10 | ++ | - | As above | As above | As above | As above |
Lamotrigine monotherapy | 20.2 | 50.4 | - | ++/+ | Rash, abdominal pain, indigestion, diarrhoea, nausea, vomiting, asthenia, ataxia, coordination problem, dizziness, headache, insomnia, sedation, tremor, vertigo, blurred vision, diplopia, anxiety, depression, dysmenorrhoea, rhinitis, pain | Erythema multiforme (<0.1%), Stevens–Johnson syndrome (0.08-0.8%), toxic epidermal necrolysis (0.08-0.8%), anaemia (<0.1%), Disseminated intravascular coagulation, Eosinophilia(<0.1%), Thrombocytopenia (<0.1%), Liver failure, Drug hypersensitivity syndrome, aseptic meningitis | Pregnancy Category:
D (Au) |
Mucous membranes, oral |
Lithium monotherapy | 6.1 | 4.4 | ++ | ++/+ | Acne, hypothyroidism, weight gain, gastritis, xerostomia, nausea, leukocytosis, fine tremor, Hyperreflexia, Deep tendon, Nephrotoxicity, Polyuria, Potential sign of toxicity, Increased thirst, Potential sign of toxicity | Bradyarrhythmia (Severe), Brugada syndrome, Sinus node dysfunction, Transient reduction in peripheral circulation as a whole, Erythema multiforme, Ataxia, Potential sign of toxicity, Coma, Pseudotumor cerebri, Increased intracranial pressure and papilledema, Seizure, Blurred vision, Potential sign of toxicity, Tinnitus, Potential sign of toxicity, Giddiness, Potential sign of toxicity, Renal interstitial fibrosis, Angioedema | Pregnancy Category:
D (Au) |
Oral |
Olanzapine monotherapy | 17.2 | 4.4 | +++ | ++/+ | Orthostatic hypotension, Peripheral edema (3% to 6%), Hypercholesterolemia (up to 24%), Hyperglycemia (0.1% to 17.4%), Increased appetite (3% to 24%), Increased prolactin level (31.2% to 61.1%), Serum triglycerides raised (up to 40%), Weight gain, Constipation, Xerostomia, Akathisia, Asthenia, Dizziness, Sedation, Tremor, Personality disorder (8%), Accidental injury (4% to 12%) | Sudden cardiac death, Diabetic coma with ketoacidosis, Diabetic ketoacidosis, Hyperglycemic hyperosmolar state, Acute hemorrhagic pancreatitis, Venous thromboembolism, Immune hypersensitivity reaction, Cerebrovascular disease, Seizure (0.9% ), Status epilepticus, Suicidal intent (0.1% to 1% ), Pulmonary embolism | Pregnancy Category: | Oral, intramuscular |
Olanzapine adjunct to lithium/valproate | 6.2 | 11.2 | +++ | - | As above | As above | As above | As above |
Quetiapine monotherapy | 3.3 | 2.4 | ++ | +++ | Orthostatic Hypertension, Tachycardia (0.5% to 7%), Serum cholesterol raised (7% to 18%), Serum triglycerides raised (8% to 22%), Weight gain (3% to 23%), Abdominal pain, Constipation, Increased appetite, Indigestion, Vomiting, Xerostomia, Increased liver enzymes, Backache, Asthenia, Dizziness, Extrapyramidal signs, Headache, Insomnia, Lethargy, Sedation, Tremor, Agitation (6% to 20%), Nasal congestion, Pharyngitis (4% to 6%), Fatigue, Pain | Syncope (0.3% to 1%), Diabetic ketoacidosis, Pancreatitis, Agranulocytosis, Leukopenia, Neutropenia (0.3%), Anaphylaxis, Seizure (0.05% to 0.5%), Tardive dyskinesia (0.1% to less than 5%), Suicidal thoughts, Priapism, Neuroleptic malignant syndrome (rare ) | Pregnancy Category: | Oral |
Quetiapine plus lithium/valproate | 5.9 | 7.1 | +++/++ | +++ | As above | As above | As above | As above |
Risperidone | 4 | 36.4 | +++ | - | Rash, hyperprolactinaemia, weight gain, constipation, diarrhoea, excessive salivation, increased appetite, indigestion, nausea, vomiting, upper abdominal pain, dry mouth, extrapyramidal side effects, dizziness, sedation, akathisia, blurred vision, anxiety, cough, nasal congestion, nasopharyngitis, pain in throat, upper respiratory tract infection, fatigue and generalised pains | Prolonged QT interval, sudden cardiac death, syncope, diabetic ketoacidosis, hypothermia, pancreatitis, Agranulocytosis, Leukopenia, Neutropenia, Thrombocytopenia, Thrombotic thrombocytopenic purpura, stroke, seizure, tardive dyskinesia, priapism, pulmonary embolism, neuroleptic malignant syndrome | Pregnancy Category: | Oral, Intramuscular |
Risperidone plus treatment as usual | 15.8 | 7.9 | +++ | - | As above | As above | As above | As Above |
Valproate monotherapy | 10.5 | 21.3 | ++/+ | - | Abdominal pain, diarrhoea, indigestion, loss of appetite, nausea, vomiting, asthenia, dizziness, feeling nervous, headache, insomnia, sedation, tremor, Amblyopia, Blurred vision, Diplopia, infectious disease, influenza | Palpitation, tachycardia, hyperammonaemia, pancreatitis, thrombocytopaenia, liver failure, immune hypersensitivity reaction, hyperammonaemic encephalopathy, deafness | Pregnancy Category:
Has the highest propensity of all anticonvulsants for causing birth defects. Around 6-11% of children born to mothers that used the drug during pregnancy are born with birth defects. |
Oral |
Ziprasidone and treatment as usual | 55.1 | 14.1 | ++/+ | - | Rash, weight gain, constipation, diarrhoea, indigestion, nausea, vomiting, xerostomia, akathisia, anxiety, asthenia, extrapyramidal side effects, dizziness, headache, sedation, abnormal vision, respiratory tract infection | Prolonged QT interval, syncope, torsades de pointes, diabetes mellitus, hyperglycaemia, hyperprolactinaemia, dysphagia, bone marrow depression, neuroleptic malignant syndrome, seizure, tardive dyskinesia, priapism | Pregnancy Category: | Oral, intramuscular |
Legend:
- negligible/very low/clinically insignificant effect
+ weak effect
++ moderate-level effect
+++ strong effect
Regulatory status of mood stabilisers
editDrug[7][10] | FDA approved for acute mania/mixed episodes? | FDA approved for bipolar depression? | FDA approved for bipolar maintenance? | TGA approved for acute mania/mixed episodes? | TGA approved for bipolar depression? | TGA approved for bipolar maintenance? | MHRA approved for acute mania/mixed episodes? | MHRA approved for bipolar depression | MHRA approved for bipolar maintenance |
---|---|---|---|---|---|---|---|---|---|
Aripiprazole | Yes | No | Yes (as an adjunct, yes) | No | No | Yes | Yes | No | Yes (for mania prevention) |
Asenapine | Yes | No | No | Yes | No | Yes | Yes | No | No |
Carbamazepine | Yes | No | No | No | No | Yes | No | No | Yes |
Cariprazine | Yes | Yes[11] | No | ||||||
Haloperidol | No | No | No | Yes | No | No | No | No | No |
Lamotrigine | No | No | Yes | No | No | Yes | No | No | Yes (depressive episodes) |
Lithium | Yes | No | Yes | Yes | No | Yes | Yes | No | Yes |
Olanzapine | Yes | No (yes when in conjunction with fluoxetine) | Yes | Yes | No | Yes (as an adjunct to valproate/lithium) | Yes | No | No |
Quetiapine | Yes | Yes | Yes | Yes | Yes | Yes | Yes | Yes | Yes |
Lurasidone | Yes | ||||||||
Risperidone | Yes | No | Yes | Yes | No | Yes | Yes | No | No |
Valproate | Yes | No | No | No | No | Yes | Yes | No | Yes |
Ziprasidone | Yes | No | No (yes as adjunct) | Yes | No | No | No | No | No |
Zuclopenthixol | No | No | No | Yes | No | No | No | No | No |
Mood stabilizers
editLithium salts
editLithium salts have been used for centuries as a first-line treatment for bipolar disorder. In ancient times, doctors would send their mentally ill patients to drink from "alkali springs" as a treatment. Although they were not aware of it, they were actually prescribing lithium, which was present in high concentration within the waters.[12] The therapeutic effect of lithium salts appears to be entirely due to the lithium ion, Li+.
Its exact mechanism of action is uncertain, although there are several possibilities such as inhibition of inositol monophosphatase, modulation of G proteins or regulation of gene expression for growth factors and neuronal plasticity.[2] There is strong evidence for its effectiveness in acute treatment and prevention of recurrence of mania. It can also be effective in bipolar depression, although the evidence is not as strong.[2] It is also effective in reducing the risk of suicide in patients with mood disorders.[13]
Potential side effects from lithium include gastrointestinal upset, tremor, sedation, excessive thirst, frequent urination, cognitive problems, impaired motor coordination, hair loss, and acne.[3] Excessive levels of lithium can be harmful to the kidneys, and increase the risk of side effects in general. As a result, kidney function and blood levels of lithium are monitored in patients being treated with lithium.[2] Therapeutic plasma levels of lithium range from 0.5 to 1.5 mEq/L, with levels of 0.8 or higher being desirable in acute mania.[14]
Lithium levels should be above 0.6 mEq/L to reduce both manic and depressive episodes in patients.[15] A recent review concludes that the standard lithium serum level should be 0.60–0.80 mmol/L with optional reduction to 0.40 0.60 mmol/L in case of good response but poor tolerance or an increase to 0.80 1.00 mmol/L in case of insufficient response and good tolerance.[16]
Monitoring is generally more frequent when lithium is being initiated, and the frequency can be decreased once a patient is stabilized on a given dose. Thyroid hormones should also be monitored periodically, as lithium can increase the risk of hypothyroidism.[3]
Anticonvulsants
editA number of anti-convulsant drugs are used as mood stabilizers, and the suspected mechanism is related to the theory that mania can "kindle" further mania, similar to the kindling model of seizures.[2] Valproic acid, or valproate, was one of the first anti-convulsants tested for use in bipolar disorder. It has proven to be effective for treating acute mania.[2] The mania prevention and antidepressant effects of valproic acid have not been well demonstrated.[2] Valproic acid is less effective than lithium at preventing and treating depressive episodes.[17]
Carbamazepine was the first anti-convulsant shown to be effective for treating bipolar mania. It has not been extensively studied in bipolar depression.[2] It is generally considered a second-line agent due to its side effect profile.[2] Lamotrigine is considered a first-line agent for the treatment of bipolar depression. It is effective in preventing the recurrence of both mania and depression, but it has not proved useful in treating acute mania.[2]
Zonisamide (trade name Zonegran), another anti-convulsant, also may show promise in treating bipolar depression.[18] Various other anti-convulsants have been tested in bipolar disorder, but there is little evidence of their effectiveness.[2] Other anti-convulsants effective in some cases and being studied closer include phenytoin, levetiracetam, pregabalin and valnoctamide.[19]
Each anti-convulsant agent has a unique side-effect profile. Valproic acid can frequently cause sedation or gastrointestinal upset, which can be minimized by giving the related drug divalproex, which is available in an enteric-coated tablet.[2] These side effects tend to disappear over time.[3] According to studies conducted in Finland in patients with epilepsy, valproate may increase testosterone levels in teenage girls and produce polycystic ovary syndrome in women who began taking the medication before age 20. Increased testosterone can lead to polycystic ovary syndrome with irregular or absent menses, obesity, and abnormal growth of hair. Therefore, young female patients taking valproate should be monitored carefully by a physician. Excessive levels of valproate can lead to impaired liver function, and liver enzymes and serum valproate level, with a target of 50–125 μg/L, should be monitored periodically.[3]
Side effects of carbamazepine include blurred vision, double vision, ataxia, weight gain, nausea, and fatigue, as well as some rare but serious side effects such as blood dyscrasias, pancreatitis, exfoliative dermatitis, and hepatic failure.[3] Monitoring of liver enzymes, platelets, and blood cell counts are recommended.[3]
Lamotrigine generally has minimal side effects, but the dose must be increased slowly to avoid rashes, including Stevens-Johnson syndrome (SJS) and exfoliative dermatitis.[2]
Atypical antipsychotic drugs
editAntipsychotics work best in the manic phase of bipolar disorder.[20] Second-generation or atypical antipsychotics (including aripiprazole, olanzapine, quetiapine, paliperidone, risperidone, and ziprasidone) have emerged as effective mood stabilizers.[2] The evidence for this is fairly recent, as in 2003 the American Psychiatric Press noted that atypical anti-psychotics should be used as adjuncts to other anti-manic drugs because their mood stabilizing properties had not been well established.[14] The mechanism is not well known, but may be related to effects on glutamate activity. Several studies have shown atypical antipsychotics to be effective both as single-agent and adjunctive treatments.[21] Antidepressant effectiveness varies, which may be related to different serotonergic and dopaminergic receptor binding profiles.[2] Quetiapine and the combination of olanzapine and fluoxetine have both demonstrated effectiveness in bipolar depression.[21]
In light of recent evidence, olanzapine (Zyprexa) has been FDA approved as an effective monotherapy for the maintenance of bipolar disorder.[22] A head-to-head randomized control trial in 2005 has also shown olanzapine monotherapy to be just as effective and safe as lithium in prophylaxis.[23]
The atypical antipsychotics differ somewhat in side effect profiles, but most have some risk of sedation, weight gain, and extrapyramidal symptoms (including tremor, stiffness, and restlessness).[2] They may also increase the risk of metabolic syndrome,[2] so metabolic monitoring should be performed regularly, including checks of serum cholesterol, triglycerides, and glucose, weight, blood pressure, and waist circumference. Taking antipsychotics for long periods or at high doses can also cause tardive dyskinesia — a sometimes incurable neurological disorder resulting in involuntary, repetitive body movements. The risk of tardive dyskinesia appears to be lower in second-generation antipsychotics than in first-generation antipsychotics but as with first-generation drugs, increases with time spent on medications and in older patients.[24]
New treatments
editA variety of other agents have been tried in bipolar disorder, including benzodiazepines, calcium channel blockers, L-methylfolate, and thyroid hormone.[2] Modafinil (Provigil) and pramipexole (Mirapex) have been suggested for treating cognitive dysfunction associated with bipolar depression, but evidence supporting their use is quite limited.[25][26] In addition, riluzole, a glutamatergic drug used in ALS has been studied as an adjunct or monotherapy treatment in bipolar depression, with mixed and inconsistent results.[27][28][29][30] The selective estrogen receptor modulator medication tamoxifen has shown rapid and robust efficacy treating acute mania in bipolar patients.[31][32][33][34] This action is likely due not to tamoxifen's estrogen-modulating properties, but due to its secondary action as an inhibitor of protein Kinase C.[31]
Cognitive effects of mood stabilizers
editBipolar patients taking antipsychotics have lower scores on tests of memory and full-scale IQ than patients taking other mood stabilisers.[35] Use of both typical and atypical antipsychotics is associated with risk of cognitive impairment, but the risk is higher for antipsychotics with more sedating effects.
Among bipolar patients taking anticonvulsants, those on lamotrigine have a better cognitive profile than those on carbamazepine, valproate, topiramate, and zonisamide.[36]
Although decreased verbal memory and slowed psychomotor speed are common side effects of lithium use[37][38] these side effects usually disappear after discontinuation of lithium. Lithium may be protective of cognitive function in the long term since it promotes neurogenesis in the hippocampus and increases grey matter volume in the prefrontal cortex.[39]
Antidepressants
editAntidepressants are used with caution in bipolar disorder, as they may not be effective and may even induce mania.[2] They are generally not used alone, but may be considered as an adjunct to lithium.[3]
A recent large-scale study found that severe depression in patients with bipolar disorder responds no better to a combination of antidepressant medications and mood stabilizers than it does to mood stabilizers alone and that antidepressant use does not hasten the emergence of manic symptoms in patients with bipolar disorder.[40]
The concurrent use of an antidepressant and a mood stabilizer, instead of mood stabilizer monotherapy, may lower the risk of further bipolar depressive episodes in patients whose most recent depressive episode has been resolved.[41] However, some studies have also found that antidepressants pose a risk of inducing hypomania or mania,[42] sometimes in individuals with no prior history of mania. Saint John's Wort, a naturally occurring compound, is thought to function in a fashion similar to man-made antidepressants, and there are reports that suggest that it can also induce mania.[43] For these reasons, some psychiatrists are hesitant to prescribe antidepressants for the treatment of bipolar disorder unless mood stabilizers have failed to have an effect, however, others feel that antidepressants still have an important role to play in treatment of bipolar disorder.
Side effects vary greatly among different classes of antidepressants.
Antidepressants are helpful in preventing suicides in people with bipolar disorder when they go in for the depressive phase.[44]
NMDA-receptor antagonists
editIn a double-blind, placebo-controlled, proof-of-concept study, researchers administered an N-methyl-d-aspartate–receptor antagonist (ketamine) to 18 patients already on treatment with lithium (10 patients) or valproate (8 patients) for bipolar depression. From 40 minutes following intravenous injection of ketamine hydrochloride (0.5 mg/kg), the researchers observed significant improvements in depressive symptoms, as measured by standard tools, that were maintained for up to 3 days, an effect not observed in subjects who received the placebo.[45] Five subjects dropped out of the ketamine study; of these, four were taking valproate and one was being treated with lithium. One patient showed signs of hypomania following ketamine administration and two experienced low mood. This study demonstrates a rapid-onset antidepressant effect of ketamine in a small group of patients with bipolar depression. The authors acknowledged the study's limitations, including the dissociative disturbances in patients receiving ketamine that could have compromised the study blinding, and they emphasised the need for further research.
A more recent double-blind, placebo-controlled study by the same group found that ketamine treatment resulted in a similarly rapid alleviation of suicidal ideation in 15 patients with bipolar depression.[46]
Ketamine is used as a dissociative anaesthetic, and is a Class C substance in the United Kingdom; as such, it is only be used psychiatrically under the direction of a health professional.
Dopamine agonists
editIn a single controlled study of twenty one patients, the dopamine D3 receptor agonist pramipexole was found to be highly effective in the treatment of bipolar depression. Treatment was initiated at 0.125 mg thrice daily and increased at a rate of 0.125 mg thrice daily to a limit of 4.5 mg per day until the patients' condition satisfactorily responded to the medication or they could not abide the side effects. The final average dosage was 1.7 mg ± 0.90 mg per day. The incidence of hypomania in the treatment group was no greater than in the control group.[47]
Psychotherapy
editCertain types of psychotherapy, used in combination with medication, may provide some benefit in the treatment of bipolar disorders. Psychoeducation has been shown to be effective in improving patients' compliance with their lithium treatment.[48] Evidence of the efficacy of family therapy is not adequate to support unrestricted recommendation of its use.[49] There is "fair support" for the utility of cognitive therapy. Evidence for the efficacy of other psychotherapies is absent or weak,[50] often not being performed under randomized and controlled conditions.[51] Well-designed[51] studies have found interpersonal and social rhythm therapy to be effective.[52]
Although medication and psychotherapy cannot cure the illness, therapy can often be valuable in helping to address the effects of disruptive manic or depressive episodes that have hurt a patient's career, relationships or self-esteem. Therapy is available not only from psychiatrists but from social workers, psychologists and other licensed counselors.
Jungian therapy
editJungian authors have likened the mania and depression of bipolar disorder to the Jungian archetypes 'puer' and 'senex'.[53][54][55][56][57] The puer archetype is defined by the behaviors of spontaneity, impulsiveness, enthusiasm or mania and is symbolized by characters such as Peter Pan or the Greek god Hermes.[53][54][55][56] The senex archetype is defined by behaviors of order, systematic thought, caution, and depression and is symbolized by characters such as the Roman god Saturn or the Greek god Kronos.[53][54][55][56] Jungians conceptualize the puer and senex as a coexistent bipolarity appearing in human behavior and imagination, but in neurotic manifestations appears as extreme oscillations and as unipolar manifestations.[53][54][55][56][58][59] In the case of the split puer-senex bipolarity the therapeutic task is to bring the puer and senex back into correlation by working with the patient's mental imagery."[53][54][55][56][57][58]
Lifestyle changes
editSufficient sleep
editIf sleeping is disturbed, the symptoms can occur. Sleep disruption may actually exacerbate the mental illness state. Those who do not get enough sleep at night, sleep late and wake up late, or go to sleep with some disturbance (e.g. music or charging devices) have a greater chance of having the symptoms and, in addition, depression. It is highly advised by psychiatric authorities to not sleep too late and to get enough high quality sleep. [60]
Self-management and self-awareness
editUnderstanding the symptoms, when they occur and ways to control them using appropriate medications and psychotherapy generally helps those diagnosed with bipolar disorder to lead a psychologically healthier life. Prodrome symptom detection has been shown to be used effectively to anticipate onset of manic episodes[61][62] and requires close monitoring of bipolar symptoms. Because the offset of the symptoms is often gradual, even subtle mood changes and activity levels are monitored to help avoid a relapse.[63] Maintaining a mood chart[64] is a specific method used by patients and doctors to identify mood, environmental and activity triggers.[65]
Stress reduction
editForms of stress may include having too much to do, too much complexity and conflicting demands among others. There are also stresses that come from the absence of elements such as human contact, a sense of achievement, constructive creative outlets, and occasions or circumstances that will naturally elicit positive emotions. Stress reduction will involve reducing things that cause anxiety and increasing those that generate happiness. It is not enough to just reduce the anxiety.[citation needed]
Co-morbid substance use disorder
editCo-occurring substance misuse disorders, which are extremely common in bipolar patients, can cause a significant worsening of bipolar symptomatology and can cause the emergence of affective symptoms. The treatment options and recommendations for substance use disorders is wide but may include certain pharmacological and nonpharmacological treatment options.[66]
The role of cannabinoids
editAcute cannabis intoxication transiently produces perceptual distortions, psychotic symptoms and reduction in cognitive abilities in healthy persons and in severe mental disorder,[67][68][69] and may impair the ability to safely operate a motor vehicle.[70]
Cannabis use is common in bipolar disorder;[71][72] and is a risk factor for a more severe course of the disease by increasing frequency and duration of episodes.[73][74][75][76] It is also reported to reduce age at onset.[77][78]
Other treatments
editOmega-3 fatty acids
editOmega-3 fatty acids may also be used as a treatment for bipolar disorder, particularly as a supplement to medication. An initial clinical trial by Stoll et al. produced positive results. However, since 1999, attempts to confirm this finding of beneficial effects of omega-3 fatty acids in several larger double-blind clinical trials have produced inconclusive results. It was hypothesized that the therapeutic ingredient in omega-3 fatty acid preparations is eicosapentaenoic acid (EPA) and that supplements should be high in this compound to be beneficial. A 2008 Cochrane systematic review found limited evidence to support the use of Omega-3 fatty acids to improve depression but not mania as an adjunct treatment for bipolar disorder.
Omega-3 fatty acids may be found in fish, fish oils, algae, and to a lesser degree in other foods such as flaxseed, flaxseed oil and walnuts. Although the benefits of Omega-3 fatty acids remain debated, they are readily available at drugstores and supermarkets, relatively inexpensive, and have few known side effects. (All of these oils, however, have the capacity to exacerbate GERD—food sources may be a good alternative in such cases.)[79]
Exercise
editExercise has also been shown to have antidepressant effects.[80]
Electroconvulsive therapy
editElectroconvulsive therapy (ECT) may have some effectiveness in mixed mania states, and good effectiveness in bipolar depression, particularly in the presence of psychosis.[3] It may also be useful in the treatment of severe mania that is non-responsive to medications.[81][82]
The most frequent side effects of ECT include memory impairment, headaches, and muscle aches.[14] In some instances, ECT can produce significant and long-lasting cognitive impairment, including anterograde amnesia, and retrograde amnesia.[83]
Ketogenic diet
editBecause many of the medications that are effective in treating epilepsy are also effective as mood stabilizers, it has been suggested that the ketogenic diet—used for treating pediatric epilepsy—could have mood stabilizing effects. Ketogenic diets are diets that are high in fat and low in carbohydrates, and force the body to use fat for energy instead of sugars from carbohydrates. This causes a metabolic response similar to that seen in the body during fasting. This idea has not been tested by clinical research, and until recently, was entirely hypothetical. Recently, however, two case studies have been described where ketogenic diets were used to treat bipolar II.[84] In each case, the patients found that the ketogenic diet was more effective for treating their disorder than medication and were able to discontinue the use of medication. The key to efficacy appears to be ketosis, which can be achieved either with a classic high-fat ketogenic diet, or with a low-carbohydrate diet similar to the induction phase of the Atkins Diet. The mechanism of action is not well understood. It is unclear whether the benefits of the diet produce a lasting improvement in symptoms (as is sometimes the case in treatment for epilepsy) or whether the diet would need to be continued indefinitely to maintain symptom remission.
See also
editReferences
edit- ^ "Bipolar disorder - Symptoms and causes". Mayo Clinic. Retrieved 2022-12-09.
- ^ a b c d e f g h i j k l m n o p q r s Stahl SM (2008). Stahl's Essential Psychopharmacology: Neuroscientific basis and practical applications. Cambridge University Press.
- ^ a b c d e f g h i j "Practice Guideline for the Treatment of Patients with Bipolar Disorder, Second Edition". American Psychiatric Association. 2002. Archived from the original on 15 April 2013.
- ^ Popovic D, Reinares M, Goikolea JM, Bonnin CM, Gonzalez-Pinto A, Vieta E (May 2012). "Polarity index of pharmacological agents used for maintenance treatment of bipolar disorder". European Neuropsychopharmacology. 22 (5): 339–46. doi:10.1016/j.euroneuro.2011.09.008. PMID 22000157. S2CID 8067809.
- ^ Galbally M, Roberts M, Buist A (November 2010). "Mood stabilizers in pregnancy: a systematic review". The Australian and New Zealand Journal of Psychiatry. 44 (11): 967–77. doi:10.3109/00048674.2010.506637 (inactive 31 January 2024). PMID 21034180.
{{cite journal}}
: CS1 maint: DOI inactive as of January 2024 (link) - ^ Cipriani A, Barbui C, Salanti G, Rendell J, Brown R, Stockton S, et al. (October 2011). "Comparative efficacy and acceptability of antimanic drugs in acute mania: a multiple-treatments meta-analysis". Lancet. 378 (9799): 1306–15. doi:10.1016/S0140-6736(11)60873-8. PMID 21851976. S2CID 25512763.
- ^ a b Ryan RS, Jordan BM, Martin J, Wagle SM, Amin S, Clarke SE, et al. (2013). British National Formulary 65. London: Pharmaceutical Press. ISBN 978-0-85711-084-8.
- ^ "Australian Medicines Handbook". Australian Medicines Handbook Pty Ltd. 2013.
- ^ Hendrick V, Keck P, Wilkins-Haug L (14 June 2013). "Bipolar disorder in pregnant women: Treatment of mania, hypomania, and mixed episodes". UpToDate. Wolters Kluwer. Retrieved 10 October 2013.
- ^ "Therapeutic Goods Administration". TGA eBusiness Services [Internet]. Australian Government Department of Health and Ageing. Retrieved 15 September 2013.
- ^ "News Center | AbbVie News Center".
- ^ Friedrich, M. J. (1999-06-23). "Lithium: Proving Its Mettle for 50 Years". JAMA. 281 (24): 2271–2273. doi:10.1001/jama.281.24.2271. ISSN 0098-7484. PMID 10386539.
- ^ Baldessarini RJ, Tondo L, Hennen J (2003). "Lithium treatment and suicide risk in major affective disorders: update and new findings". The Journal of Clinical Psychiatry. 64 (Suppl 5): 44–52. PMID 12720484.
- ^ a b c Hales E, Yudofsky JA, eds. (2003). The American Psychiatric Press Textbook of Psychiatry. Washington, DC: American Psychiatric Publishing, Inc.
- ^ Nolen WA, Weisler RH (February 2013). "The association of the effect of lithium in the maintenance treatment of bipolar disorder with lithium plasma levels: a post hoc analysis of a double-blind study comparing switching to lithium or placebo in patients who responded to quetiapine (Trial 144)" (PDF). Bipolar Disorders. 15 (1): 100–9. doi:10.1111/bdi.12027. PMID 23228201. S2CID 22324571.
- ^ Nolen, Willem A.; Licht, Rasmus W.; Young, Allan H.; Malhi, Gin S.; Tohen, Mauricio; Vieta, Eduard; Kupka, Ralph W.; Zarate, Carlos; Nielsen, René E.; Baldessarini, Ross J.; Severus, Emanuel (2019). "What is the optimal serum level for lithium in the maintenance treatment of bipolar disorder? A systematic review and recommendations from the ISBD/IGSLI Task Force on treatment with lithium". Bipolar Disorders. 21 (5): 394–409. doi:10.1111/bdi.12805. ISSN 1399-5618. PMC 6688930. PMID 31112628.
- ^ Kessing LV, Hellmund G, Geddes JR, Goodwin GM, Andersen PK (July 2011). "Valproate v. lithium in the treatment of bipolar disorder in clinical practice: observational nationwide register-based cohort study". The British Journal of Psychiatry. 199 (1): 57–63. doi:10.1192/bjp.bp.110.084822. PMID 21593515. S2CID 4696036.
- ^ Lieberman DZ, Goodwin FK (16 September 2005). "The Accurate Diagnosis and Long-Term Treatment of Bipolar Depression". Medscape. Archived from the original on 8 December 2008.
- ^ Clinical trial number NCT00140179 for "Valnoctamide in Mania" at ClinicalTrials.gov
- ^ Geddes JR, Miklowitz DJ (May 2013). "Treatment of bipolar disorder". Lancet. 381 (9878): 1672–82. doi:10.1016/s0140-6736(13)60857-0. PMC 3876031. PMID 23663953.
- ^ a b "Guideline Watch: Practice Guide for the Treatment of Patients with Bipolar Disorder, 2nd ed". American Psychiatric Association. Archived from the original on 15 April 2013.
- ^ "Now Approved: ZYPREXA for maintenance therapy for bipolar disorder". www.zyprexa.com.
- ^ Tohen M, Greil W, Calabrese JR, Sachs GS, Yatham LN, Oerlinghausen BM, et al. (July 2005). "Olanzapine versus lithium in the maintenance treatment of bipolar disorder: a 12-month, randomized, double-blind, controlled clinical trial". The American Journal of Psychiatry. 162 (7): 1281–90. doi:10.1176/appi.ajp.162.7.1281. PMID 15994710. S2CID 20932562.
- ^ Correll CU, Leucht S, Kane JM (March 2004). "Lower risk for tardive dyskinesia associated with second-generation antipsychotics: a systematic review of 1-year studies". The American Journal of Psychiatry. 161 (3): 414–25. doi:10.1176/appi.ajp.161.3.414. PMID 14992963.
- ^ Sanchez-Moreno J, Martinez-Aran A, Vieta E (January 2017). "Treatment of Functional Impairment in Patients with Bipolar Disorder". Current Psychiatry Reports. 19 (1): 3. doi:10.1007/s11920-017-0752-3. PMID 28097635. S2CID 42872706.
- ^ Solé B, Jiménez E, Torrent C, Reinares M, Bonnin CD, Torres I, Varo C, Grande I, Valls E, Salagre E, Sanchez-Moreno J, Martinez-Aran A, Carvalho AF, Vieta E (August 2017). "Cognitive Impairment in Bipolar Disorder: Treatment and Prevention Strategies". The International Journal of Neuropsychopharmacology. 20 (8): 670–680. doi:10.1093/ijnp/pyx032. PMC 5570032. PMID 28498954.
- ^ Park LT, Lener MS, Hopkins M, Iadorola N, Machado-Vieira R, Ballard E, Nugent A, Zarate CA (June 2017). "A Double-Blind, Placebo-Controlled, Pilot Study of Riluzole Monotherapy for Acute Bipolar Depression". Journal of Clinical Psychopharmacology. 37 (3): 355–358. doi:10.1097/JCP.0000000000000693. PMC 5392145. PMID 28338546.
- ^ Zarate CA, Quiroz JA, Singh JB, Denicoff KD, De Jesus G, Luckenbaugh DA, Charney DS, Manji HK (February 2005). "An open-label trial of the glutamate-modulating agent riluzole in combination with lithium for the treatment of bipolar depression". Biological Psychiatry. 57 (4): 430–2. doi:10.1016/j.biopsych.2004.11.023. PMID 15705360. S2CID 32075426.
- ^ Pittenger C, Coric V, Banasr M, Bloch M, Krystal JH, Sanacora G (2008). "Riluzole in the treatment of mood and anxiety disorders". CNS Drugs. 22 (9): 761–86. doi:10.2165/00023210-200822090-00004. PMID 18698875. S2CID 17221832.
- ^ Brennan BP, Hudson JI, Jensen JE, McCarthy J, Roberts JL, Prescot AP, Cohen BM, Pope HG, Renshaw PF, Ongür D (February 2010). "Rapid enhancement of glutamatergic neurotransmission in bipolar depression following treatment with riluzole". Neuropsychopharmacology. 35 (3): 834–46. doi:10.1038/npp.2009.191. PMC 3055603. PMID 19956089.
- ^ a b Khan MM (2018-10-08). "Translational Significance of Selective Estrogen Receptor Modulators in Psychiatric Disorders". International Journal of Endocrinology. 2018: 9516592. doi:10.1155/2018/9516592. PMC 6196929. PMID 30402099.
- ^ Yildiz A, Guleryuz S, Ankerst DP, Ongür D, Renshaw PF (March 2008). "Protein kinase C inhibition in the treatment of mania: a double-blind, placebo-controlled trial of tamoxifen". Archives of General Psychiatry. 65 (3): 255–63. doi:10.1001/archgenpsychiatry.2007.43. PMID 18316672.
- ^ Yildiz A, Aydin B, Gökmen N, Yurt A, Cohen B, Keskinoglu P, Öngür D, Renshaw P (March 2016). "Antimanic Treatment With Tamoxifen Affects Brain Chemistry: A Double-Blind, Placebo-Controlled Proton Magnetic Resonance Spectroscopy Study". Biological Psychiatry. Cognitive Neuroscience and Neuroimaging. 1 (2): 125–131. doi:10.1016/j.bpsc.2015.12.002. PMC 4876725. PMID 27231722.
- ^ Zarate CA, Singh JB, Carlson PJ, Quiroz J, Jolkovsky L, Luckenbaugh DA, Manji HK (September 2007). "Efficacy of a protein kinase C inhibitor (tamoxifen) in the treatment of acute mania: a pilot study". Bipolar Disorders. 9 (6): 561–70. doi:10.1111/j.1399-5618.2007.00530.x. PMID 17845270.
- ^ Donaldson S, Goldstein LH, Landau S, Raymont V, Frangou S (January 2003). "The Maudsley Bipolar Disorder Project: the effect of medication, family history, and duration of illness on IQ and memory in bipolar I disorder". The Journal of Clinical Psychiatry. 64 (1): 86–93. doi:10.4088/JCP.v64n0116. PMID 12590629.
- ^ Dias VV, Balanzá-Martinez V, Soeiro-de-Souza MG, Moreno RA, Figueira ML, Machado-Vieira R, Vieta E (November 2012). "Pharmacological approaches in bipolar disorders and the impact on cognition: a critical overview". Acta Psychiatrica Scandinavica. 126 (5): 315–31. doi:10.1111/j.1600-0447.2012.01910.x. PMID 22881296. S2CID 24193259.
- ^ Pachet AK, Wisniewski AM (November 2003). "The effects of lithium on cognition: an updated review". Psychopharmacology. 170 (3): 225–234. doi:10.1007/s00213-003-1592-x. PMID 14504681. S2CID 6939642.
- ^ Honig A, Arts BM, Ponds RW, Riedel WJ (May 1999). "Lithium induced cognitive side-effects in bipolar disorder: a qualitative analysis and implications for daily practice". International Clinical Psychopharmacology. 14 (3): 167–71. doi:10.1097/00004850-199905002-00003. PMID 10435769.
- ^ Moore GJ, Bebchuk JM, Wilds IB, Chen G, Manji HK, Menji HK (October 2000). "Lithium-induced increase in human brain grey matter". Lancet. 356 (9237): 1241–2. doi:10.1016/S0140-6736(00)02793-8. PMID 11072948. S2CID 36289314.
- ^ Sachs GS, Nierenberg AA, Calabrese JR, Marangell LB, Wisniewski SR, Gyulai L, Friedman ES, Bowden CL, Fossey MD, Ostacher MJ, Ketter TA, Patel J, Hauser P, Rapport D, Martinez JM, Allen MH, Miklowitz DJ, Otto MW, Dennehy EB, Thase ME (April 2007). "Effectiveness of adjunctive antidepressant treatment for bipolar depression". The New England Journal of Medicine. 356 (17): 1711–22. doi:10.1056/NEJMoa064135. PMID 17392295.
- ^ Altshuler L, Suppes T, Black D, Nolen WA, Keck PE, Frye MA, McElroy S, Kupka R, Grunze H, Walden J, Leverich G, Denicoff K, Luckenbaugh D, Post R (July 2003). "Impact of antidepressant discontinuation after acute bipolar depression remission on rates of depressive relapse at 1-year follow-up". The American Journal of Psychiatry. 160 (7): 1252–62. doi:10.1176/appi.ajp.160.7.1252. PMID 12832239.
- ^ Truman CJ, Goldberg JF, Ghaemi SN, Baldassano CF, Wisniewski SR, Dennehy EB, Thase ME, Sachs GS (October 2007). "Self-reported history of manic/hypomanic switch associated with antidepressant use: data from the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD)". The Journal of Clinical Psychiatry. 68 (10): 1472–9. doi:10.4088/jcp.v68n1002. PMID 17960960. S2CID 31963466.
- ^ Nierenberg AA, Burt T, Matthews J, Weiss AP (December 1999). "Mania associated with St. John's wort". Biological Psychiatry. 46 (12): 1707–8. doi:10.1016/S0006-3223(99)00233-4. PMID 10624554. S2CID 19546656.
- ^ Leon AC, Fiedorowicz JG, Solomon DA, Li C, Coryell WH, Endicott J, Fawcett J, Keller MB (July 2014). "Risk of suicidal behavior with antidepressants in bipolar and unipolar disorders". The Journal of Clinical Psychiatry. 75 (7): 720–7. doi:10.4088/JCP.13m08744. PMC 4142755. PMID 25093469.
- ^ Diazgranados N, Ibrahim L, Brutsche NE, Newberg A, Kronstein P, Khalife S, Kammerer WA, Quezado Z, Luckenbaugh DA, Salvadore G, Machado-Vieira R, Manji HK, Zarate CA (August 2010). "A randomized add-on trial of an N-methyl-D-aspartate antagonist in treatment-resistant bipolar depression". Archives of General Psychiatry. 67 (8): 793–802. doi:10.1001/archgenpsychiatry.2010.90. PMC 3000408. PMID 20679587.
- ^ Zarate CA, Brutsche NE, Ibrahim L, Franco-Chaves J, Diazgranados N, Cravchik A, Selter J, Marquardt CA, Liberty V, Luckenbaugh DA (June 2012). "Replication of ketamine's antidepressant efficacy in bipolar depression: a randomized controlled add-on trial". Biological Psychiatry. 71 (11): 939–46. doi:10.1016/j.biopsych.2011.12.010. PMC 3343177. PMID 22297150.
- ^ Zarate CA, Payne JL, Singh J, Quiroz JA, Luckenbaugh DA, Denicoff KD, Charney DS, Manji HK (July 2004). "Pramipexole for bipolar II depression: a placebo-controlled proof of concept study". Biological Psychiatry. 56 (1): 54–60. doi:10.1016/j.biopsych.2004.03.013. PMID 15219473. S2CID 19613411.
- ^ Cochran SD (October 1984). "Preventing medical noncompliance in the outpatient treatment of bipolar affective disorders". Journal of Consulting and Clinical Psychology. 52 (5): 873–8. doi:10.1037/0022-006X.52.5.873. PMID 6501672.
- ^ Justo LP, Soares BG, Calil HM, et al. (Depression, Anxiety and Neurosis Group) (October 2007). "Family interventions for bipolar disorder". The Cochrane Database of Systematic Reviews. 2007 (4): CD005167. doi:10.1002/14651858.CD005167.pub2. PMC 6669265. PMID 17943843.
- ^ Parikh SV, Kusumakar V, Haslam DR, Matte R, Sharma V, Yatham LN (August 1997). "Psychosocial interventions as an adjunct to pharmacotherapy in bipolar disorder". Canadian Journal of Psychiatry. 42 (Suppl 2): 74S–78S. PMID 9288439.
- ^ a b Goodnick PJ (2002). "Psychosocial Treatments for Bipolar Disorder: Is There Evidence That They Work?". In Sartorius N, Maj M, Akiskal HS, Hagop S, López-Ibor JJ (eds.). Bipolar disorder. WPA Series in Evidence & Experience in Psychiatry. Vol. 5. Chichester: John Wiley & Sons. p. 338. ISBN 978-0-471-56037-1.
- ^ Frank E, Swartz HA, Mallinger AG, Thase ME, Weaver EV, Kupfer DJ (November 1999). "Adjunctive psychotherapy for bipolar disorder: effects of changing treatment modality". Journal of Abnormal Psychology. 108 (4): 579–87. doi:10.1037/0021-843X.108.4.579. PMID 10609422.
- ^ a b c d e Hillman J, ed. (1979). Puer Papers. Spring Publications.
- ^ a b c d e Hillman J (2005). Senex and Puer. Spring Publications. pp. 30–66.
- ^ a b c d e Zoja L (January 1987). "Analytical psychology and the metapsychology of feelings: possible connections between Jung and Melanie Klein". The Journal of Analytical Psychology. 32 (1): 47–55. doi:10.1111/j.1465-5922.1987.00047.x. PMID 3804855.
- ^ a b c d e Vitale A (1973). "Saturn: The Transformation of the Father". In Berry P (ed.). Fathers and Mothers: Five Papers on the Archetypal Background of Family Psychology. Spring Publications. pp. 5–39.
- ^ a b Thompson J (2012). A Jungian Approach to Bipolar Disorder. Soul Books. pp. 1–10.
- ^ a b Zoja L (1995). Growth and Guilt. Routledge Press. pp. 131–132.
- ^ Thompson J (2012). A Jungian Approach to Bipolar Disorder. Soul Books.
- ^ "The Effects of Lack of Sleep on Bipolar Disorder | HealthyPlace". www.healthyplace.com. Retrieved 2022-12-08.
- ^ Morriss RK, Faizal MA, Jones AP, Williamson PR, et al. (January 2007). "Interventions for helping people recognise early signs of recurrence in bipolar disorder". Depression, Anxiety and Neurosis Group. The Cochrane Database of Systematic Reviews. 2010 (1): CD004854. doi:10.1002/14651858.CD004854.pub2. PMC 6544804. PMID 17253526.
- ^ Sahoo MK, Chakrabarti S, Kulhara P (February 2012). "Detection of prodromal symptoms of relapse in mania and unipolar depression by relatives and patients". The Indian Journal of Medical Research. 135 (2): 177–83. PMC 3336848. PMID 22446859.
- ^ Schwartz J (20 July 2017). "Can People Recover From Bipolar Disorder?". U.S. News & World Report.
- ^ "Daily Mood Chart" (PDF). Good Health Guidelines for People With Bipolar Disorder. CignaBehavioral. February 2008. Retrieved 2014-06-23.
- ^ Miklowitz D (2002). The Bipolar Disorder Survival Guide. New York: The Guilford Press. p. 154. ISBN 978-1-57230-712-4.
- ^ Cerullo MA, Strakowski SM (October 2007). "The prevalence and significance of substance use disorders in bipolar type I and II disorder". Substance Abuse Treatment, Prevention, and Policy. 2: 29. doi:10.1186/1747-597X-2-29. PMC 2094705. PMID 17908301.
- ^ D'Souza DC, Abi-Saab WM, Madonick S, Forselius-Bielen K, Doersch A, Braley G, Gueorguieva R, Cooper TB, Krystal JH (March 2005). "Delta-9-tetrahydrocannabinol effects in schizophrenia: implications for cognition, psychosis, and addiction". Biological Psychiatry. 57 (6): 594–608. doi:10.1016/j.biopsych.2004.12.006. PMID 15780846. S2CID 33125224.
- ^ Ranganathan M, D'Souza DC (November 2006). "The acute effects of cannabinoids on memory in humans: a review". Psychopharmacology. 188 (4): 425–44. doi:10.1007/s00213-006-0508-y. PMID 17019571. S2CID 10328820.
- ^ Grotenhermen F (August 2007). "The toxicology of cannabis and cannabis prohibition". Chemistry & Biodiversity. 4 (8): 1744–69. doi:10.1002/cbdv.200790151. PMID 17712818. S2CID 45115368.
- ^ Mann RE, Stoduto G, Macdonald S, Brands B (2008). "Cannabis use and driving: implications for public health and transport policy" (PDF). In Sznitman SR, Olsson B, Room R (eds.). A cannabis reader: global issues and local experiences, Volume 2. pp. 173–98. doi:10.2810/15648. ISBN 978-92-9168-312-3.
- ^ Lagerberg TV, Sundet K, Aminoff SR, Berg AO, Ringen PA, Andreassen OA, Melle I (September 2011). "Excessive cannabis use is associated with earlier age at onset in bipolar disorder". European Archives of Psychiatry and Clinical Neuroscience. 261 (6): 397–405. doi:10.1007/s00406-011-0188-4. PMC 3159738. PMID 21267743.
- ^ Najt P, Fusar-Poli P, Brambilla P (April 2011). "Co-occurring mental and substance abuse disorders: a review on the potential predictors and clinical outcomes". Psychiatry Research. 186 (2–3): 159–64. doi:10.1016/j.psychres.2010.07.042. PMID 20728943. S2CID 1030276.
- ^ Tohen M, Vieta E, Gonzalez-Pinto A, Reed C, Lin D (March 2010). "Baseline characteristics and outcomes in patients with first episode or multiple episodes of acute mania". The Journal of Clinical Psychiatry. 71 (3): 255–61. doi:10.4088/jcp.08m04580. PMID 19709503.
- ^ Strakowski SM, DelBello MP, Fleck DE, Arndt S (September 2000). "The impact of substance abuse on the course of bipolar disorder". Biological Psychiatry. 48 (6): 477–85. doi:10.1016/s0006-3223(00)00900-8. PMID 11018221. S2CID 17315802.
- ^ Baethge C, Hennen J, Khalsa HM, Salvatore P, Tohen M, Baldessarini RJ (September 2008). "Sequencing of substance use and affective morbidity in 166 first-episode bipolar I disorder patients". Bipolar Disorders. 10 (6): 738–41. doi:10.1111/j.1399-5618.2007.00575.x. PMID 18837869.
- ^ Henquet C, Krabbendam L, de Graaf R, ten Have M, van Os J (October 2006). "Cannabis use and expression of mania in the general population". Journal of Affective Disorders. 95 (1–3): 103–10. doi:10.1016/j.jad.2006.05.002. PMID 16793142.
- ^ Lagerberg TV, Kvitland LR, Aminoff SR, Aas M, Ringen PA, Andreassen OA, Melle I (January 2014). "Indications of a dose-response relationship between cannabis use and age at onset in bipolar disorder". Psychiatry Research. 215 (1): 101–4. doi:10.1016/j.psychres.2013.10.029. PMID 24262665. S2CID 25675185.
- ^ De Hert M, Wampers M, Jendricko T, Franic T, Vidovic D, De Vriendt N, Sweers K, Peuskens J, van Winkel R (March 2011). "Effects of cannabis use on age at onset in schizophrenia and bipolar disorder". Schizophrenia Research. 126 (1–3): 270–6. doi:10.1016/j.schres.2010.07.003. PMID 20674280. S2CID 2657010.
- ^ Stuart, Annie. "Omega-3s and Fish: Facts on DHA and EPA in Fish". WebMD. Retrieved 2022-10-28.
- ^ Reynolds G (2011-08-31). "Prescribing Exercise to Treat Depression". The New York Times. Retrieved April 29, 2013.
- ^ "Bipolar disorder: the assessment and management of bipolar disorder in adults, children and young people in primary and secondary care. | National Guideline Clearinghouse". guideline.gov. Archived from the original on 2017-02-24. Retrieved 2017-02-23.
- ^ Small JG, Milstein V, Klapper MH (1986). "Electroconvulsive therapy in the treatment of manic episodes". Annals of the New York Academy of Sciences. 426 (1): 37–49. Bibcode:1986NYASA.462...37S. doi:10.1111/j.1749-6632.1986.tb51237.x. PMID 2871794. S2CID 7478248.
- ^ MacQueen G, Parkin C, Marriott M, Bégin H, Hasey G (July 2007). "The long-term impact of treatment with electroconvulsive therapy on discrete memory systems in patients with bipolar disorder". Journal of Psychiatry & Neuroscience. 32 (4): 241–9. PMC 1911194. PMID 17653292.
- ^ Phelps JR, Siemers SV, El-Mallakh RS (2013). "The ketogenic diet for type II bipolar disorder". Neurocase. 19 (5): 423–6. doi:10.1080/13554794.2012.690421. PMID 23030231. S2CID 28007202.
Further reading
edit- Mitchell PB, Malhi GS, Ball JR (August 2004). "Major advances in bipolar disorder". The Medical Journal of Australia. 181 (4): 207–10. doi:10.5694/j.1326-5377.2004.tb06238.x. PMID 15310256. S2CID 18993165.
External links
edit- Guzman F (2012-01-27). "Video Lecture: First and Second Generation Antipsychotics for the Treatment of Bipolar Disorder". Psychopharmacology Institute. Retrieved 2012-08-04.
- "Bipolar Disorder Information". Psych Central. 2016-08-29.