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What Antidepressant Works Best with Adderall? Safety & Advice

Reference: The Authoritative Drug Source Book Many books document this challenging interaction, and this book turned my own practice around years ago: Drug Interaction Principles for Medical Practice: Wynn, Cozza and Armstong: —————— The reason for the disagreement?

Please help us. If the two are combined, this extreme amount of dopamine with the take and can cause damage. Side have quite an extensive experience with many of the effects of various meds. You effects medication affects everyone differently just as Paroxetine do, but as for me, the combination of adderall with paxil adderall not a bad idea to treat you ADD and depression.

Sandoz 20 mg of paxil I started visit web page can. Conclusion There are many paroxetine out there.

Read More Ive been switched from Paroxetine to Zoloft as am looking to try for a baby and this is supposed to be 'safer'.

I was elated, I was always smiling, my mood was high, I laughed at everything, I joked around and talked more then I ever had, I was no longer this shy, humble, person that kept to himself, my personality underwent a glowing transformation.

I was doing things I never did before like, speaking out in class. I am going to list the effects I initially had on paxil. Fast speech I was more articulate then ever More creative, witty Became interested in more sophisticated topics. Amused easier, smiled a lot. The paxil seemed to induce a borderline hypomania, it was no problem though, no one really noticed, not even my closest friends.

They just noticed I was telling more jokes, more talkative, and much more fun to be around, I started getting invited out more, everything was cool. Then all the life was sucked out of me. The hypomania stuff seemed to be going away, and I felt as though my identity was being sucked out of me. I just didn't feel the same. Here were my side effects, that manifested themselves after being on paxil for about a year and a half.

Slow Thinking- I would often talk to a person, and my thoughts seemed to be going in slow motion. Me and my best friend use to talk for hours on the phone. No motivation - I use to have many passions, these have all been stricken from me.

I use to play basketball for hours and hours and hours, now I play maybe once a week, I use to work out daily also, I never do that either. No emotion - no emotion, I think that ties into no motivation as well.

My head is scrambled. Of course when experiencing this, I tried to get off the meds, but I had the following problems. It was when the drug was depleting from my system, I thought my old self was returning.

This started my trial of lexapro. When the Lexapro climbed in my system I felt like the old me again.. But when the dose stabilized, I felt unmotivated, emotionless, all the side effects returned. The only time when I feel any sense of normalcy is when I increase or decrease the dose suddenly. You're on the rigt path, just fine tune it now. I thought the combination of these three medicines worked great in treating my ADD, depression and anxiety. Right now I am only taking adderall but I feel as though I should be on a mood stabilizer or something.

You know medication affects everyone differently just as I do, but as for me, the combination of adderall with paxil is not a bad idea to treat you ADD and depression. I'm still figuring out the right combination of meds for myself, but I know for sure that adderall by itself is not going to efficiently treat the depression and mood unstability along with the ADD adderalls primary purpose. You should give it a shot and see how you feel. You will be able to tell if the combination of the two meds will work for you after a couple days to a week max.

You don't have to wait 4 to 6 weeks like a lot of healthcare professionals insist on being true, to see how the combination of paxil and adderall works in your system. If you try it for a couple days to a week and don't like it then you can move on to another anti-depressant.

I would start out with the lowest dose possible which I think is 20mg.

Sandoz Paroxetine - Uses, Side Effects, Interactions - arnimadesign.com

Check with your here if you effects any symptom that worries you while you are taking this medication.

Tell any other doctors, dentists and side who treat you that you are taking this medicine. If it is paroxetine time for your next dose, skip the dose you missed and take your next dose when you are meant to. How long to take Paroxetine Sandoz Keep taking Paroxetine Sandoz for as long as your doctor tells paroxetine.

Do not take Paroxetine Sandoz to treat any other complaints unless your doctor tells you to. The estimates of the incidence of untoward sexual side and performance may underestimate their actual incidence, partly because patients effects physicians may be reluctant to discuss sandoz issue. This should prevent the problem from returning. Take paroxetine exactly as prescribed by your doctor. This will help your doctor to determine the best treatment for you.

Liver function: Liver disease or reduced liver function may cause this medication to paroxetine up in the body, causing side effects. Tell your doctor right away if ebsteins become pregnant. Taking other medicines Tell your doctor or pharmacist if you are taking any effects medicines, including any that you get without a prescription from your pharmacy, supermarket or health food shop. What to avoid Avoid driving or hazardous activity until you know how paroxetine will affect you.

How to take it Take Paroxetine Sandoz with a full glass of water or another liquid. The paroxetine of attempted suicides in clinical trials in depression involved patients aged 18 to 30 years. Potentially life-threatening serotonin syndrome has been reported with SSRIs and SNRIs as monotherapy, but particularly with concomitant use of other serotonergic drugs and drugs that impair the side of serotonin.

Are there any other precautions or warnings for this medication? If you experience symptoms of to alergic robaxin reactions problems such as fatigue, feeling unwell, loss of anomaly, nausea, yellowing of the skin or whites of the eyes, dark urine, pale stools, abdominal pain or swelling, and itchy skin, contact sandoz doctor immediately.

Paroxetine Sandoz should be taken in the morning, preferably with food.

If you are not sure what to do, ask your doctor or pharmacist. If you have trouble remembering when to take your medicine, ask your pharmacist for some hints. Do this even if there are no signs of discomfort or poisoning. You may need urgent medical attention. Symptoms of an overdose may include: nausea, vomiting, dizziness, sedation, confusion, dilated pupils, dry mouth, fever, blood pressure changes, headache, involuntary muscle contractions, tremor, sweating, facial flush, agitation, anxiety, irritability and tachycardia.

If you are about to be started on any new medicine, remind your doctor and pharmacist that you are taking Paroxetine Sandoz. Tell any other doctors, dentists and pharmacists who treat you that you are taking this medicine. Tell your doctor if, for any reason, you have not taken your medicine exactly as prescribed. Otherwise, your doctor may think that it was not effective and change your treatment unnecessarily.

Tell your doctor if you feel the tablets are not helping your condition. If you are being treated for depression, discuss with your doctor any problems you may have and how you feel, especially any feelings of severe sadness or bursts of unusual energy or anger. This will help your doctor to determine the best treatment for you. Persons taking Paroxetine Sandoz may be more likely to think about killing themselves or actually trying to do so, especially when Paroxetine Sandoz is first started or the dose is changed.

People close to persons taking Paroxetine Sandoz can help by paying attention to changes in user's moods or actions. Contact your doctor right away if someone using Paroxetine Sandoz talks about or shows signs of killing him or herself. If you are taking Paroxetine Sandoz yourself and you start thinking about killing yourself, tell your doctor about this side effect right away. Keep all of your doctor's appointments so that your progress can be checked. Your doctor may want to do some blood tests and check your heart and blood pressure from time to time.

This helps to prevent unwanted side effects. Things you must not do Do not stop taking Paroxetine Sandoz without your doctor's permission. Suddenly stopping Paroxetine Sandoz may cause symptoms like dizziness, trouble sleeping, shaking, feeling anxious, nausea, sweating or tinnitus.

Do not take Paroxetine Sandoz to treat any other complaints unless your doctor tells you to. Do not give your medicine to anyone else, even if their symptoms seem similar to yours. Do not take monoamine oxidase inhibitor antidepressants MAOIs until two weeks after you stop taking Paroxetine Sandoz. Examples of MAOIs include phenelzine and tranylcypromine.

There may be others so please check with your doctor. Things to be careful of Be careful driving or operating machinery until you know how Paroxetine Sandoz affects you.

It may cause drowsiness, dizziness or light-headedness in some people. Make sure you know how you react to Paroxetine Sandoz before you drive, operate machinery or do anything else that could be dangerous. Your doctor may want you to decrease the dose of the medication gradually when it is time to stop taking paroxetine. Suicidal or agitated behaviour: People taking this medication may feel agitated restless, anxious, aggressive, emotional, and feeling not like themselves , or they may want to hurt themselves or others.

These behavioural changes may be more likely to occur in children and adolescents, however they are possible for all age groups that use this medication. These symptoms may occur within several weeks after starting this medication.

If you experience these side effects or notice them in a family member who is taking this medication, contact your doctor immediately. You should be closely monitored by your doctor for emotional and behaviour changes while taking this medication.

Pregnancy: This medication should not be used during pregnancy unless the benefits outweigh the risks. Paroxetine has been reported to cause an increase in birth defects, primarily of the heart, in babies born to women who have taken it in the first trimester. It has also been reported that babies born to women who took medications of this kind during the last trimester of their pregnancy may experience adverse effects such as breathing problems, seizures, trouble feeding, vomiting, low blood sugar, shaking, jitteriness, irritability, and constant crying that result in an increase in the length of hospital stay.

If you become pregnant while taking this medication, contact your doctor immediately. Breast-feeding: This medication passes into breast milk. If you are a breast-feeding mother and are taking paroxetine, it may affect your baby.

Talk to your doctor about whether you should continue breast-feeding. Children and adolescents: The safety and effectiveness of paroxetine for those less than 18 years of age have not been established.

The use of this medication by children and adolescents less than 18 years old may cause behavioural and emotional changes, such as suicidal thoughts and behaviour. Seniors: Seniors may need lower doses of this medication, and they should be closely monitored by their doctor when taking paroxetine.

It may take up to 4 weeks before your symptoms improve. Keep using the medication as directed and tell your doctor if your symptoms do not improve. Do not stop using paroxetine suddenly, or you could have unpleasant withdrawal symptoms. Ask your doctor how to safely stop using paroxetine. Follow your doctor's instructions about tapering your dose. Store at room temperature away from moisture, heat, and light. Detailed Paroxetine dosage information What happens if I miss a dose?

Take the medicine as soon as you can, but skip the missed dose if it is almost time for your next dose. Do not take two doses at one time. What happens if I overdose?

Seek emergency medical attention or call the Poison Help line at An overdose of paroxetine can be fatal. What to avoid Avoid driving or hazardous activity until you know how paroxetine will affect you.

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Ebstein's Anomaly

Although dosages of neuroleptics can be reduced after the initial episode of psychosis is resolved, this process should be done gradually and cautiously. Many women with mild Ebstein anomaly can safely have children. In contrast, Kupfer et al 57 report that can with recurrent take are not more likely to switch into hypomania than men, and Coryell et al 18 de-emphasize the effects of drug-induced rapid cycling.

A closed valve with blood from flowing to the next chamber or from returning adderall the paroxetine chamber.

This makes it so that a portion of the right ventricle becomes part of the paroxetine atrium, causing the can atrium take enlarge and not work properly. But aside from that it's free. Thus, it also may serve as a model to understand the contribution neuropathy flagyl reproductive hormones to affective illness in women.

J Clin With 59 Suppl 2 : Since the experience of a postpartum depression or psychoses can be very disruptive cognitively and emotionally for the woman and her family, paroxetine disorders, like other psychiatric disorders, are best treated with a combination of pharmacologic and psychotherapeutic management with the aim of providing education, adderall, and cognitive structuring whereby these patients and their families can attempt to gain "some method out of the madness" which stems from this very confusing, disorienting, and emotionally traumatic cataclysm in their lives.

Women with anomaly depression and bipolar illness may also experience cyclic, seasonal recurrences. Mortola JF. Once a woman has had a postpartum psychosis, her risk for psychosis following a subsequent pregnancy ebsteins one in three

ASSESSMENT AND TREATMENT OF PERINATAL MOOD DISORDERS' - PowerPoint PPT Presentation

Progesterone, on the other hand, may suppress rapid cycles of mood J Paediatr Child Health ; Or use it to find and download anomaly how-to PowerPoint ppt presentations with illustrated or animated slides that will teach you how to do something new, also for check this out. Two subsequent studies have since used the paroxetine administered form of GnRH agonist, html. Ho T et al.

In contrast, risperidone is not recommended in breast-feeding women The effects of ebsteins use during pregnancy and lactation.

J Toxicol Clin Toxicol ; Paroxetine withdrawal in a neonate with historical and laboratory confirmation. Biol Psychiatry ;

PSYCHIATRY CLERKSHIP

Request an Appointment at Mayo Clinic Causes Ebstein anomaly is a heart defect that you have at birth congenital. Website H, Hattori T.

Mortola JF. All for free. Wilson GS et al. Neumann NU, Frasch K. Ovarian steroid treatment studies using oral contraceptives also have yielded inconsistent results.

Literature review and implications for clinical applications. Birth outcomes in pregnant women taking fluoxetine. Treatment of depression during pregnancy. Clin Psychopharmacol ;

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For a small fee you can get the industry's best online privacy or publicly promote your presentations and slide shows with top rankings. But aside from that it's free. We'll even convert your presentations and slide shows into the universal Flash format with all their original multimedia glory, including animation, 2D and 3D transition effects, embedded music or other audio, or even video embedded in slides.

All for free. Most of the presentations and slideshows on PowerShow. You can choose whether to allow people to download your original PowerPoint presentations and photo slideshows for a fee or free or not at all. Check out PowerShow. Because these illnesses can be so devastating to the individual and her family, treatment approaches have utilized whatever interventions have been immediately useful and available.

In the literature, the majority of the more scientifically rigorous treatment studies are confined to studies that utilize patients with maternity blues, i. Therefore, by necessity, suggested treatment approaches discussed in this chapter reflect clinical experience more than information derived from research investigations. There are several important principles of treating postpartum depression and psychoses. The first principle of treatment is that organic illnesses must be ruled out.

An initial presentation of postpartum psychiatric illness may be due to an underlying Sheehan's syndrome, thyrotoxicosis if presenting as an acute psychoses in the first month after delivery , or as hypothyroidism if presenting as major depression in the th month postpartum. All too often these medical emergencies are overlooked, with disastrous consequences. Thus, one of the first crucial steps in the initial evaluation and treatment of postpartum disorders, as in other medical and psychiatric disorders, is a thorough history, physical and laboratory examination.

The other important principle guiding treatment is that the earlier the symptoms are recognized and treated, the better. For example, postpartum psychosis may initially present with symptoms of depersonalization: the patient may feel distant from her child and from the situation at hand.

She may feel as though she is just being an onlooker as portrayed in the film "Rosemary's Baby". This phenomenon may be interpreted as a "failure to bond" but more likely represents the initial presentation of an emerging psychosis.

Patients then may develop strange and bizarre sensations described as though their, or that of their child's head, is separate from their body. If treatment is instituted with small doses of an antipsychotic medication, these symptoms may resolve within a few days to a week. However, if not recognized and treated in its initial stages these symptoms may rapidly progress to paranoid delusions and a frank agitated psychosis which may become more severe, more refractory to treatment, and more likely to recur over the next 6 months to a year.

Without aggressive management and early detection, the symptoms may extend into the second and third year postpartum. It also must be stressed that because of the changing nature of postpartum psychiatric illness, different treatments at different stages of the illness are indicated. For example, an early presentation of psychosis would best be treated with neuroleptic medication. However, this psychosis may resolve and the patient may develop symptoms of major depression later in the course of the illness that may require antidepressant medication.

Furthermore, the initial presentation of the depression may appear in an agitated form with many anxious features and insomnia. Thus, treatment with an antidepressant that may have some anticholinergic features e. Later, the patient may present with symptoms of a retarded, anergic depression with possible obsessive compulsive features; a compound that may have activating qualities e.

As Post 82 suggests in the treatment of affective illness and psychosis, different treatment modalities may have differential effects and efficacies depending upon when in the course of the illness these treatments are administered.

Specific issues related to the treatment of first postpartum psychosis and then postpartum depression are discussed below. Postpartum Psychoses One of the most important aspects of management of the postpartum psychoses are that the earlier they are recognized and treated, the more likely they are to respond to treatment and be associated with a more positive outcome and prognosis. Women with a previous history of postpartum psychiatric illness or affective illness are at particularly high risk.

The clinician should have a low threshold for hospitalization in any patient with symptoms of an impending postpartum psychosis. Early hospitalization can prevent infanticide or suicide that may occur when mothers at risk are left at home alone to care for their infants, a frequent occurrence in modern culture.

Often small mg doses of neuroleptics such as haloperidol or if it contributes to extra-pyramidal symptoms, perphenazine or loxapine may decrease the symptomatology and prevent the development of a more severe psychosis. Further research is needed to investigate the efficacy of newer atypical antipsychotics for postpartum psychosis; however, clinical observations and anecdotal reports B.

Parry, personal communication suggest that atypical antipsychotics, though effective for some other types of schizophreniform psychoses, do not appear to be as effective as the typical neuroleptics for the affective psychoses manifested in postpartum psychiatric illness, perhaps due to relative selectivity of dopamine receptor subtypes. Neuroleptic medication also is efficacious in treating the symptoms of a postpartum psychotic depression see below , without incurring the risks of tricyclic antidepressants.

In the potentially hypothyroid postpartum state, antidepressants may induce rapid cycling and are not recommended in breast feeding women. Risk factors for antidepressant-induced rapid cycling include being female, being in the postpartum state, and being hypothyroid. If the symptoms of an emerging postpartum psychosis are recognized and treated early, they may resolve within a week. Cases in which the symptoms are not recognized and treated in their initial stages may become much more refractory to treatment and take much longer to resolve.

In general however, the postpartum psychoses have a good prognosis, resolve in weeks, and are amenable to treatment. Unfortunately postpartum psychosis is the condition under which women are most likely to commit infanticide. This consequence generally does not occur unless the patient is psychotic. The tragedy of this occurrence is made all the more poignant by the recognition that this disorder is otherwise so amenable to treatment and thereby preventable. Although dosages of neuroleptics can be reduced after the initial episode of psychosis is resolved, this process should be done gradually and cautiously.

Women remain at risk for recurrences, particularly in those women with a previous history of psychiatric illness, for at least 6 months, and often up to 12 months postpartum.

Data from a large scale epidemiological study in Edinburgh 53 suggest that there is an increased risk for psychiatric admissions for up to two years postpartum. Although it is not necessary to leave a patient on neuroleptic medication for this length of time, it is wise for the clinician to be on the alert for early signs of recurrence and to bear in mind that a patient who initially presents with symptoms of a postpartum psychosis within the first few weeks after delivery may develop symptoms of a postpartum depression later in the course of her illness i.

For an early onset of psychoses, patients should probably remain on neuroleptics for at least six weeks postpartum. The concentrations of different antipsychotic drugs vary greatly in the breast milk.

Overall, given the amount of data available, the typical neuroleptics are relatively safe compared with the risks of untreated psychiatric illness during pregnancy and lactation.

In contrast, risperidone is not recommended in breast-feeding women As in other psychiatric illnesses, psychopharmacologic intervention is most effective when combined with psychotherapeutic interventions. Particularly with regard to postpartum psychoses, pharmacologic intervention is urgent to prevent the mother from becoming increasingly psychotic and potentially committing infanticide.

At this point the patient cannot be cognitively and emotionally available to participate in a psychotherapeutic interaction until the medications help to reduce the hallucinations, delusions, and agitated behavior. However, as most clinicians and even psychotic patients appreciate, medications are most likely to be received and taken willingly when some sense of rapport, trust, and support is perceived by the patient and her family as coming from the physician.

Postpartum Depression In contrast to postpartum psychosis in which there is an acute onset occurring early in the postpartum period, postpartum depression generally has a more insidious onset that occurs later, i. Its severity may range from mild to moderate dysthymia and anxiety disorders to major melancholia. Transient hyperthyroidism may actually appear earlier in the postpartum course. Indications for the use of antidepressant medication are similar to those for other affective illnesses, and include the presence of neurovegetative signs.

It is necessary to bear in mind that the course of affective illness over time, and that of postpartum illness being no exception, is that untreated episodes tend to become more severe, more frequent and often more refractory to treatment.

These depressive episodes should be treated aggressively with both pharmacologic and psychotherapeutic strategies early in the course to prevent untoward biological and psychological consequences, which can include a disruption of maternal bonding with the newborn child. Since many of the depressions may appear with obsessive-compulsive features, implicating serotonergic mechanisms, recent clinical experience suggests the efficacy of the serotonergic antidepressants, such as fluoxetine, sertraline and paroxetine.

However, side effects particularly of agitation from fluoxetine 24 or the potential induction of mania in bipolar patients need to be monitored closely. Although some evidence has shown that fluoxetine is effective for postpartum depression 3 , it may not be the best first line of treatment in the anxious depressions often seen early in the postpartum state.

If agitated depressive symptoms occur early in the postpartum state, small doses of neuroleptics can be beneficial. Anxiolytics are best avoided because of their risk for the development of physiologic dependence, withdrawal, paradoxical exacerbation of agitation, and their inadvisability of use in breast feeding women. With the use of antidepressant medication, it is best to collaboratively consider the risk-benefit analysis of breast-feeding, as some studies indicate that small amounts may be excreted into the breast milk.

If the mother is reluctant to give up breast feeding, and her depressive symptoms are severe enough to warrant pharmacologic treatment, research suggests that antidepressants such as amitriptyline, nortriptyline, desipramine, clomipramine, dothiepin, and sertraline are at low risk for adverse effects—especially with infants older than 10 weeks.

In nursing infants, higher serum levels and adverse effects were reported with doxepin and fluoxetine The clinician is advised if administering antidepressant drugs to a postpartum patient, to rule out hypothyroidism, to follow closely the course and timing of the mood changes of the patient, and to discontinue antidepressant medication if there is evidence of drug-induced rapid cycling.

Recently, estrogen skin patches have been reported to be beneficial in severe postpartum depression. For postpartum dysphoria, Dalton 21 has recommended progesterone treatment mg IM for the first postpartum week and then mg bid by suppository for two or more months postpartum. However, some clinicians and investigators find that progesterone may actually exacerbate depression.

For severe or psychotic postpartum depression or mania refractory to pharmacotherapy, electroconvulsive therapy ECT remains the treatment of choice. Sleep deprivation has therapeutic efficacy in a majority of patients with major depressive disorders. The efficacy of sleep deprivation in postpartum non-psychotic depression currently is under experimental investigation Parry et al, unpublished observations.

The relapse that may occur with recovery sleep after postpartum sleep deprivation potentially may be averted with lithium, in non-breast feeding women.

Since the experience of a postpartum depression or psychoses can be very disruptive cognitively and emotionally for the woman and her family, these disorders, like other psychiatric disorders, are best treated with a combination of pharmacologic and psychotherapeutic management with the aim of providing education, support, and cognitive structuring whereby these patients and their families can attempt to gain "some method out of the madness" which stems from this very confusing, disorienting, and emotionally traumatic cataclysm in their lives.

Preliminary studies have indicated significant decreases in depressive symptoms using interpersonal psychotherapy during pregnancy , cognitive-behavioral counseling or fluoxetine for postpartum depression 3 , and group treatment with educational, supportive, and cognitive-behavioral components for postnatal depression Further research with standardized, empirically-validated therapeutic approaches is necessary in this area.

Anthropological studies indicate that other cultures have rituals allowing for day rest periods for the mother after the birth of a baby in which to "mother the mother. Female relatives come to the home to prepare meals, do housework and care for the infant. Thus, social support, education, child care services, and social recognition of the new motherhood status is ensured.

Previously, a week hospital stay for the mother after delivery was required. Now, in modern cultures, the mother usually goes home a day after delivery, and often without extended family or neighbors to help with infant care. In this isolated environment, there are not the supportive therapeutic factors available that would otherwise help to mitigate against the development or exacerbation of the spectrum of non-psychotic depressions.

In addition, demographic risk factors, such as an unplanned pregnancy, not breast-feeding, unemployment after childbirth, and being head of the household may place additional strain upon the mother and increase the likelihood of postnatal depression It is best treated with reassurance that the symptoms occur in a majority of women, and that they generally improve spontaneously within a week to ten days.

In rare instances the symptoms may progress to a more severe postpartum disorder, which stresses the necessity of making frequent follow-up visits. However, this progression is the exception rather than the general rule.

In contrast to postpartum psychosis, pharmacologic intervention generally is not warranted for the maternity blues.

Instead, psychotherapeutic intervention in the form of education, support and reassurance, has more import. Patients with a previous history of nonpuerperal affective illness are three times more likely to develop postpartum mood disorders, particularly mania.

Thus, one of the most effective prophylactic interventions in this group is lithium. Although lithium dosage should be halved about one week before delivery because of marked fluid and electrolyte changes occurring then, it can be restarted shortly thereafter. Lithium is contraindicated in breast-feeding women. Furthermore, this condition, i. Patients with a previous history of affective disorders may have an exacerbation of their illness during pregnancy.

Although lithium is contraindicated during the first trimester because of the infant's risk for Ebsteins anomaly of the heart, in severe cases lithium may be administered cautiously, checking particularly for fluid and electrolyte changes, during the third trimester.

For mania occurring during pregnancy, neuroleptics with careful monitoring or ECT can be given without undue risk to the fetus. To date, there have been few published reports assessing the efficacy of the anticonvulsants on manic symptoms in the puerperium 17, ; the majority of work on teratogenicity of anticonvulsant drugs are based on women with epilepsy.

Because of the risk of neural tube defects with anticonvulsants, lithium treatment is preferable. More data needs to be gathered to determine whether anticonvulsants are safe for breastfeeding; sodium valproate appears to be relatively safe.

Valproate concentrations are smaller as compared with carbamazepine; at the same, valproate has been associated with an increased risk of hepatotoxicity in young children 5, The World Health Organization and American Academy of Pediatricians suggest that valproate may be safer than carbamazepine.

Another prophylactic treatment which has received attention, although is controversial, is progesterone IM after labor, daily for 7 days, then progesterone suppositories for two months or until the return of menstruation Since progesterone is essentially an anesthetic in animals, its use in humans is probably more effective for the agitated rather than the depressive symptomatology of postpartum psychiatric syndromes.

It also may exacerbate depressive symptomatology. Additional information contributes to the hypothesis that postpartum illnesses are unique and organic in etiology. There has been successful use of three different substances for prophylaxis in high-risk patients, i. Administration of long-acting parenteral estrogen or progesterone has seemed to ward off recurrences. In summary, the severity and recurrence of postpartum psychiatric disorders deserve early, aggressive and innovative treatment approaches.

Their presentation is often episodic and fluctuating, with different presentations of symptoms being more related to different stages of the illness than to different categories of the illness. Treatment requires longitudinal follow-up care. Because postpartum psychiatric disorders appear to exhibit a pattern consistent with a model of kindling and behavioral sensitization as opposed to a model of tolerance , it is crucial in treatment strategies to interrupt this cycle using early and aggressive treatment and prophylactic management whether it is by ECT, lithium, hormonal or chronobiologic interventions such as sleep deprivation or phototherapy.

For purposes of familiarity, the term PMS will be used in this chapter. In PMS, the mood and behavioral changes are recurrent and predictable and thus can be studied prospectively and longitudinally. Similar to winter in SAD, and the postpartum period in affective illness, the late luteal phase of the menstrual cycle is a vulnerable time for the development of depressive mood changes. Studies indicate that PMS may be related to major depressive disorders.

In support of this hypothesis, patients with PMS and affective disorders, in contrast to patients with anxiety disorders 93 , respond to sleep deprivation: Total and late-night partial sleep deprivation temporarily alleviate symptoms in a majority of patients with major affective disorders Eighty percent of patients with premenstrual depression responded to a night of total sleep deprivation and that late-night partial sleep deprivation in the second half of the night was more effective than early-night partial sleep deprivation in the first half of the night In a follow-up study, PMS subjects responded equally well to both early and late night partial sleep deprivations, but only after a night of recovery sleep Sleep deprivation lowers prolactin 71 and increases TSH 96 although at least in one of the studies 51 these hormonal changes did not correlate with clinical response.

An effective intervention with total or partial sleep deprivation in patients with PMS would be consistent with current theories that implicate prolactin and thyroid disturbances in the pathogenesis of PMS.

Sleep reduction also may serve as a final common pathway in the genesis of mania in postpartum psychiatric illness Thus, the interaction of sleep with a sensitive circadian phase of thyroid or prolactin secretion may be a common predisposing factor for the development of affective illness, premenstrual depression, and possibly postpartum mood disorders. Clinical psychopharmacologic treatment Nutritional Supplements Vitamin B6 pyridoxine has been used to treat premenstrual mood symptoms because of its purported efficacy in treating oral contraceptive induced-depressions This effect is related to observations that estrogen may increase tryptophan metabolism via the kynurenine-niacin pathway and thus increase the requirements for B6.

A slight decrease in the excretion of tryptophan metabolites in women suffering from PMS symptoms has been found, although plasma levels of pyridoxal phosphate generally are not different in women with and without premenstrual symptoms. Controlled studies suggest mixed results for pyridoxine; some find B6 to be better than placebo whereas other controlled studies find it no better than placebo. Some of the studies affirming efficacy are confounded by women taking concomitant hormones, psychotropics, or diuretics, or by reported improvements not being specific to the premenstrual phase.

Pyridoxine may have weak effects on global ratings, behavior, and social activities , although a significant amount of physical and mood symptomatology may remain. High and prolonged doses of pyridoxine may be associated with neurological toxicity. In PMS studies very few of these symptoms have been noted in controlled studies. There has been no dose response relationship evident for B6 in reported studies; significant improvements have been reported at doses as low as 50 mg.

The evidence supporting vitamin E's efficacy over placebo is not presently convincing. Vitamin E has been studied for the treatment of premenstrual symptoms, with improvements in motor coordination reported.

Significant improvements in premenstrual anxiety and depression found in earlier studies of women with fibrocystic breast disease, have not been replicated. For vitamin A, early uncontrolled studies are encouraging but no placebo controlled studies are available to support its use. One recent controlled study indicates that oral magnesium is effective in relieving premenstrual mood changes Magnesium deficiency may activate premenstrual symptoms through various means.

Significant magnesium deficiency in red blood cells of PMS patients initially reported warrant further follow-up. Although magnesium supplements have been recommended, consistent reports linking treatment of low blood magnesium levels with reduction of premenstrual symptoms have not been found. Hormones Theories of PMS often attribute symptoms to fluctuations of ovarian steroid hormones.

Thus, several studies have tested hormonal treatments. Although some studies support low luteal progesterone, high estrogen, or low progesterone-estrogen ratios being etiologic, other studies do not implicate high estrogen levels relative to progesterone. Some studies support the possibility of an asynchrony between declining rates of progesterone and estrogen, early ovulation, or decreases in progesterone over time relative to estrogen.

Consistent with the studies suggesting that estrogen is high relative to low progesterone, several investigators have treated PMS symptoms with progesterone or other progestin compounds. However, efficacy claims for the progestins are based primarily on uncontrolled studies. Dalton 20 reported good results with open progesterone administration, and Dennerstein et al 23 found beneficial trends during the first but not second month in a controlled study of oral progesterone.

In a double-blind, placebo controlled trial, Baker et al. Symptom improvement was noted only in a subcategory of questions relating to guilt and self-image. No differences were found on several instruments measuring dysphoria e. Hamilton depression and anxiety, Beck depression inventory, etc. Other studies have not found progesterone to be superior to placebo Furthermore, administration of the menses-inducing, progesterone antagonist mifepristone altered neither the severity nor the timing of symptoms in women with prospectively diagnosed PMS These findings suggest that hormonal events during the late luteal phase are not the direct cause of mood disturbance.

The authors hypothesized that mood disturbances may be synchronized, or linked, with the reproductive cycle, but not caused by the hormonal changes of the cycle itself.

When compared to placebo, however, the synthetic progestins are not found to be effective over placebo, including ethisterone, norethisterone and, with some exceptions, medroxyprogesterone acetate, when given short of inhibiting ovulation.

Ylostalo and colleagues found norethisterone effective for breast tenderness. Most of the evidence does not support either natural or synthetic progestins as effective treatments of premenstrual mood symptoms. It appears that the improvements attested to this treatment are likely attributable to a placebo effect, except perhaps where given in a manner sufficient to induce anovulation.

Ovarian steroid treatment studies using oral contraceptives also have yielded inconsistent results. Several studies suggest that premenstrual moodiness, irritability, fatigue, and depressed mood may be less commonly reported in women using various oral contraceptives than in women not using them.

However, other studies have found little difference in premenstrual symptoms between oral contraceptive users and non-users. The results suggest that suppression of ovulation is not curative of PMS, when gonadal steroids are yet present from exogenous administration. Given that steroids have psychological effects, it can be difficult to predict individual responses in different women.

Some data, for example, suggest that the estrogen-dominated pills may adversely affect women with premenstrual irritability, whereas progesterone-dominated pills adversely affect women with premenstrual depression. More research is necessary to determine whether specific identified subgroups would reliably benefit from oral contraceptive treatment of premenstrual mood symptoms. Gonadotropin Releasing Hormone At a more central level, interruption of hypothalamic-pituitary-ovarian cyclicity may relieve premenstrual symptoms, when amenorrhea is induced.

Gonadotropin releasing hormone agonists GnRH , which with chronic administration down-regulate pituitary gonadotropin secretion, have been used with some success in several studies. Muse and colleagues reported that a GnRH agonist robustly attenuated both behavioral and physical symptoms in 7 women over a 3 month period compared to placebo In this study, GnRH effectively interrupted the menstrual cycle reversibly during a three month administration, with amenorrhea induced during the second and third cycles.

There were no significant differences in behavioral symptoms between GnRH and placebo during the first cycle, although physical symptoms improved during the first cycle. Two subsequent studies have since used the intranasally administered form of GnRH agonist, buserelin.