Pathological & Therapeutic Crying

This post is in response to a previous comment:

...So, maybe if there was a medication that would stop you from crying, depression levels could be taken down?

----
Antidepressants can directly reduce crying, probably independent of other effects on emotion.

There is a condition called "pathological crying" which can occur after a stroke or other brain damage; in this condition the afflicted person may be weeping uncontrollably, with or without a subjectively sad or negative emotional state. SSRI antidepressants can help greatly with this, here is a reference:

http://www.ncbi.nlm.nih.gov/pubmed/10576464

Here is a reference showing that mirtazapine could be an alternative:

http://www.ncbi.nlm.nih.gov/pubmed/16239769

A similar antidepressant-induced "reduction in crying" may sometimes be one of the sources of relief in depression. But such an effect could be unwelcome if it leads to a subjective restriction of emotional range.
Are tears therapeutic? Most of us would agree that crying is often a relief, or even a necessary emotional outlet. Many psychotherapists would consider a patient's tearfulness in a session to be therapeutic.

In my opinion, tears can sometimes be a relief, and can sometimes be very therapeutic -- but sometimes tearfulness can feed a cycle of exhausting, out-of-control sadness or despair. And sometimes tearfulness can be so reflexive that almost any event or trigger in daily life can bring it on. Occasionally tearfulness may be a type of "defence" which prevents dialog (with self or others) about an underlying experience or emotion.

I would add, as a formal personal opinion, that tearfulness need not be a sign of "loss of emotional control" (though sometimes it could be). A person who is confident, stable, mature, and sensitive may feel quite at ease with tearfulness. Tearfulness, in this case, is a normal, and often healthy, emotional display. For some individuals, tearfulness happens more naturally, for others they may be more comfortable experiencing emotion without tearfulness.


What does some of the evidence have to tell us:
http://www.emotionalprocessing.org.uk/tears/is%20crying%20good%20for%20you.htm
(a website with an introduction to the subject)

http://www.ncbi.nlm.nih.gov/pubmed/18509370
(here's a case study showing that crying can be therapeutic -- even if it is the therapist who cries; this is a position I strongly support, for a variety of reasons, most of all because I believe in the "Rogersian" idea of genuineness and transparency, also I believe that crying need not be considered a form of weakness, but a symbol of sensitivity and compassion, whether the tear is shed by the patient or by the therapist. Too many therapists are, in my opinion, so defended by various tactics of emotional detachment, that they become aloof, and in some cases ironically afraid of emotional intensity--this may in some cases lead to dismissive, or ineffectively cold, postures towards tearful or suffering patients. Of course, if the therapist is not functioning, and is tearful due to emotional fragility or depression, then the tearful therapist needs to take a break and seek therapy himself or herself.)

http://www.ncbi.nlm.nih.gov/pubmed/17587475
(an interesting look--from an anthropological perspective-- at a phenomenon called "wailing", a type of crying & lamentation which is part of a group ritual of mourning in the Yemenite Jewish community; this article includes interesting perspectives about crying and its theoretical role in bereavement. It suggests that the idea of "healthy bereavement" has been heavily influenced by Freudian, and largely "male", ideas, viewing emotions in a kind of "hydraulic" way -- as forces to be directed, or cathartically released, and in particular pronouncing healthy grief as a process involving letting go of the relational bond with the deceased. In the "wailing" phenomenon the author suggests that the group crying, accompanied by lyricism and dialog, may act to build a kind of emotional or relational "cradle" where the bereaved person may maintain a continuing loving bond with the deceased, rather than aim to let the bond go)

Beta-Blockers

Here's a link to a very interesting study which shows that the beta-blocker propranolol can interrupt the consolidation of fear in humans:

http://www.nature.com/neuro/journal/vaop/ncurrent/pdf/nn.2271.pdf

This study suggests a novel use for beta-blockers, which could facilitate behavioural therapy for PTSD. The study demonstrates a variety of things:
1) as was well-known before, when people experience something fearful or traumatic, it sensitizes them to react more strongly to the same fearful stimulus in the future
2) when people re-experience a fearful or traumatic memory, this re-experience consolidates, or strengthens, the strong fearful reaction. This is consistent with the evolution of PTSD and other anxiety disorders, in which an expanding variety of daily events can trigger and consolidate the fear (e.g. a survivor of a bad traffic accident may constantly re-experience traumatic symptoms when hearing traffic noise, loud sounds, etc.--and may start to avoid these situations. Every time this happens, the anxiety disorder becomes more entrenched).
3) Fears can be "extinguished" by re-experiencing the feared stimulus repetitively, in a safe setting. But the fear can be "re-kindled" after extinction more easily than in non-traumatized people (this suggests a permanence to "emotional memory" that can be only temporarily over-ridden by psychological techniques)
4) If the consolidation phase of fear or traumatic memory could be interrupted, then a person might not develop ongoing post-traumatic symptoms at all. In this experiment, there is evidence that propranolol can interrupt this consolidation.
5) Propranolol may disrupt the "emotional memory" consolidation but not the "declarative memory"--the former process may occur primarily through the amygdala, whereas declarative memory is consolidated mainly in the hippocampus. So, the use of propranolol would not "erase the memory" of a traumatic event--the facts of the event would still be remembered normally--but it might reduce the painful, reflexive feeling of emotional trauma associated with the event.

The study does NOT show that "propranolol erases memories", as some of the news headlines seem to be proclaiming. It DOES suggest that adjunctive propranolol may greatly enhance the effectiveness of behavioural therapy. It requires that the person use propranolol while engaging in exposure therapy. So, for example, a possible technique for treating PTSD or panic (especially new-onset) might be to use a 40 mg dose of propranolol 1-2 hours before a therapy session. In the therapy session, the memories of the upsetting events could be discussed. The propranolol might interrupt the process of these upsetting memories getting further consolidated, might facilitate a behavioural therapy process which would help the person feel emotionally comfortable with their thoughts and memories. This process may occur because of direct beta-blockade in the amygdala, which may interrupt consolidation of emotional memory directly.

Despite this encouraging study, there are a number of negative studies looking at using propranolol similarly, for example:
http://www.ncbi.nlm.nih.gov/pubmed/18761097

http://www.ncbi.nlm.nih.gov/pubmed/19060728

I think the main thing to take from the first study is that propranolol may help, but probably only as an augmentation to enhance the effectiveness of behavioural therapy (or CBT) for treating post-traumatic stress or other anxiety disorders.

Beta-blockers are drugs used primarily in cardiology. Some beta-blockers, such as atenolol, act only peripherally, that is they do not enter the brain very much. Others, especially propranolol, can more easily enter the brain, and therefore can act in the central nervous system as well as peripherally.

In psychiatry, propranolol has been useful to treat performance anxiety, especially if there is a component of tremor (e.g. shaking hands) accompanying the anxiety. Many musicians use doses of propranolol to reduce tremor during performances. The anti-tremor mechanism is most likely peripheral beta-blockade (i.e. outside the brain), but the accompanying reduction of subjective anxiety may also be due to central beta-blockade (i.e. inside the brain). This is consistent with some studies which show that peripherally-acting beta-blockers reduce tremor as well as propranolol, but people subjectively prefer the propranolol.
(Reference: http://www.mdconsult.com/das/citation/body/121508141-4/jorg=journal&source=&sp=6333536&sid=0/N/6333536/1.html?issn= )

Beta-blockers have been studied in the treatment of panic disorder, decades ago. They don't work. Here's a link to one of the many studies showing this:
http://www.ncbi.nlm.nih.gov/pubmed/2651490

Yet, these old studies don't look at the possibility that the beta-blocker could work as an "augmentation" to psychological therapy. Many effective treatments do not work on their own, they work only in conjunction with something else.

Beta-blockers have also been used to treat irritability or rage problems. Here are a few references:

http://www.ncbi.nlm.nih.gov/pubmed/15764868
{one of the studies in the geriatric psychiatry literature, showing possible benefit for using propranolol to help agitated dementia patients}

http://www.ncbi.nlm.nih.gov/pubmed/2136070
{an example of a study showing some benefit of propranolol treatment for reducing rage outbursts -- however the study is of low quality}

http://www.ncbi.nlm.nih.gov/pubmed/3546964
{another study from the Mayo Clinic in 1985, showing some success using propranolol to treat patients with rage outbursts}

http://www.ncbi.nlm.nih.gov/pubmed/9196923
{a review paper from 1997, looking at various pharmacologic treatments for aggression; some of the research about beta-blockers is reviewed here}

In summary of the above studies, beta-blockers may help a bit for irritability, aggression, rage outbursts, and agitation, due to a variety of causes, but the evidence base is mainly from before 1990, and the studies are not very rigorous.

Beta-blockers also help diminish a very uncomfortable symptom called "akathisia". Akathisia is a state of external, and internal, restlessness, that can be caused by older antipsychotic drugs.

Beta-blockers are also useful in migraine prophylaxis. Migraine is associated with depression, so a beta-blocker could be a good therapeutic choice in someone with migraines as well as anxious, irritable, or agitated depression.

There were a few studies suggesting beta-blockers could cause or worsen depression, but many of these studies are weak. Here is a review:
http://www.ncbi.nlm.nih.gov/pubmed/16466322

In a more recent major JAMA review, beta-blockers were not found to be causative of depression or fatigue:
http://www.ncbi.nlm.nih.gov/pubmed/12117400

In my opinion, beta-blockers should be used cautiously in people who have or develop depressive symptoms, but I don't think they are contraindicated, since they may be beneficial overall if they help other symptoms. Also, if there are depressive effects, these may be dose-dependent, and may disappear just by reducing the dose.

---

Beta-blockers literally "block" beta-adrenergic receptors in the body. These beta receptors are normally stimulated by the catecholamines adrenaline and noradrenaline (also called epinephrine and norepinephrine), which are hormones secreted by the adrenal glands and by a small area of cells deep in the brain called the locus ceruleus. There is always a little bit of these hormones in circulation (in quantities in the order of parts per trillion, concentrations which would be achieved by adding a single drop of hormone to the volume of 1-10 olympic-sized swimming pools).**

Here is a reference showing resting adrenaline and noradrenaline levels in healthy subjects:
http://hyper.ahajournals.org/cgi/content/abstract/30/1/71

These tiny quantities of hormone are nevertheless enough to stimulate beta receptors; such stimulation is required to maintain or increase the output of the heart, also many other actions in the body, including in kidneys and muscle tissue.

http://www.psychosomaticmedicine.org/cgi/content/abstract/52/2/129
{An excellent study looking at peripheral catecholamine levels (norepinephrine and epinephrine) in groups of patients with anxiety, patients with pheochromocytoma (a disease causing huge increases in catecholamine levels), and normal controls; they found that peripheral norepinephrine levels correlate with anxiety, but NOT in the pheochromocytoma patients; this supports a theory that anxiety states cause central, and secondary peripheral, stimulation of catecholamine release--but the catecholamines themselves do not necessarily CAUSE the anxiety, but are a RESULT of it. Incidentally, Psychosomatic Medicine is another excellent journal worth following}

http://www.psychosomaticmedicine.org/cgi/reprint/66/5/757
{a study showing that norepinephrine levels in the brain correlate highly with blood pressure in normal controls; but do not correlate at all with blood pressure in people with PTSD, suggesting that in PTSD there is an abnormality in catecholamine regulation}

http://ajp.psychiatryonline.org/cgi/reprint/158/8/1227.pdf
{a study from The American Journal of Psychiatry showing that people with PTSD have levels of CSF norepinephrine almost twice as high as normal, and that the norepinephrine levels correlate with the severity of PTSD symptoms}

http://www-personal.umich.edu/~nesse/Articles/AdrenFunctPanic-ArchGenPsychiatry-1984.PDF
{a study from Archives of General Psychiatry in 1984, showing higher levels of plasma catecholamines in panic disorder subjects; but less responsiveness to further adrenergic stimulation in the panic subjects--this suggests that anxious subjects have chronically high catecholamines, and consequently are actually LESS sensitive to catecholamine changes}

http://www.csbmb.princeton.edu/ncc/PDFs/Locus%20Coeruleus/Aston-Jones%20&%20Cohen%20(ARN%2005).pdf
(an article about the role of norepinephrine released in the brain's locus ceruleus, and its importance for optimizing performance of tasks)

**For the math, let us assume that the resting concentration of epinephrine is 100 pMol, or 10^-10 moles/litre; a litre of water has about 55.5 moles of water, so the concentration can be expressed as one part in (55.5 / 10^-10) or one part in 555 billion. A drop of water has a volume of about 1/20 mL. So this concentration of epinephrine corresponds to an analagous concentration of one drop in (555 billion/20) mL, which is about 1 drop in 28 million litres. An olympic swimming pool has a volume of about 2.5 million litres (http://en.wikipedia.org/wiki/Olympic_size_swimming_pool). So this concentration corresponds to 1 drop in a volume of over 10 swimming pools.

Brainstem Stimulation - cranial nerves

There are some novel therapies such as vagal nerve stimulation or deep brain stimulation, which can improve symptoms of depression. These treatments may be increasingly important sources of relief for chronically suffering depressed patients-- particularly as the technology advances, becomes safer and more refined.

Here are a few links to references about these treatments:

http://www.ncbi.nlm.nih.gov/pubmed/16641939

http://www.ncbi.nlm.nih.gov/pubmed/19137233

Of greater interest to me in an outpatient office psychiatry practice, is an idea based on looking at trivially available techniques to accomplish "deep brain stimulation" or "vagal nerve stimulation", etc. All parts of the brain -- even the "deep brain", and even the vagal nerve -- are connected to all other parts of the body! Specific life events can obviously affect deep brain or vagal nerve stimulation, without requiring an implanted electrical device or neurosurgery! Some of these life events could be deliberately sought out as therapeutic strategies.

Something I've noted about some of these new, radical techniques, is that they involve stimulation of brainstem structures, often involving the cranial nerves. It seems to me that the cranial nerves are an extremely visceral set of portals through which stimuli are exchanged between the environment and the deep structures of the brain which regulate mood and consciousness. Here's a summary of all the cranial nerves, with speculations about techniques to "stimulate" them in a way that might be therapeutic:

Cranial Nerve I (olfactory): Stimulation of this nerve requires exposure to different scents. Aromatherapy is a familiar component of alternative health strategies. Here is some evidence from the mainstream medical literature, showing that aromatherapy can be helpful:
http://www.ncbi.nlm.nih.gov/pubmed/19125379
(a review article)
http://www.ncbi.nlm.nih.gov/pubmed/18178322
(a randomized study showing that the scent from lemon oil improves mood, compared to water or lavender, and regardless of expectancies or past experience with aromatherapy)
http://www.ncbi.nlm.nih.gov/pubmed/18713168
(a study showing improvement with lavender oil aromatherapy vs. controls in neuropsychiatric symptoms of elderly dementia patients)
http://www.ncbi.nlm.nih.gov/pubmed/17342790
(another study showing improvements in dementia patients with lavender)

Given the fact that there is virtually no risk to aromatherapy treatments, why not give it a try? It could help with sleep, relaxation, studying, or as a conditioning device (e.g. associating a particular odor with sleep, or with studying a particular subject, etc.)

Cranial Nerve II (Optic): Bright light therapy has a considerable evidence base. Probably looking at beautiful things in nature is good for your mood (I'll need to find a reference to prove this!). These images would have to pass through Cranial Nerve II, on their way to your brain.

Cranial Nerves III, IV, and VI: these innervate the muscles which move the eyes. There is a type of therapy called "EMDR" which calls upon patients to move their eyes back and forth as an essential part of the therapeutic technique. I suspect this acts as a conditioning phenomenon, which at once distracts the person, while perhaps permitting exposure therapy regarding uncomfortable thoughts or PTSD symptoms to take place in a more relaxed state, or in a state associated with therapeutic benefit. But maybe the "brainstem stimulation" from eye movements is an integral part of EMDR's therapeutic effect.

Here are some links to review papers or meta-analyses looking at EMDR:
http://www.ncbi.nlm.nih.gov/pubmed/16740177
(here, EMDR and CBT are both shown to be substantially and similarly effective in the treatment of post-traumatic stress disorder)

http://www.ncbi.nlm.nih.gov/pubmed/17636720
(a Cochrane review also showing EMDR and CBT to be the psychological treatments of choice in post-traumatic stress disorder)


Cranial Nerve V (trigeminal): this nerve transmits tactile sensations from the face into the brainstem. I do not know of any deliberate psychiatric therapy involving this nerve. But there is acupuncture. Also, there is massage, and in particular "facial treatments" (involving massage, aromatherapy, moisturizing creams, etc.) available in health spas--these seem to have a positive effect on overall well-being. I'd be curious to see a controlled study on this: in the meantime, though, it seems another risk-free thing to try.
http://www.ncbi.nlm.nih.gov/pubmed/19129675
(well, this is a pretty weak study -- but it's a start, and it involves a totally harmless treatment -- it shows reduction of anxiety in women receiving facial massage)

Cranial Nerve VII (facial): this nerve innervates the muscles of the face. As noted in a previous post, actions which affect facial musculature can affect emotion, just as emotion changes facial muscle tone (it's always interesting how these phenomena can work both ways). A branch of Nerve VII also conducts information about taste (gustatory sensation) from the tongue to the brain. I have no doubt that enriching one's culinary sensations in life has a positive impact on mood. But I'll have to look for a study to prove it.

Cranial Nerve VIII: the cochlear branch of this nerve transmits information about sounds from the ears to the brain. Hearing music, soothing sounds, and speech clearly affect mood and cognition. Noise, as I claimed in an earlier post, has a negative impact on mental health. Silence itself "rests" the cochlear nerve, which could itself be therapeutic (in moderation).
The vestibular branch of nerve VIII seems interesting to me as a prospective therapeutic target. This nerve transmits signals about balance, head position, and head movement to the brain. Sometimes individuals in an autistic or highly agitated psychotic state will stimulate their vestibular nerve by rocking repetitively. The action of a parent rocking a baby to sleep, or calming an agitated, crying baby, involves stimulating the baby's nerve VIII. It would be interesting to see if various stimulations of the vestibular nerve could be useful in adults, to treat anxiety, agitation, insomnia, or mood disorder. Balance exercises could be a start (perhaps some of yoga's therapeutic effects come from this). Maybe something like sleeping in a hammock, which would rock slowly, could be more soothing on this level, compared to a regular bed. Some people might find a boat to be very soothing (for others it would just cause nausea). If there are any engineers out there, reading this, it would be an interesting project to design a device which could be programmed to gently rock an adult back and forth (with different waveforms and frequencies).

Cranial Nerve IX: Glossopharyngeal. This nerve innervates your throat. The action of swallowing involves this nerve. People with anxiety states often have uncomfortable throat sensations, or problems with swallowing. It's hard to come up with therapeutic ideas directly relating to this one. Except perhaps the idea of eating really spicy food -- which stimulates not only taste buds but also sensory nerves (partly from Cranial Nerve V) in the mouth and throat. Strong culinary sensations can be a source of pleasure, and perhaps can also teach one to be more open about new things (I remember taking a long time getting used to wasabi on sushi after being introduced to Japanese food upon moving to Vancouver in 1995).

Cranial Nerve X: This is the vagus nerve that is stimulated electronically in an advanced surgical treatment for depression. The vagus nerve innervates the parasympathetic system of the body's viscera (e.g. it slows the heart, speeds up the bowel, etc.). One can train the vagus nerve through activities such as yoga, meditation, biofeedback, and through physical exercise.

Cranial Nerve XI: this nerve allows you to turn your head back and forth. Perhaps this could be an element not to forget in your exercise regime -- do some stretching and gentle exercises involving rotation of your head.

Cranial Nerve XII: this nerve allows you to move your tongue. Speech, singing, eating, and a variety of other pleasurable activities -- all involve your tongue. In anxiety states, people can have an exaggerated awareness of their tongue movements. Taking voice lessons or attending a voice coach can help build confidence, reduce social anxiety, literally help you "strengthen your voice"--a strong and clear voice, both metaphorically and literally, can be part of a healthy emotional life.

In conclusion, perhaps there are a variety of readily available techniques that can accomplish "deep brain stimulation" in ways that benefit your mental health, without actually requiring a neurosurgical procedure!

Singing

There are a number of reasons why singing (out loud!) can be beneficial for mood:

1) the parts of the brain, as well as the facial and pharyngeal muscles, involved in singing, are similar to those most active in positive mood states. This may seem a trite or ridiculous association, but it is supported by evidence, namely that voluntary actions associated with happiness, even if unconsciously initiated, lead to more positive mood. Here's a link to the abstract of a classic, amusing, 1988 paper by Fritz Strack, published in The Journal of Personality and Social Psychology (another great journal that I recommend following), demonstrating that changing the position of facial muscles leads to a change in emotional response:
http://psycnet.apa.org/journals/psp/54/5/768/

2) singing is active, yet relaxing; potentially social, yet individual; creative, yet structured

3) Fellow singers--if singing is done in a group--are likely themselves to be emotionally positive and encouraging, leading to a positive social environment.

Here's a link to an abstract demonstrating that choir singing leads to improved mood and reduced stress hormone levels:
http://www.ncbi.nlm.nih.gov/pubmed/15669447

Of note, actively singing music -- not merely listening to music -- was required to produce a beneficial effect.

Bipolar Depression

The depression which occurs in the context of bipolar disorder may have a variety of unique features (sometimes such a depression may occur BEFORE a clear manic episode has ever happened, so a depression with these features can sometimes be a warning sign of latent bipolarity, or a risk sign that bipolar disorder may develop in the future):

1) excessive sleep (rather than insomnia), along with marked physical lethargy
2) depression beginning early in life (during teenage or young adult years)
3) depressive episodes of short duration
4) depressive episodes having psychotic features (e.g. delusions)
5) other "atypical" depressive features, such as increased eating
6) Sometimes a very rapid response to antidepressants (e.g. within one or two doses)

Nevertheless, these features are not invariably present in bipolar depression; and many people may have depressive episodes with these features, who do not have bipolar disorder.

Conversely, in my opinion, there is one significant element from a person's history which points strongly away from a diagnosis of bipolar depression:

If a person has taken an antidepressant, especially at a high dose, and especially for a long period of time (over 3 months), and especially a tricyclic antidepressant or venlafaxine -- if a person has taken such an antidepressant on its own, without a mood stabilizer, and WITHOUT developing overt symptoms of mania, this is fairly strong evidence against underlying bipolarity.

Some of the recent evidence about treating bipolar depression leads us to question the role, value, or safety of antidepressants in the bipolar population.

http://www.ncbi.nlm.nih.gov/pubmed/18727689
(a 2008 review, showing little effect of antidepressants when added to mood stabilizers in treating bipolar disorder over at least 6 months of follow-up)

http://www.ncbi.nlm.nih.gov/pubmed/17392295
(this is from the New England Journal of Medicine--one of the world's leading medical journals--in 2007, and it showed, over 26 weeks of follow-up, that adding antidepressants to a mood stabilizer regime did not improve outcome, in fact the antidepressant group did not do quite as well)

Which treatments have an evidence base in bipolar depression?

1) Lamotrigine. It has the advantage of helping modestly with depressive symptoms with a low risk of causing mania. It may be true that some of the studies over the past few years have exaggerated the benefit of lamotrigine, however. In any case, it appears quite safe, and can be helpful for some people. There is a small risk of a very serious skin rash with this drug, otherwise it is quite safe and well-tolerated.

http://www.ncbi.nlm.nih.gov/pubmed/19200421
(a recent study looking at Lithium + Lamotrigine vs. Lithium + Placebo over 8 weeks of follow-up; the benefits of lamotrigine are significant but modest)

http://www.ncbi.nlm.nih.gov/pubmed/15003074
(this study also showed a benefit from lamotrigine, over a whole year, but there was no placebo group, so the results carry much less weight)

2) Other mood stabilizers, e.g. lithium, valproate, and carbamazepine. Unfortunately these drugs are probably more effective for preventing manic episodes than for preventing or treating depression. Yet, the combination of a standard mood stabilizer with another agent such as lamotrigine could be a valid step.

3) Atypical antipsychotics, e.g. olanzapine, quetiapine, and risperidone. These drugs undoubtedly are beneficial as mood stabilizers, possibly more so than the standard mood stabilizers such as lithium or valproate. There is evidence that antipsychotics + other mood stabilizers are additively effective in combination. They can be worth a try for treating bipolar depression. Unfortunately, if the bipolar depression is already characterized by excessive sleep, tiredness, and appetite, antipsychotics can sometimes make these symptoms worse. But if there are psychotic features with the depression, an antipsychotic can be an essential part of the treatment.

4) Omega-3 supplements : see my previous post

5) Light therapy: I have seen this be helpful at times. The light exposure may need to be carefully titrated (e.g. just a few minutes at a time), to prevent overstimulation or agitation. Light therapy requires the purchase of a 10 000 Lux light box, which could cost about $200-300.
http://www.ncbi.nlm.nih.gov/pubmed/18076544

6) Cognitive-behavioural therapy. Elements of CBT help with most anything, it seems to me (from learning to play the violin, to doing mathematics, to treating anxiety or depression from any cause). CBT can be adapted so as to be more tolerable and interesting (some of the workbooks can be hard to get through). I think its core features require daily written work, journaling, conducting a dialog with oneself about thoughts and emotions (hopefully to work at identifying forms of depressive thinking, and being willing to challenge such thoughts if they occur), and deliberately challenging oneself behaviourally to face fears, a little at a time. In bipolar disorder CBT may work best in conjunction with ideas that help to stabilize or structure daily behavioural rhythms (e.g. getting up regularly in the morning, having a routine, eating regularly, exercising, doing some intellectually challenging work, doing some creative work, going to bed around the same time, etc.). Of course, in depression of any sort, it can be extremely hard to initiate or maintain such lifestyle habits--if there is too much fatigue or lack of motivation to get started with very much, I encourage getting started with the very smallest of tasks or daily structures, and building from there; consistency is more important than amount.

http://www.ncbi.nlm.nih.gov/pubmed/18324665

7) Other psychotherapy: basic supportive care can be very important, provided there is a resilient, trusting therapeutic relationship

8) Antidepressants: despite the negative results of late, there are selected individuals for whom antidepressants may be very helpful. Over the past decade, bupropion has perhaps been the first antidepressant to consider, due to its lower rate of causing a manic switch, and possibly its higher likelihood of helping with the low energy states characteristic of bipolar depression. SSRI antidepressants have been the second-choice agents. MAOI's are probably lower risk with respect to causing manic switch, and the reversible MAOI moclobemide could be a good option. Venlafaxine and tricyclic antidepressants have been agents to avoid, due to their high risk of causing a manic switch.

References:
http://www.ncbi.nlm.nih.gov/pubmed/16449476

http://www.ncbi.nlm.nih.gov/pubmed/16880481

9) Stimulants: I have found that stimulants can be quite useful in bipolar depression, provided that they are not increasing psychotic symptoms or agitation. They have the advantage of working quickly, helping immediately with energy and attention, and often helping with mood. Furthermore, they can be withdrawn quickly if manic symptoms or agitation arises; if stimulants are withdrawn quickly, it causes a relative state of sedation. (Note that there is some evidence from a few older studies that stimulant treatment can actually reduce symptoms of mania) There are several older stimulants, such as methylphenidate (Ritalin), and dextroamphetamine (Dexedrine), and several newer formulations of these older drugs (e.g. Adderall). A newer, atypical stimulant called modafinil can be an option as well. However, modafinil is quite expensive and often not covered by medication plans in Canada.

References:
http://www.ncbi.nlm.nih.gov/pubmed/15383134
http://www.ncbi.nlm.nih.gov/pubmed/18980736

http://www.ncbi.nlm.nih.gov/pubmed/16974196

http://www.ncbi.nlm.nih.gov/pubmed/367183

http://www.ncbi.nlm.nih.gov/pubmed/3312177

(the above two references are to older, interesting studies showing that stimulant treatments actually helped REDUCE manic symptoms acutely--I cite this as evidence that stimulants are reasonable to use in bipolar patients, however I would not go so far as to recommend stimulants in the treatment of mania, as other anti-manic treatments are much more effective and accepted as a standard of care)


10) ECT:electroconvulsive therapy is unequivocally effective for treating both depression and mania. However, there may be a higher risk of mild but persistent cognitive side-effects in the bipolar population:
http://www.ncbi.nlm.nih.gov/pubmed/17653292

If there are "borderline" phenomena occuring in the context of bipolar depression, once again some of Dawson's ideas may be helpful (see my previous postings about borderline personality); these involve emphasizing the role and competence of the individual patient in choosing treatment options, and avoiding an authoritarian stance on the part of the therapist.

Other references:

http://www.ncbi.nlm.nih.gov/pubmed/18992784
(A recent study correlating early age of onset for depression with bipolarity, severity, recurrence, etc.)

http://www.ncbi.nlm.nih.gov/pubmed/18199233
(A review of diagnostic issues regarding bipolar depression)