In case you missed my psych meds 101 series, here’s the post on antidepressants.
In case you missed my psych meds 101 series, here’s the post on antidepressants.
Faith Trent explains that she wrote Be There For Me: An Insight Into My Journey With Depression to “1. Show sufferers they are not alone. 2. Provide advice and guidance for those trying to support a sufferer. 3. Try to remove some stigma around depression.” At the time of writing she was in the midst of a depressive episode and was off work, and she thought writing would be a good way to make something positive out of something horribly difficult.
The author’s depression journey captures common elements shared by many of us living with depression. When she first became depressed, she had no idea what was happening, especially since there was no identifiable trigger or reason for her to be depressed. She was initially reluctant to try medication, a view that she’d picked up from her mother. There are chapters devoted to various different features of her illness, including anxiety and self-harm. For her, self-harm was a way to somehow legitimize the way she was feeling.
She describes what it feels like to live with depressive symptoms such as fatigue, apathy, poor concentration, and the pervasive shadow of guilt. She also explains common thought patterns in depression, including self-doubting, feeling like a burden, and drowning in shoulds. These are not textbook definitions, but rather descriptions of the subjective experience.
She writes about the challenges of parenting young children with depression, and how the illness makes the daily parenting tasks feel like a mountain that must be climbed. She finds it hard to be fully present with her children, and she regrets the distance from them that has created. She also crying in front of them. I’ve always wondered, though, if there isn’t benefit in children seeing what mental illness actually looks like, and perhaps this helps to prevent the propagation of stigma.
She identifies the essential elements she has found for managing her illness: becoming aware of her triggers and early red flags of worsening illness, maintaining work-life balance, getting enough rest, talking to a close circle of friends, exercising, and doing things that make her happy. When her illness hits hard, she says “it cripples my whole life… It causes me to question every part of my life, doubt my value, and make me feel like I am a burden to all I encounter.” This struck me as such classic depressive thinking.
As is far too often the case for those of us living with mental illness, the author has experienced stigma directly. Some people made her feel “truly inadequate and small for suffering from something that I feel they didn’t believe was real. I was patronised and made to feel like I was making it up at times.” It was disturbing to read that a teaching colleague of hers questioned whether she should be allowed to be at work because she might pose a danger to her students. As a nurse I have faced questions about my safety to my patients, but somehow no one realizes (or cares?) that with depression most often the real risk is to ourselves.
The main focus of the book is breaking down stigma. She concludes that the only way to do this is for people with depression to share their stories to counter the misconceptions others may have. I wholeheartedly agree.
You can find the author on her blog Shatter the Stigma.
You can find my other book reviews on my blog index.
Image credit: Amazon.com
Content warning: This post openly discusses suicide and suicide attempts
You can find info here on where to reach out for help if you’re in crisis.
It’s suicide prevention week, so it seems like an appropriate time to talk about suicide in all its ugliness. I have attempted suicide multiple times; most were associated with my first episode of depression just over 10 years ago. Suicidal thinking is a symptom of my illness, and one that will most likely continue to pop up when things get really dark. It’s something abnormal that unfortunately has come to be all too familiar.
In 2007 I had three suicide attempts outside of hospital, plus multiple attempts while in hospital that resulted in me being sent to psych ICU. At the time of the first attempt. I hadn’t been diagnosed with depression yet, but I was fairly certain that’s what was going on. The suicidal thinking had been building, and then it got to the point where I had a plan. The next step was getting pills, and finally I ended up taking those pills. Each of these steps was well thought out and took some time; there was nothing impulsive about any of it. I tried to hold off as long as I could out of a sense of responsibility to my family and other people in my life, but things were just so bleak and hopeless that the idea of remaining alive seemed totally untolerable. The suicidal thinking was something new to me at that point in my life, so it was hard to figure out ways to cope with it. I went through a brief phase of cutting in an attempt to find an alternate way to deal with the pain.
When I became depressed in 2010, initially suicidality wasn’t among the symptoms I was experiencing. However, as the episode extended over the next year I began having ever-increasing thoughts of suicide. I took myself to hospital voluntarily, but had a very negative experience and ended up being discharged without feeling any better. I developed a suicide plan involving my psych meds. At the time, I was working Monday to Friday with every other Friday off, and my plan was to take the pills on one of my Fridays off so no one would notice anything out of the ordinary until Monday. Each Friday off, I would evaluate whether or not I thought I could make it through until the next Friday off. Eventually one Friday I decided I just couldn’t take the pain anymore, and I took the pills. Over the next few days I alternated between sleeping and wandering around delirious, and then when I didn’t show up for work on Monday they called the police. When the police showed up at my door I was totally loopy, and they hauled me off to hospital.
I haven’t attempted suicide since then, but there have been a few occasions when I have taken steps towards enacting a plan to kill myself. What has stopped me has been fear – not fear of dying, but fear of “failing” to kill myself. I generally don’t tell people when I feel suicidal, partly because I don’t feel like talking will help, and partly because I have a strong aversion to going to hospital. I’ve come to the conclusion that given the history of my illness, chances are fairly good that I will eventually, at some nebulous point in the future, end up dying by suicide. I don’t say this because I desire this outcome or because I’m suicidal right now, but in terms of simple probability it seems the most likely.
That brings me back to what I said in my post yesterday. To really decrease the risk of suicide in those of us living with mental illness, we need better treatment. We need more than just an ear to listen to us; we need something tangible that will truly make a difference and create a bright light of hope. And that can’t come soon enough.
Image credit: American Foundation for Suicide Prevention
Wouldn’t it be nice if the treatment of depression was simple? Unfortunately, there’s nothing simple about depression treatment in the real world Treatment resistant depression (TRD) refers to illness that hasn’t respond to trials of adequate duration and dosage of at least two antidepressants. The STAR*D research study found that only about 1/3 of people get well with one anti-depressant trial, a further 1/4 get well with a second trial, and only 67% get well after a fourth medication trail. That’s a whole lot of people not getting well. So if you fall into that category of TRD, what are your options?
If depression isn’t responding to treatment, it’s important that the diagnosis be re-evaluated. Could this be bipolar depression? In that case, the treatment strategy may need to be quite different, and antidepressants alone are seldom effective for bipolar depression. Is there a medication, medical condition (e.g. hypothyroidism), or substance use that could be contributing to the problem that needs to be addressed in order to properly treat the depression? Is there unaddressed trauma that needs to be targeted?
Let’s say the diagnosis is major depressive disorder and no complicating factors can be identified. Has psychotherapy been tried? If not, that’s always a great place to start. Other first steps might be to increase dose, switch antidepressants, or try antidepressant combos. Another strategy is augmentation, which refers to medications that are added onto an antidepressant regimen to achieve a greater therapeutic effect. Options include lithium, thyroid hormone, antipsychotics, and stimulants.
Ok, so what if you’ve tried, maxed out, and failed on these various treatment strategies? Ketamine, a dissociative anaesthetic, has a novel mechanism of action, affecting the glutamate system in the brain. It is a relatively new treatment and availability can be limited, but there is some good research supporting its effectiveness.
There are a number of other drugs that have been studied that are potential options although there isn’t a large body of research evidence to support them. D-cycloserine is an antibiotic that at high doses acts on the same NDMA receptors that ketamine works on. Minocycline is another antibiotic that has shows some benefit, as it calms inflammatory microglia in the brain. I wouldn’t be all that keen to use an antibiotic for a prolonged period, particularly when there’s not much evidence to back it up. Infliximab, which is used for autoimmune diseases, has shown some antidepressant effect in depressed people with elevated levels of inflammation. As a biological agent, it is quite expensive. Botox has also been shown to be helpful, and I feel like I’ve had some positive results from it.
Scopolamine, which is used for nausea, appears to have an antidepressant effect via its action on muscarinic receptors in the brain. Studies have primarily involved 3 doses via IV infusion, with a rapid but not sustained effect. This is something I’ve considered trying in the form of an intramuscular injection, as the oral version of scopolamine that’s available in Canada can’t cross the blood-brain barrier to enter the brain.
Blocking kappa-type opioid receptors has been associated with an antidepressant effect. This is different from the µ-type opioid receptors which are associated with effects like analgesia and respiratory depression. Buprenorphine, which is found in Suboxone, is a kappa antagonist but also has effects on µ receptors, and research is being done to develop drugs that are selective for kappa receptors with no activity at µ receptors.
There are a number of over-the-counter supplements which have shown some effectiveness in depression. These include L-methylfolate, which may be most useful in those with elevated inflammation or impaired methylation cycles, S-adenosyl methionine (SAMe), omega-3 fatty acids, creatine, and n-acetyl cysteine, which decreases oxidative stress. I take L-methylfolate along with vitamin B12 by injection every 2 weeks, and have noticed that if I go longer than 2 weeks my thinking and my energy start to slow down. I also take omega-3’s, although I’m nor sure if it’s actually helping me or not.
Other options involve the application of energy to the brain. Probably the best known is electroconvulsive therapy (ECT). ECT has been helpful for me in the past, but it’s difficult to manage on an outpatient basis, both because of the effects on memory and because you’re required to essentially have a babysitter on ECT days. Another option is transcranial magnetic stimulation (TMS), which stimulates the brain through the creation of a magnetic field.. It has demonstrated good results in research studies, and because there’s no anaesthesia involved that decreases the pain-in-the-butt factor compared to ECT. It brings about its own pain-in-the-butt factor, though, as it’s more frequent, and at least where I live it’s not covered by insurance. Deep brain stimulation (DBS) is another option that I have very limited familiarity with. This involves the surgical implantation of a neurostimulator device that sends electrical impulses to target areas in the brain. DBS is also used for other conditions including Parkinson’s disease. The potential complications sound a bit frightening, but a quick google search shows it’s the most common operation performed for Parkinson’s Disease at the major local hospital in my area.
How is your treatment working for you? If it’s not working, what other options have you considered?
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The Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial studied 2876 people with major depressive disorder to evaluate their response to depression treatment in a real-world setting. Unlike the randomized controlled trials that are often used to evaluate a drug’s efficacy, there were few exclusion criteria, the patient and their physician knew which drug they were taking, and patient choice was incorporated. Four sequential levels of treatment were established, and if a patient failed to achieve remission after 12-14 weeks, they would be moved to the next level. The target was full remission, unlike many other studies which measure response (i.e. a ≥50% reduction in symptom rating scale scores). Remission rates can be substantially lower than response rates, but are useful because there are better long-term outcomes for people who do achieve full remission.
Level 1 treatment consisted of citalopram, and 28% of patients achieved remission based on the Hamilton Rating Scale for Depression (HAM-D). Certain factors were identified, such as other comorbid mental illnesses, that were associated with lower or higher remission rates.
In level 2, patients were offered cognitive psychotherapy, a switch to another antidepressant (randomly selected), or the addition of another medication to augment the treatment. Among level 2 patients who switched to another medication, remission rates were 21.3% for bupropion, 17.6% for sertraline, 24.8% for venlafaxine. Rates were similar among those patients who switched to cognitive psychotherapy. Among the patients who received augmentation treatment, the remission rates were approximately 30% for both bupropion and buspirone. Augmentation with medication produced more rapid remission than augmentation with cognitive psychotherapy.
In level 3, patients who switched medication were randomly assigned to mirtazapine or nortriptyline, and patients who received an medication for augmentation were randomly assigned to lithium or the T3 form of thyroid hormone (liothyronine). Remission rates were 12.3% for mirtazapine, 19.8% for nortriptyline, 15.9% for lithium, and 24.7% for thyroid hormone.
In level 4, patients were randomly assigned to switch to either tranylcypromine (an MAOI antidepressant) or venlafaxine plus mirtazapine. Remission rates were 6.9% for tranylcypromine and 13.7% for venlafaxine plus mirtazapine.
Altogether, 67% of patients were able to achieve remission. The study found that people may still remit by 12 weeks even if there’s only a modest symptom reduction at 6 weeks. However, the more treatment steps that are required, the lower the chance of a patient achieving remission and the higher the chance of intolerable side effects and relapse.
Personally I found the take-home message from this study rather discouraging. During my last hospitalization I argued that my suicide attempt was supported by the STAR*D’s not so subtle hint that I was shit outta luck. I think it’s crucial that we find new kinds of treatment that will help that 33% of people who are treatment-resistant and just aren’t achieving remission with many currently available antidepressant medications. This study doesn’t consider all potential treatments; for example, atypical antipsychotics, ketamine, and ECT aren’ included, and psychotherapy plays a limited part. Still, we deserve better. A lot better.
For more info on the research terminology I’ve used in this post, see my post on research literacy.
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The title is a kind of weak ripoff from the Seinfeld-ian Pimple Popper MD, but still, it’s fairly apt. I have major depressive disorder, and I take a boatload of pills. Because my memory isn’t that great and I don’t want to forget to take them, I have them all laid out on a shelf in my bookcase. If anyone comes into my living room chances are they’ll notice the mini pharmacy I’ve got going on, but I am so beyond caring about what people think about that.
In this post I’m going to break down the various things I’m putting into my body to try and stay afloat with my depression. Medications will never be all of the picture, but for me they are an important part of my treatment plan.
Mirtazapine 30mg and venlafaxine 300mg: These are my two antidepressants. I have always responded better to antidepressants with more activity related to norepinephrine than serotonin, so these two fit the bill. The combo is sometimes referred to as “California rocket fuel” because of its potency. Mirtazapine is actually most sedating at lower doses, so I’ve settled on the middle of the road 30mg dose because I didn’t sleep as well on higher doses.
Lithium 1200mg: I don’t have bipolar disorder, but lithium has actually been recognized for a long time as an effective augmentation strategy in major depressive disorder. If I start feeling worse one of the first things my doctor and I consider is increasing my lithium, since I tend to respond fairly quickly to dose increases. When my serum levels get higher, though, I tend to have increased problems with tremor and coordination, turning me into a complete klutz, complete with wipeouts on the sidewalk and falling down stairs.
Quetiapine 600mg: Atypical antipsychotics are also effective for treatment augmentation in depression. Of the ones I have tried, quetiapine has been most effective for me. It helps with my mood and is very reliable for getting to sleep.
Dextroamphetamine 15mg: I first tried dextroamphetamine a year and a half ago when I was really slowed down in both movement and thinking. It helped, but I wasn’t keen on taking “speed” any longer than needed, so I only took it for about a month. I restarted it earlier this year when I got really slowed down again. It helped, but when I tried to decrease the dose my mood dropped. Research has shown that it tends to be effective as an antidepressant augmentation strategy for only a couple of months or so, and then the effect tends to wear off; however, I’ve tried several times to decrease the dose and it makes me feel worse. My doctor has a good attitude about it, and has no problem with me taking it on an ongoing basis when it’s clearly working.
Propranolol 10mg prn (as needed): Lithium gives me an intention tremor, which occurs with intentional movement as opposed to a resting tremor. It’s worse if my lithium level is higher or if I’m worn out, and probably the dextroamphetamine doesn’t help either. Propranolol helps keep it in check, and I tend to use it mostly for days that I’m working, since patients generally aren’t reassured about getting an injection if the nurse drawing it up has shaky hands.
Lorazepam 0.5-1mg prn: Anxiety is generally not a prominent feature of my illness, so I’ve never needed to use lorazepam (Ativan) on a regular basis. I find for me it’s most effective to get a bit of a numbing effect when I’m going into particularly stressful situations. Since I use it so seldom, I’m able to get away with a small dose.
Min-Ovral: I have spent much of my adult life on birth control, but decided a couple of years ago to take a break. When I got depressed last year, my hormones went crazy. I was getting my period every 3 weeks and PMS was having a big impact on my mood. Now I’m back on birth control and my hormones are steady and happy. The estrogen in the Min-Ovral may also give my neurotransmitters a bit of a boost.
Omega-3 fatty acid plus vitamin D supplement: There have been research studies that have shown that omega-3’s have some beneficial effect on depression. Vitamin D may also play a role in depression, and since I live on the Wet Coast of Canada where it rains for a good chunk of the year supplementation seems like a good way to go.
Multivitamin/mineral/antioxidant supplement: Besides helping my overall health, the goal with this is to have some effect on decreasing oxidative stress, which may play a role in depression.
L-methyfolate and vitamin B12 supplementation: I get these in an intramuscular injection every 2 weeks from my naturopath. Both play a role in the methylation cycle that’s involved in neurotransmitter synthesis, and L-methylfolate in particular has been shown to be useful in depression.
So that’s me, Pill Popper RN. What’s in your medicine cabinet?
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I will freely admit that I’m a bit of an organization nut. It’s a trait that has served me very well in terms of maintaining functioning while bogged down in an episode of depression. I’ve been doing this depression thing long enough that I know what my deficits tend to be when I’m unwell, and I draw on that knack for organization to create a sort of safety net for myself.
Mental illness can wreak havoc on memory. When I’m ill, my brain feels like a strange hybrid of Swiss cheese and mashed potatoes. Since I am aware of this, I can try to plan ahead for it. I do this by setting up an organizational system that can compensate for some of my deficits. When it comes to important things, my backup plan needs its own backup plan, since I know that I might not always remember to put things in my calendar, for instance. This has come to the rescue a few times, including saving me from being a no-show for visits I’d booked with my patients for my home care nursing job.
I rely heavily on my Google calendar. Everything goes in there as soon as it’s arranged (unless I’m really scattered and forget this crucial part of my system). I use color-coding to separate work and personal, and have recurring reminders set up for things like bill payments. I’m also a great lover of lists, and use Google Keep along with Apple Notes. I’ve got checklists breaking more complex tasks into individual components for those days when I’m feeling too overwhelmed to know how to do anything. The goal is to rely as little as possible on my brain to remember things. Working on getting/staying well is hard enough, and any brainpower I can free up is a good thing.
When depression muddles my thinking, making simple decisions can seem overwhelming and impossible. If I haven’t decided ahead of time what kind of yogurt I’m going to buy, I might stand in front of the yogurt section at the grocery store for 10 minutes with a blank stare on my face and absolutely no idea how to make a decision about what to buy. It’s not a matter of anxiety over what the right decision is, but more like that part of the brain that knows how to make decisions has decided to close up shop and take a siesta. There has been many a time that I have simply left a store empty-handed, because the default decision is do/buy nothing. I’ve learned that when I’m feeling like this, I need to decide exactly what I’m going to get ahead of time, when I’m not faced with an array of options. It feels a bit silly to be so rigid, but it’s a lot less silly than staring stupidly at a sea of yogurt containers.
Mental illness can warp how we see the present in relation to both past and future. It can be very hard to see a pattern in our symptoms and what might be triggering them. Technology can be a powerful tool to gain insight into what is happening both inside and outside the mind and body. I use apps to track almost everything I do: sleep, mood, diet, activity, menstrual cycle, medication changes, alcohol, stressful events, work, etc, etc. Again, it feels kind of silly to be this rigid, but it helps me understand how I’m doing, and makes it s lot easier to answer questions that my health care providers might ask. When my depression leaves me feeling totally powerless, tracking things on my apps can help me feel a little bit more in control.
Having a routine is very important to me, especially when I’m not well. It gives me a sense of peace, and makes it easier to turn down the volume on my thoughts. Most important is my morning routine. I drink tea, tea, and more tea, read the discussion forums on a mental health app I use, meditate, and do crossword puzzles. Even my pet guinea pigs support me in sticking to the ritual – they know that their veggies come at the same time as mama’s first and second cups of tea, and if I happen to forget, they will give me loud squeaky reminders.
We all have our little tricks to help us cope with the day to day experience of mental illness. These are some things that have worked for me, but it’s always great to learn new strategies from other people who are dealing with the same sorts of issues. Together we can be stronger, and our bags of tricks can help us make it through.
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We’re supposed to dream big, aim high, reach for the sky, and all that crap. But what about those days when your mental illness is kicking your butt and you barely have the energy, motivation, interest, or presence of mind to haul your a** out of bed, much less hold yourself up for the duration of a shower?
Let me be clear, setting goals is a good thing. Pushing yourself to do more than you think you’re capable can allow you to do things you thought you could only dream of. However, the goals you set should be realistic, and what’s realistic is going to change based on how your illness is currently affecting you. If you’re setting yourself up for failure, how is that doing you any favours?
When my depression is severe, just getting out of bed can be a gargantuan effort. If I were to try to go outside for a walk because that’s what you “should” do when you’re depressed, I probably wouldn’t make it beyond the front door. That would make me feel even more negative about myself, and reinforce the thoughts that I’m useless, pathetic, etc., etc. I find that I don’t tend to devote a lot of energy to comparing myself to others (perhaps because I hate people when I’m depressed), but I do compare myself to my level of functioning when I’m well. Realistically, though, that’s not a fair comparison.
The way I try to look at it is that goals should be proportionate to the amount of energy you have and the amount of energy it would take to complete a task. If depression is sucking the life out of you and your energy level is so low that if it were a gas tank you’d be running on fumes, is it reasonable to plan on going for a 4-hour drive on that empty tank? Hmm, not so much.
So I say, if taking a shower when you’re severely depressed takes about the same amount of energy that it would take you to climb Mount Kilimanjaro when you’re well, then taking a shower is a huge goal and an accomplishment worth celebrating. The fact that showering when you’re well is easy is totally irrelevant. It’s not an apples to apples comparison or even an apples to watermelons comparison; it’s more of an apples to mountains comparison.
As I nurse I try to tell both myself and my patients to aim low and dream small when feeling really unwell. Achieving a “small” goal will serve you better than failing at a bigger goal. And don’t forget to congratulate yourself for that mountain-summit-equivalent shower that you didn’t think you could do. You absolutely earned it.
Growing up, I absolutely loved Christmas. The tree, the traditional Christmas baking and other yummy treats, Christmas carols, the excitement of Christmas morning, turkey dinner… the list went on and on. As I grew into adulthood, some of the sparkle faded to more of a soft happy glow, but there was a new form of sparkle in things like rum and eggnog and ice wine.
My first non-Christmas, or Christmas that wasn’t, happened in 2008, when my partner at the time was in ICU following a suicide attempt. My Christmas dinner that year was a hotdog from 7-Eleven, because nothing else was open near the hospital. My next non-Christmas was in 2012, when I was locked up in the psych ward. My family chose to have Christmas at my parents’ place in another city, which I understood but couldn’t help but feel some resentment over.
Depression next stole Christmas away from me last year. I was completely indifferent, and joined a friend for turkey dinner more because I thought it would satisfy her than out of any desire on my own part to celebrate Christmas. This year seems to be headed toward another indifferent Christmas. The large collection of Christmas tree ornaments that are a mix of childhood favourites and new additions is tucked away in my closet, and I haven’t felt any desire to fire up my old ritual of Christmas tree decorating accompanied by carols and eggnog.
While I don’t feel much of anything about Christmas itself, I do feel a sense of loss that something I used to care about and enjoy so much now means nothing. Maybe if I forced myself to follow the rituals anyway the Christmas spirit would sneak back into my life. Or maybe it would all just feel like a farce and remind me that I am broken.
I have a small family, and our Christmases have always been intimate affairs rather than a chaotic bustle. My parents almost always host Christmas, and they live 4 hours away, so I have the options of just not going. They haven’t said anything about it yet, and I know they’re worried that if I feel pressured it will scare me off. I probably “should” go home for Christmas, but shoulds just don’t really hold water with me these days.
I suppose what I have to accept is that my depression makes it almost impossible for me to enjoy anything at this point. Whether I put up a tree or not that isn’t going to change. But that doesn’t mean some rum and eggnog and butter tarts can’t lighten things up a little bit.
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I can be a bit (okay more than just a bit) of a geek, and one of my big interests is how medications work. Throw in the fact that I’m a mental health nurse, former pharmacist, and person who has tried piles of different psychiatric medication, and you get someone who will quite happily watch hours of continuing education webinars on the topic.
It can be really useful to understand how medications work, because it can make both the therapeutic effects and side effects make more sense. This is the first of a series of psych meds 101 posts I’m going to write that will break down different classes of medications. I’ll also address antipsychotics, mood stabilizers, anti-anxiety meds, and sleep meds.
Most antidepressants affect the three major neurotransmitters implicated in depression: serotonin, norepinephrine, and dopamine. Nerve cells (neurons) communicate with other neurons via connections known as synapses. The neuron sending the signal is referred to as presynaptic, and the neuron receiving the signal is referred to as postsynaptic. The presynaptic neuron releases neurotransmitter molecules in the synaptic cleft (the space between the two neurons), and the neurotransmitters act at specific receptors on the postsynaptic neuron.
Why does that matter? Many antidepressants are reuptake inhibitors, meaning they block recycling pumps on the presynaptic side that would normally take up and recycle some of the neurotransmitter that had been released. This means there is more neurotransmitter floating around the synaptic cleft, available to act at receptors on the postsynaptic neuron. Over time, this actually changes the number of receptors that the postsynaptic neuron produces, which may explain the delayed onset of action for antidepressants.
Other antidepressants may block certain types of receptors on either pre- or post-synaptic neurons, and this may influence the release of one or more types of neurotransmitters.
A lot of medications are messy, in the sense that they don’t only do want them to. Some antidepressants affect histamine receptors, and this can cause side effects such as sedation and weight gain. Activity at muscarinic receptors can cause sedation, dry mouth, and constipation.
There are multiple different kinds of serotonin and norepinephrine receptors, and they impact various processes in the body. When serotonin gets busy at certain types of receptors it can do things that we don’t want it to, causing things like insomnia, weight gain, or sexual dysfunction. Norepinephrine can act at certain receptors to affect things like blood pressure, causing lightheadedness.
These inhibit the activity of the presynaptic serotonin recycling pumps. Escitalopram is the most “clean” in that it does what it’s supposed to and not much else. Other medications in this class include citalopram, sertraline, fluoxetine, and paroxetine.
These inhibit the presynaptic recycling pumps for both serotonin and norepinephrine. Some people are not as responsive to meds that act on serotonin alone, and respond better when there is action on norepinephrine. Drugs in this class include venlafaxine, desvenlafaxine, and duloxetine.
Bupropion inhibits the presynaptic recycling pumps for norepinephrine and dopamine. Because of the different mechanism of action, it can be used in combination with SSRI for a triple-whammy sort of effect.
These inhibit the recycling pumps for serotonin and norepinephrine. However, they are quite “messy” and affect a number of different receptors, meaning they tend to cause more side effects. They are dangerous in overdose because they can potentially disrupt the heart rhythm. Several years ago a psychiatrist wanted to put me on nortriptyline, and while I reluctantly agreed, I soon stopped it because I didn’t think it was a safe medication to have at home given that I do get suicidal thoughts in the context of depression. Other examples of TCAs include amitriptyline and imipramine. This class of medications is also used to manage nerve pain.
These inhibit the monoamine oxidase (MAO) enzyme, which acts inside neuronal cells and is involved in breaking down serotonin, norepinephrine, and dopamine. They are an older class of medications and despite being very effective antidepressants they are seldom used because of the need to restrict dietary intake of tyramine. Tyramine is normally broken down in the gut by MAO, but if MAO is blocked by medication, tyramine is absorbed into the bloodstream and sends blood pressure through the roof. This condition is referred to as hypertensive crisis. Tyramine is found in a number of different foods, including aged cheeses and fermented foods.
Tranylcypromine is the most commonly used MAOI. Moclobemide is a variation of an MAOI called a RIMA (reversible inhibitor of monoamine oxidase) that acts reversibly on the MAO enzyme, so that tyramine is still able to get broken down safely by MAO in the gut.
There are a variety of other medications such as mirtazapine and vortioxetine that work in novel ways, which I won’t get into here. The combination of mirtazapine and venlafaxine is sometimes referred to as “California rocket fuel”; this is part of my current treatment plan, and while I’m not getting a rocket fuel effect it has helped. There are also other medications that can be used to augment antidepressant therapy, including lithium, atypical antipsychotic medications, and liothyronine (a form of thyroid hormone).
There are also new outside of the box treatments being studied such as ketamine, which affects the action of the neurotransmitter glutamate. I am really excited about this, and will write more about it in future posts.
If you’ve made it this far, good for you! I hope you’ve found some of this useful, and maybe it’s even given you some added insight into medications you have taken or are taking. In the upcoming post Psych Meds 101: Mood Stabilizers, I’ll talk about the treatment of bipolar depression, and why antidepressants have a limited role to play.
Ask anyone of a certain age what comes to mind first when they hear the term electroconvulsive therapy (aka ECT, aka electroshock therapy, aka shock therapy), and chances are they will mention the film One Flew Over the Cuckoo’s Nest starring Jack Nicholson. Given the lack of more realistic portrayals of this treatment, ECT may be viewed as a dangerous, obsolete treatment.
Except it not. ECT is a very effective treatment option for depression, and can also play a role in mania and psychosis. One of the biggest benefits is that it works fast, much faster than antidepressants could be expected to start working. That’s why I first received ECT; it was my first hospitalization, I was highly suicidal, and the treatment team just wasn’t prepared to wait the weeks it would take to see if I would respond to the antidepressant that had been started. I was too ill to be able to remember any of those first few weeks, and I was being treated on an involuntary basis, but being a mental health nurse I probably knew at least on some level that this was a good idea.
The ECT process itself is fairly simple, and very different from Jack Nicholson’s ECT scene in One Flew Over the Cuckoo’s Nest. In the movie a bite block was roughly shoved in his mouth, a shock was applied with no anaesthetic, and he began wildly thrashing about. None of this is representative of current ECT practice.
As a patient, they put you out cold with a general anaesthetic (such as propofol) and a muscle relaxant (succinylcholine). These are given by IV and knock you out within seconds. I had the odd experience of getting a yummy smoky sort of smell after they injected the meds, even though the only thing coming through the mask on my face was oxygen. One of the reasons I like ECT is because I love that smell. This is not something I’ve heard anyone else report, but I experienced it every single time. Once you’re anaesthetized, they fit the rubber bit guard into your mouth to protect your teeth and tongue. The shock is delivered via two electrodes placed on the head. The muscle relaxant means there is not a visible seizure; instead, the intensity of the seizure is measured via EEG (electroencephalogram). You wake up feeling fairly clear-headed (at least in relation to how you were feeling beforehand); sometimes I haven’t even realized the ECT had already been done.
There are various parameters that can be adjusted in the delivery of ECT, one of which is the electrode placement. Unilateral ECT, which involves both electrodes being placed on the same side of the head, is less likely to cause side effects. Bilateral ECT, which involves one electrode on each side of the head (on either the temples or forehead), is more effective but also more likely to cause side effects. Unilateral didn’t work very well for me, so after my first few treatments I’ve always had bilateral ECT. I’ve also required relatively long courses of ECT; instead of the typical 8, I’ve needed 15+ during a couple of my hospitalizations.
I am one of those mental health professionals who tells clients that ECT typically doesn’t have significant effects on memory. That’s absolutely true, but my experience was not typical. I have experienced a lot of memory loss from ECT, although it hasn’t impacted my ability to form new memories after completing treatment. Mostly it was short-term memory that was effected, but some of the memory loss has gone farther back. There have been substantial chunks of time that have gone missing from the months leading up to my first hospitalization. Some of these eventually did return, but many didn’t. It was truly bizarre to have people tell me things that I did or even show me photographs taken of me, and I would have sworn that these events never occurred. I feel absolutely certain I’ve never been snow-tubing, yet there’s a photo of me doing exactly that at a local ski hill. My family tends to notice the memory loss the most, as I say the same things and ask the same questions over and over. On a lighter note, after each discharge from hospital after a course of ECT, it was kind of fun to return home to an assortment of what seemed like brand new clothes/shoes/household items that I had no memory of purchasing.
Despite the disruptive effects of the ECT-induced amnesia, it remains very much on the table as a treatment option for me. I would probably ask for outpatient ECT right now if it weren’t for the requirement that someone be available to take you home after treatments and keep an eye on you (a safety precaution because of the use of general anaesthetic). This is just not feasible in my circumstances right now, and it bothers me that this restriction limits my access to effective treatment.
So, that’s my journey over the cuckoo’s nest. A lot less movie-worthy than Jack Nicholson’s, but a lot more real.
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This has been a busy week for me. I mean that very much in a relative sense rather than an absolute sense, as I doubt anyone else looking at my calendar would use the term “busy” to describe it.
I have always found the cognitive symptoms of depression to be among the most disruptive to my overall functioning. When I’m really unwell it feels like I can’t think my way out of a paper bag. I tend to describe the effect on my thinking as “mashed potato brains”; it seems like a fairly apt analogy. My current depressive episode has stretched over the last year and a half, and the cognitive symptoms have ebbed and flowed over that time. When my thinking starts to get clearer I’m able to feel a bit of hope and optimism, but then a week like this week comes along.
It wouldn’t bother me as much if there was something stressful that triggered the decompensation (I use this psychiatry term because it’s the only one that comes to mind). That might seem logical. But no, I don’t have that excuse. I have just asked my brain to do a little bit of outside-the-routine thinking, and I get totally overwhelmed. Hello mashed potato brains. When I went on Pixabay to look for an image for this post, I couldn’t even remember how to spell potatoes (although I did realize that potatos looked a bit funny).
Just before I started writing this post, I was looking through my WordPress Reader feed, and I saw the post Losing My Mind on Travis and the Brain. I felt relieved – relieved that I’m not the only one losing my mind, and relieved that even if we’re drowning we can help pull each other out of the water.
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I can get pretty irritable sometimes because of my depression. I seem to lose access to all of my more mature self, and revert to what may have worked best when I was five years old. This can have a major impact on my behaviour, and sometimes I have let fly with yelling, screaming, and swearing. This has occurred most often when I’ve been hospitalized, and has been directed at nurses and doctors whom I perceived as making things more difficult for me. One of my former community psychiatrists once told me “you can be a real bitch when you’re not well”.
Several years after my first hospitalization, I learned that one of the diagnoses on that first discharge summary was borderline personality traits. Subsequent psychiatrists have disagreed with that diagnosis, as the maladaptive coping mechanisms only make an appearance when I am ill, as opposed to personality disorders involving traits that are consistent over time. It begs the question, though – to what extent do our coping strategies and behaviour when ill reflect (or not reflect) our core selves?
I am not generally an irritable person, so when I become irritable due to my depression, I’m not sure if things are suddenly bothering me that I never would have noticed, or if I’m just more disinhibited about expressing irritation that I would normally just brush off. In other words, is something new happening, or is there just an amplification of what’s already there? While in the end it probably doesn’t make a whole lot of practical difference, it’s worth thinking about in terms of self-identity.
Is my mental illness part of me or is it something that happens to me, a monster on my back that I have to carry around? I have always tended to lean toward the latter view, because I don’t think my illness should define me. Perhaps it’s also in part because I don’t want the real me, my core self, to be responsible for my bad behaviour. Then again, no one is responsible for my actions but me, although the options I have to choose from seem to be very much influenced by my illness.
The perspective that I’ve sort of settled on is that we all have our inner caveman brain, including bits like the amygdala, and in times of stress and difficulty, that is what gets activated. Our prefrontal cortex, the most advanced part of our brain in terms of evolution, is what generates our most adaptive coping mechanisms. In personality disorders, factors such as trauma can impair the development over time of these sorts of adaptive coping mechanisms. In conditions such as mood disorders, our ability to access our adaptive coping mechanisms seems to be impaired in the acute illness phase, leaving us to default to what caveman brain can provide us.
So am I a bitch, or is it my illness? In the end, probably some of both.
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Okay, so I completely made up a new word in the title of this post, but I’m guessing you can tell what I mean. Depression is a profoundly isolating illness, as many mental illnesses can be, and as my illness progresses in many ways I find myself evolving into a hermit of sorts.
I have always been an introvert, but I used to really value time spent with close friends. And then depression hit, and everything changed. When I am depressed, I hate being around people. Depending on my particular set of symptoms at the time, being around others can be exhausting, irritating, overstimulating, anxiety-provoking, or mood-lowering. I used to try to push through this, thinking that I “should” socialize even if it made me feel worse, because that’s one of the things you’re “supposed to” do to get better. But that now feels like a dead horse that’s been beaten long enough. Over the last year and a half of this current episode of depression, I have systematically cut almost everyone out of my life. I don’t have the internal strength or resources to have a mature adult conversation with anyone about this, so I have taken the path of least resistance and just stopped responding to calls/texts/emails.
I don’t like being this person that depression has made me. My family and friends (now former friends) certainly deserved better. I feel like they must hate me for my ghosting behaviour. Yet that hasn’t been enough to stop me from this pattern of behaviour, because it’s not about them as much as it’s been about retreating as a perceived path to self-preservation.
Looking forward into the future, it’s hard to imagine how I would ever rebuild a social life, knowing that I will get depressed again, and I will hide out in my figurative cave again. Why would I let people in knowing that I would most likely at some point just slam the door shut in their face? Guilt plays into this too – if I am such a terrible daughter/sister/friend, why should I even deserve to have people in my life?
As much as I might wish to be able to hide out 24/7, it’s just not feasible. Yet even when I venture out into the world, it feels like there is a self-imposed barrier that isolates me. I either am not able or don’t remember how to have a genuine connection with another human being. So I put on the mask to try to hide the darkness inside of me, and struggle with those superficial social interactions that normally wouldn’t merit a second thought. It makes for a very lonely existence, one that is entirely of my own making.
Strangely enough, the only setting in which I feel comfortable emerging from my cave is with my patients (I’m a nurse). Somehow that part of me is still able to function interpersonally, and I’m not sure why that is. I think it might have to do with spontaneity. I’ve been a nurse for 13 years, and by now I don’t even have to think about what my response is going to be; I just know, and I do it. At least it gives me reassurance that i haven’t fully transitioned to hermit mode. Not yet, anyway.
While fear may not be a symptom of depression, it is certainly something that has become tightly woven into the fabric of my illness. When I am well, I am fearful of when the next relapse might be, when the ground might disappear beneath my feet. When that relapse happens, I am terrified – here we go again with yet another tidal wave to wash my life away. And as a depressive episode stretches out, I am scared that I won’t get better, that I will drown in this mental pain.
What is probably the most frightening is the lack of control. I can be doing what would appear to be all the right things, and I will still get sick. As the years have passed it has become harder and harder to control my illness, so the fear only escalates. This current episode has lasted for almost a year and a half, and I am utterly terrified that I will never get my well self back again. I miss her so much, but she is either gone, washed away in the tsunami of my depression, or drowning in a dark basement somewhere. If only there was a “find my iPhone” for the real me, to give me a life preserver to hold on to.
A few years ago I was making my case before a review board about why I should not remain committed to the psychiatric ward. As a mental health nurse, I’m a bit of a research geek, so I was talking about the STAR*D research study, which essentially showed that the more treatment failures a patient has the worse the prognosis. I argued that my suicide attempt stemmed from “evidence-based hopelessness” (although looking back, I’m not sure why I thought that would help my case). Perhaps a better way to put it, though, would be evidence-based fear – fear based in the evidence of my personal experience and reinforced by the research evidence I was reading. If I am already fearful that I won’t get better, it becomes very hard to challenge that kind of thinking.
I’ve been learning recently about acceptance and commitment therapy (Russ Harris’s ACT Mindfully site is a great resource if you’re interested in reading more), and contemplating how fear fits in with this idea of acceptance rather than resistance. Is this fear a form of resistance? And if so, maybe it’s resistance in a good way – a reason to keep fighting for recovery. Or maybe acceptance lies in making space for this fear, acknowledging it as a neighbour that’s not going to be moving away any time soon.
As I struggle to tread water in the sea of my depression, perhaps I have to both accept and resist. Resist the urge to stop struggling and just drown already, and accept that another wave might come at any time and push me under. In the end, whether I feel fear or not, que sera sera.
As a mental health nurse, I always hope that my clients will feel comfortable and safe enough to be open and honest with me.
As a person with depression, though, being open and honest is likely to go straight out the window if it appears to conflict with whatever goal feels most pressing to me at the time. While this may sound manipulative, it is something I do for the purpose of self-protection and self-preservation. It is part of the armor that I put on when my illness leaves me feeling weak and defenseless.
The topic I lie the most about is suicidal thinking. Based on past experiences, I never want to be hospitalized again. Disclosing thoughts of suicide is probably one of the quickest ways to get committed to hospital, so I keep my mouth shut. Is that a safe, healthy way to approach the issue? Of course not. But in the balance of pros and cons that goes on in my head, there is little that would win out against my desire to avoid hospitalization. I try to consider this in my professional life and be very mindful of how I’m reacting when clients disclose suicidal thoughts to me.
I also omit symptoms that I either do not want or do not feel ready to talk about. At one point I had gone off meds for a while after a 3-strikes-you’re-out series of negative experiences with doctors. After a couple of sleepless months I realized that I really needed to find someone to order some drugs for me. I didn’t want to talk about my depression for fear of getting a similar reaction to the last few doctors I’d seen, so I only admitted to being unable to sleep. In doing so I could get my mirtazapine and quetiapine back on board, and after a while I felt safe enough to disclose the rest of what was going on.
In the end, I can only conclude that we just try to do the best we can with the situation we’re faced with. And I think the more that health care providers understand that, the easier it might be for us to start to remove some of that armor. It’s not realistic to think that we will never feel the need to resort to lies and secrets, but it’s worth reflecting on what underlies them so they don’t end up coming back to bite us in the butt.
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“Sticks and stones may break my bones but words can never hurt me.”
That may have worked in the school yard at recess, but language has tremendous power, both to communicate and to miscommunicate. Take the word “depression” for example.
Depression is often used in everyday language to describe an emotion like sadness. This is a very different creature from major depressive disorder, which can be debilitating and affect almost every aspect of a person’s functioning. Similarly, bipolar disorder is a whole different can of worms from short-term mood fluctuations. If people are lightly tossing these words around to describe transient emotional blips, it dilutes the social understanding of these terms and minimizes the experience of those suffering from mental illness.
When we use language that minimizes mental illness, we are likely to propagate stigma. If we think someone is “just depressed”, the same way we might be if our favourite sports team didn’t win the championship, then we’re more likely to think “they’re just not trying hard enough”, and they could feel better if they would “just get over it already”. But in reality, we’re not comparing apples and apples, we’re comparing mice and elephants.
Depression is the example that resonates the most with me, since it’s the illness that I have, but there are many other examples, many of which are pejorative. “Psycho.” “Crazy.” Or perhaps using the word “suicidal” to describe feeling disappointed over some minor event. People may be describes as “schizophrenic” as if that defines who they are as a person.
We could all do well to reflect a bit on the language we choose to use and what that might mean for those around us. Sticks and stone may break my bones, but words can wound me far deeper.
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There have been a lot of horrific events in the news lately. Hurricanes, the mass shooting in Las Vegas, terror attacks… As I saw these events on the news, I knew cognitively how terrible they were, but on an emotional level, I just felt nothing. I am not a cruel, heartless sort of person, but I still felt nothing.
Many people have some idea of the “gifts” that depression gives: low mood, anxiety, suicidal thoughts. There is often less familiarity with what depression steals away from those who suffer from it. Anhedonia refers to the inability to feel pleasure, and apathy refers to a lack of interest. These deficits that people can experience due to depression may sound relatively minor, but in fact they can be soul-destroying.
Part of what makes us human is the ability to feel things in response to what is happening around us. If depression takes that away, what does that do to our humanity? I feel like a monster for not caring about tragic devastation and loss of life, but it’s as though the ability to feel in that way has been turned off in my brain and my heart, and for the life of me I can’t figure out how to turn it back on.
Depression can leave a darkness and emptiness on the inside that can’t be lit up no matter how bright the sun shines. Perhaps that is harder to understand than that which depression giveth, but the greatest impact on my life has without question come from that which depression taketh away.