Akathisia is a clinical term for extreme inner restlessness. People who are experiencing akathisia have great difficulty sitting still, or maybe even sitting at all. I first experienced akathisia on Abilify (which I ultimately discontinued because it gave me a facial dyskinesia), and it continued to plague me as I tried different antipsychotics, such as Haldol. I found myself unable to do anything except to go outside, pacing back and forth and smoking cigarettes. Propranolol offered me some relief from the worst of it, but the effect eventually faded.
The medications that are most likely to cause extrapyramidal side effects (EPS) — including tardive dyskinesia — are also the most likely suspects for akathisia. In fact, you might even say akathisia is a type of EPS, even though it does not cause per se involuntary movements. Common suspects would include Haldol and probably also Abilify, which has much greater risk of EPS than we once believed.
It’s excruciating to live with akathisia, and yet most people have never even heard the term. A common descriptor is the feeling of “wanting to crawl out of your skin”.
I’ve had some trouble over the years differentiating between akathisia and hyperactivity associated with my ADHD. The main difference between these two scenarios is the cause, but when you’re on a regimen of multiple antipsychotics plus lithium plus stimulants plus benzodiazepines it becomes difficult to discern cause and effect. No doubt in my mind, at its worst akathisia feels worse and even more frustrating than ADHD — but what about those days where it’s just kind of there?
I’ve also experienced restless leg syndrome. Some scholars believe there is a link between RLS and akathisia — essentially, that akathisia is like RLS experienced during the day (as well as at night — akathisia has kept me awake many nights). I would say this is a pretty apt comparison.
When I first started propranolol, and was able to sit and rest for a few minutes for the first time in weeks. It was like getting your first pair of glasses, and realizing you can see clearly now. The relief was nearly immediate. Unfortunately, it faded somewhat over time. But I’ll remember that instant where it hit me, the moment I put on the glasses, forever. I hadn’t even realized how bad it was until then.
Traditionally, it has been thought that bipolar disorder emerges most typically in the early to mid 20s of a person’s life. It has been known since the time of Emil Kraepelin (circa 1921), however, that children can be affected by this illness. While adolescent onset (mid-to-late teens) is now recognized as common and similar to the presentation of adult bipolar disorder, pediatric onset bipolar disorder remains the subject of debate, and its presentation is somewhat different than adult bipolar disorder.
Why do some children get bipolar disorder?
We do have some idea why some people get bipolar disorder as adults, and others get it much younger. The effect is known as genetic anticipation, which occurs when certain genes accumulate in later generations. We know that bipolar youth are highly likely to have members of their family belonging to previous generations (parents, grandparents, aunts, uncles) with bipolar disorder. When those genes add up over successive generations, and the person has a LOT of the polymorphisms that cause bipolar disorder, they tend to get it a) younger and b) more severely. This also helps to explain why pediatric onset bipolar tends to be a clinically severe manifestation.
How does pediatric-onset differ from adult bipolar disorder?
Pediatric onset bipolar is commonly characterized by very rapid cycling. This is an uncommon phenotype (what the disorder “looks like”) in adults, but the majority of children with bipolar disorder are rapid cyclers. Chronic irritability is also common and is part of the reason pediatric bipolar disorder is so controversial. An episodic pattern of moods — whether the manias are dysphoric or euphoric — is arguably the hallmark of bipolar disorder; chronic irritability doesn’t seem to fit the bill, and in children who do not experience depression, an alternative diagnosis may be more appropriate. Nonetheless, irritability is a common symptom even among those children who seem to clearly meet the criteria for bipolar disorder.
In my anecdotal experience (my symptoms started before the age of 10) I still have rapid cycling and dysphoric mixed manias as an adult. I urge those who are doubtful that rapid cycling bipolar is “real” or that it is somehow less valid to consider that many adults with this phenotype first experienced bipolar symptoms as children.
Recommended reading about bipolar in children
If you want to learn more about bipolar disorder in kids, I recommend the book The Bipolar Child by Demitri Papolos. It is really informative and helped me to better understand myself, as someone who had pediatric onset. I sat down in a library and read it all within a couple of hours.
I’m medication resistant, meaning that meds don’t fully stabilize my cycling. I’ll never be the person who can say “nobody even knows I am bipolar”. In fact, I have to disclose my bipolar disorder to most of the people I work with, due to how it impacts my working hours.
I’ve tried every atypical antipsychotic approved for use in psychiatric patients in the United States except for clozapine (although that has been on the table) plus two typical antipsychotics, three anticonvulsant mood stabilizers, and many other drugs including benzodiazepines, antidepressants, hypnotics, lithium, and so on. I’ve taken the tour.
Currently, this is my regimen: olanzapine, risperidone, lithium, diazepam, and amphetamine salts. I continue to experience symptoms, even with all of that on board. So how do I live and continue to work? The answer is not one-size-fits-all, but for me there are a few key components.
1. Consistent sleep times
I try to go to sleep at the same time every night, and wake up at the same time every morning. Of course it doesn’t always work out that way, but I try. I also make sure not to schedule any meetings that are too late at night, and not to stay out too far into the evening, as both of these things will keep me awake. Each person’s natural bedtime is different, so I can’t tell you what time is correct for you, but for me it’s usually between 10 PM and 12 AM (a fairly wide window, I know).
2. Structure during the day
It helps me if I am able to maintain some regularity and consistency throughout my days. Since I’m an academic and my work schedule is flexible, this is something I largely have to impose on myself. When I’m really struggling I’ll schedule events in my Google Calendar, even for things I don’t “have” to do — recreational activities, like video games or watching anime. The point is to stay busy, but not too busy. Make sure to build in plenty of breaks. This also helps me get the things on my to-do list for work done efficiently.
3. Take meds religiously
This one doesn’t need a whole lot of explanation, but it’s an important point. Don’t stop taking your meds. At least for me, it always ends in hospitalization, and that’s a huge disruption to my life even though I’m quite used to it by now. Don’t get me wrong — sometimes hospitalization is necessary. However, it’s best to avoid it as much as possible, so that I can stay in contact with my friends and family.
4. Light and darkness
Research has shown that light/dark cycles have a dramatic impact on bipolar moods. I use a light box (or “sun lamp”) for a couple hours daily in the winter. You can buy a clinical strength sun lamp on Amazon (I am not affiliated, and do not gain anything from this) but be aware that the market is flooded with lamps that are not full clinical strength. The recommended protocol for bipolar disorder is to start at noon for 10 minutes, then add 10 minutes every day until you reach 1 hour. This is because the sun lamp does run some risk of triggering mania. At the same time, when you go to sleep (or ideally, when it’s naturally dark outside) there is an equivalent if not more important factor: darkness. Total darkness at night has been shown to dramatically stabilize patients who did not respond to conventional treatments.
5. Mindfulness and psychoeducation
The point of mindfulness in this context is to be able to recognize what mood state you’re in. Likewise, it helps me to be as educated as possible. I read tons of papers, but these are not super accessible to everyone; if you trust your psychiatrist, I recommend asking lots and lots of questions so that you can understand as much as possible. I also compiled a list of some of my favorite bipolar books. The insight into what you’re going through can save your life, even if it doesn’t change what you’re going through.
Ah, lithium; it’s been our gold-standard treatment for bipolar disorder for many years, and can work for people who have failed other drug trials. It is also one of the only drugs known to decrease the risk of suicide1. But how does it work?
It’s a bit more complicated to understand than, for example, an SSRI (which, ultimately, increases serotonin in the synapse, through a fairly intelligible mechanism of stopping reuptake). Despite knowing since 1949 that lithium was an effective treatment for bipolar disorder, we still don’t fully understand its mechanism of action.
One of the difficulties in determining this is that lithium goes everywhere in your body. Within the brain, it can cause an absurd number of changes through numerous signalling pathways. Like other drugs, it can cross the brain-blood barrier (an important quality for psychiatric medications, since they target the brain) but, uniquely among psych meds, it can also enter your intracellular space — hiding inside your cells, instead of just floating around in your blood.
It is excreted by the kidneys in urine, although it is also known to be excreted in human sweat and tears2. (I’ve had hyper-salty tears caused by lithium every so often.)
Lithium appears to increase the concentration of some neurotransmitters (potentially serotonin and GABA) while moderating the effects of dopamine and norepinephrine through its effects on voltage-gated channels3. This action causes a broad cascade of effects throughout the entire brain that restores balance in people with bipolar disorder. Lithium can get into any cell in your body, and it goes inside your neurons (brain cells) too. This is how it affects voltage-gated channels and moderates the activity of all neurotransmitters.
Although we usually call it a mood stabilizer, it’s not related to any other drug we put in this class, since it is not an anticonvulsant. Lithium is probably most accurately classified as a neuroprotective drug4, like memantine (a drug typically used for Alzheimer’s disease). There is even some speculation that memantine could augment the effect of lithium, due to its similar mechanism of action, but specific to the NMDA receptors.
A key point to understanding the pharmacodynamics of lithium is that lithium, in the human body, can use the same transporters as sodium. It fits where sodium should go — therefore, it exits cells through active transport systems designed for sodium, but at about half the speed of sodium. The similarity of lithium and sodium explains why lithium is excreted by the kidneys and not metabolized by the liver.
This is also why activated charcoal will not absorb lithium. Your body sees it as a metallic salt (it has a positive charge), and metals (or charged ions) are not attracted to charcoal. In addition, the similarity of sodium and lithium creates a sort of sodium-lithium ecosystem in your body; if you maintain a steady dose of lithium but drastically reduce your intake of sodium, your lithium levels can rise to toxicity.
Kessing, L. V., Søndergård, L., Kvist, K., & Andersen, P. K. (2005). Suicide risk in patients treated with lithium. Archives of General Psychiatry, 62(8), 860–866. https://doi.org/10.1001/archpsyc.62.8.860
Fraunfelder, F. T., Fraunfelder, F. W., & Jefferson, J. W. (1992). The effects of lithium on the human visual system. Cutaneous and Ocular Toxicology, 11(2), 97–169. https://doi.org/10.3109/15569529209042704
Lenox, Robert H., H. C.-G. (2000). Overview of the Mechanism of Action of Lithium in the Brain: Fifty-Year Update. 61.
Gray, J. D., & Mcewen, B. S. (2013). Lithium’s role in neural plasticity and its implications for mood disorders. Acta Psychiatrica Scandinavica, 128(5), 347–361. https://doi.org/10.1111/acps.12139
I. Dirty Dyl, known for his ostentatious attitude (typical of a manic persona) wants to have a rap battle in the middle of the TV room.
Dirty Dyl, who lost phone privileges on his first night dialing 911: I’m being held hostage at South Oaks Hospital, he said & then screamed & shouted & started to cry —
I ask him if poetry will do.
II. I read my poem in art therapy.
Soon, three other patients are scribbling in the small hospital-issue composition notebooks & the backs of napkins in pencil, crayon, or markers (the washable, non-toxic kind) simply because it’s better than passing the time weakly magnetized by television game shows.
III. I know Dirty Dyl, or at least I know his face from a gay hookup app. He with his crooked swagger & snapback caps is Not My Type.
Only I know he is bisexual. Only I know that he fucks people like me.
Somehow, maybe just in Dyl’s mind, being the keeper of this secret inspires trust.
IV. Depressives squint at their words with tired souls, heavy hands & looks of consternation. It’s not beautiful, you know — it’s bedhead & stubble & hospital slippers with the little treads on the bottom — but as they write, they are inspired, their eyes grow bright,
they know of ink on the page, the spark of a fire in their blood & they are increasingly, if just a little bit, alive.
V. Dyl went home before I did. I saw him the other day. He got his job back at the dining hall, where he once came to work on shrooms. He smiled at me & asked, How’s poetry?
I smiled politely back, thinking of a line from Whitman
(I too am not a bit tamed, I too am untranslatable)
I am bipolar type 1. 🎭 That is the most severe form of bipolar disorder. (Bipolar 2 can have very severe depression, but because it doesn’t have severe mania it doesn’t progress along the same course. Something like that.) I’ve been inpatient 18 times, and I’ve been discharged from the ER a few additional times as well.
Interestingly, I don’t have what most people would think of if you said “classic bipolar disorder”. I have mostly dysphoric manias (and sometimes euphoric hypomania), so no grandiose delusions or belief that I can see the flow of energy that connects all things. Just bugs that… may or may not be real. 🐜 But, the dysphoric mania type is actually sliiiiiightly more common than euphoric (feel-good) mania in real-world bipolar 1 people, according to one study1.
The main reason my bipolar is unusual is that it is so FAST. My psychiatrist describes it as “brittle” — a medical term often applied to highly unstable diabetes patients, where blood sugar skyrockets but then drops with intervention but then skyrockets again. It follows the same kind of course.
Usually, I think my cycle (including both mania, which almost always comes first for me, and then depression — most bipolar people have one type of episode almost always come first, but it’s a 50/50 split which one2) is 2 to 4 weeks long. If it’s a lot faster than that it’s considered a mixed episode.
I rarely ever have euthymic (normal mood) periods and I don’t have any asymptomatic periods. (I have persistent problems with memory and executive functioning and other stuff.)
💊 Currently every day I take: lithium, Thorazine (chlorpromazine), Zyprexa (olanzapine), Valium (diazepam), and Adderall (amphetamine salts). 💊
What causes bipolar disorder?
A lot of research links bipolar disorder to various things: a) circadian instability, sleep problems ⏰ b) inflammatory processes in the brain 🔥 c) epilepsy 📈 — they have a lot in common, and medications used to treat epilepsy are often used to treat bipolar disorder; I think you can think of bipolar as being similar to some kind of epileptogenic brain activity but on a more macro scale. Similarities to Temporal Lobe Epilepsy include age of onset and genetic cause among other things and they do have a very very high comorbidity rate. d) genetics 🧬 — 97% of bipolar disorder is explained by genetic variance alone and it is more heritable than autism or schizophrenia (I believe it might be the most heritable psychiatric disorder in DSM-5)
Most people get bipolar disorders in their 20s, but I got it early. I had suicidal depression sometime before the age of 10 and had my first clear hypomanic episode when I was 16. My parents were anti-psychiatry, so I wasn’t in treatment until I went to college and I almost became an emancipated minor because I was still 17 and it was that serious 🙃
Unlike autism, which is a fairly new concept (although autistic people have almost certainly existed for thousands of years) bipolar disorder is a very old idea for a distinct illness that occurs in all cultures that I know of. Other English names for it have been “manic depression” (a term I actually prefer), “manic-depressive psychosis”, “circular insanity” 🔁, all referring to a highly organized and unusually patterned occurrence of severe disturbances in mood.
That’s actually what I study now in my PhD program! I’m looking for patterns in bipolar disorder. I’m very good at patterns 🧩
1. Grant BF, Stinson FS, Hasin DS, et al. Prevalence, correlates, and comorbidity of bipolar I disorder and axis I and II disorders: Results from the National Epidemiologic Survey on Alcohol and Related Conditions. J Clin Psychiatry. 2005;66(10):1205-1215. doi:10.4088/JCP.v66n1001
2. Koukopoulos A, Reginaldi D, Tondo L, Visioli C, Baldessarini RJ. Course sequences in bipolar disorder: Depressions preceding or following manias or hypomanias. J Affect Disord. 2013;151(1):105-110. doi:10.1016/j.jad.2013.05.059
A lot of people with conditions that are defined in the DSM (Diagnostic and Statistical Manual of Mental Disorders) disagree with what their condition is called. In this post, I’m going to muse over changing the names of psychiatric disorders.
When the DSM-III was published, the DSM committee decided that the term “manic depression” had become overly stigmatized and abused. There was little to no change in the diagnostic features or description of the disorder (which has actually been fairly consistent for a very long time!), the only reason for changing the terminology was political. Many years later, I feel this has resulted in the term “bipolar” being just as stigmatized as “manic depression” ever was — except it’s even more abusable, since “bipolar” can be used as an adjective to describe many things, famously including the weather.
It should’ve been obvious that the stigma of manic depression didn’t originate from the term “manic depression” — and therefore not shocking that the same stigma followed, not the term that was used, but the people who live with the disorder. It was always the people, never the term. On top of that, I feel “manic depression” is more accurate as the term “bipolar disorder” doesn’t portray the common reality of mixed episodes and mixed mood presentation. “Bipolar” seems to imply a state of bistability, where two states representing opposite ends of one dimension (mania and depression) are cleanly and abruptly switched between; bipolar can be like this, but it is often messier.
ADHD is a controversial term for some advocates and it’s understandable why. While attention and hyperactivity/impulsivity are characteristics that are used to diagnose the disorder, they’re downstream of the real difference experienced by people who live with the condition — which is developmental effects on executive functioning. Broadening the term to define it by its root cause would probably feel more accurate of the experience of living with the condition.
Inadvertently, if the diagnostic criteria were changed accordingly to reflect other developmental disorders of executive dysfunction, there may be groups of people who didn’t meet the criteria before who now do. This is something to be interested in, of course. Attention and hyperactivity/impulsivity could still be used as specifiers, and the developmental history aspects would probably still be required so that people with executive dysfunction of non-developmental origin aren’t accidentally included. Additionally, we know that autism is associated with some kinds of executive dysfunction and this change would probably blur the lines between them even more — but in reality, those lines are pretty blurry.
Autism Spectrum Disorder?
There is a lot of controversy over this one, and to be honest I don’t have all of the answers. I think “Asperger’s” was a term of limited utility because many studies could not find clear differences between “Asperger’s” and “High Functioning Autism” even though supposedly the Asperger’s group had no language delay and the HFA group did. Their outcomes, though, were the same. So it was decided that we would collapse autism into one diagnosis that represents a gradient or spectrum of features and levels of impact on the person’s life.
However, I actually agree with some advocates who say that this has proven obtrusive for people with high support needs as the common conception of autism drifts further and further from Rain Main to Sheldon Cooper. There are many people out there who no longer believe autism is a disability. I can’t fully reconcile myself with this stance when we’re talking about a nonverbal adult with an IQ of 40: this person’s life is much, much different than mine, and I genuinely want to help them in the most effective way I can. At this venture, I believe we need a term for people with high support needs. But, the options thus far have been problematic (for example, I do see the reasons why “high functioning” and “low functioning” are much too simplistic to capture meaningful differences).
In the end, the best I can come up with right now is to include Verbal IQ score as a specifier. It’s not perfect (we know IQ means something specific, and can’t be generalized to “intelligence”), but it’s one of the better indicators we reliably have of how disabled this person is, how many barriers they’re going to face to get treated fairly and with respect. And, it doesn’t create a competition where someone is more or less autistic than I am. We’re both autistic; it’s just that one of us has an IQ of 40 and that information isn’t trite. Despite the risks of increasing discrimination, I think we’ve seen with the bipolar fiasco that changing terms merely to avoid stigma (which is attached to people, not to terms) is not a good idea.
I had always thought I had ADHD inattentive type. However, when I recently asked my psychiatrist (out of curiosity) she chuckled and said that, in her clinical opinion, I have the combined type.
Part of my perception may come from that fact that, due to my mild cerebral palsy, I move at a much slower pace than other people — thereby masking some apparent “hyperactivity”. To complicate matters, I’m currently taking two antipsychotics (Thorazine/chlorpromazine and Zyprexa/olanzapine) both of which can cause side effects that are phenotypically similar to hyperactivity (this is called akathisia). But how much of that is the drug per se, and how much of it is my ADHD (which may, in turn, be worsened by the drug)?
I think there’s a broader misconception at play. We simply do not know how to identify hyperactivity in developmental adults.
First off, let’s get some facts straight. In adults with ADHD, it’s more common to have symptoms of inattention (about 90% have these kinds of symptoms in a prominent way) while only about half of adults display clinically relevant hyperactivity or impulsivity1. By implication, we can assume that the population of adults with ADHD breaks down something like this: 10% have hyperactive type, 40% have combined type, and 50% have inattentive type. Those numbers may be a little off, but it’s a good place to start.
Yet, even though it is acknowledged that adults have hyperactivity and impulsivity, these symptoms are not well understood in adults — at least, they aren’t characterized as well as they are for children. And the presentation of these symptoms changes over the lifespan. It is thought by researchers that hyperactivity decays as the ADHD child becomes an adult, while inattention persists1.
Here are diagnostic criteria for hyperactivity and impulsivity in ADHD1:
Without a doubt these symptoms intentionally mirror those used for children, with some addendums (instead of running and climbing excessively, we just think about doing it — leading to “subjective feelings of restlessness”). Somehow, some adults with ADHD have internalized our externalizing behaviors. Instead of running from wall to wall like a four-year-old, I just feel this incredible tension in my body created by Not Moving. But it’s all inside my head. You can’t see it unless you look very closely.
I can see myself in this list of symptoms, nonetheless. I fidget, I stim, I stand when I’m supposed to remain seated, I feel restless constantly, I interrupt others when they are speaking, I feel a kind of somatic pain or intense pressure and frustration when I have to wait a long time for something that’s right in front of me.
But there is an element here that we are not capturing.
We know from literature in children that hyperactivity/impulsivity and inattention are correlated. But, it’s not so clear what the relationship is, and it really gets at the core deficit we’re trying to get at with an ADHD diagnosis: poor executive functioning and self-regulation. I can’t focus my attention, so I pace around for hours, smoking cigarettes on the patio. I feel like I have to keep moving; I constantly have to be doing something, even if I’m doing nothing. I can’t relax. That isn’t good for a child, and it’s even less so for an adult. My body feels tense and worn, like a pair of old shoes.
It turns out, too, that ADHD in adults is associated with lower socio-economic status, lower levels of academic achievement, problems with relationships, and even poorer driving ability and more traffic violations1.
Not long ago children with ADHD were presupposed to exist in a liminal state: it was thought that ADHD was a disorder of childhood, and that it diminishes with developmental advancement. Yet research (including various brain anatomy, neuroimaging, and genetics studies) is showing that this is not the case1.
Ironically enough, it’s time to turn our attention to adults with ADHD. Although it does make some sense that classic symptoms of hyperactivity decline with age, I am interested in how hyperactivity later manifests in adults who no longer fit the typical, child-centered definition of hyperactivity.
Personally, I think inwardly-turned hyperactivity may be one of the driving forces behind high levels of depression and anxiety seen in adults with ADHD. Around half of adults with ADHD have had one or more major depressive episode, and around half of adults with ADHD have one or more clinical anxiety disorder2.
There’s also a fascinating overlap with bipolar disorder, which may be a blog post for another day!
Are you an adult with ADHD? Have you ever met criteria for hyperactive or combined type ADHD, either now or as a child? Share your experiences!
Sobanski, E. (2006). Psychiatric comorbidity in adults with attention-deficit/hyperactivity disorder (ADHD). European Archives of Psychiatry and Clinical Neuroscience, 256(SUPPL. 1), i26–i31. https://doi.org/10.1007/s00406-006-1004-4
Caution: this post contains explicit discussion of suicide
Two days ago (on September 10th) was World Suicide Prevention Day. Although it is important to address prevention of suicide attempts, the strongest predictor of a fatal (or “completed”) suicide is a history of previous, non-fatal suicide attempts. The risk factors for suicide attempts are more diverse and include: family history of suicide, early onset of bipolar disorder, extent of depressive symptoms, increasing severity of affective [mood] episodes, the presence of mixed affective [mood] states, rapid cycling, comorbid Axis I disorders, and abuse of alcohol or drugs1
Most suicide prevention effort focuses on people who are naive to psychiatric treatment and have reached a crisis point: people who don’t already have a psychiatric point of contact, and usually people who have never been treated in an inpatient setting before. In my experience, most people do not continue using crisis lines or similar services after they have been hospitalized once. Surmounting the fear and stigma around hospitalization itself is a primary reason crisis lines exist. Crisis lines are staffed by severely underqualified volunteers, who are usually following a script, and only have two action moves: call an ambulance, or tell you to go talk to someone else (sometimes your health insurance company). Yet, people find calling a crisis hotline less formidable than simply admitting themselves voluntarily.
But what about those of us with chronic illnesses, with volumes of psychiatric history, who have been admitted many times? This service is clearly not meant for me. If I spoke to a crisis line on what to me is an an average day, I might find myself being dragged to the ER and with an $800 ambulance fee to boot. There is no exception for chronicity. The stakes of a mistake are high, and the crisis line operator is equipped with a high school diploma.
There’s a gap between services for first-episode patients and services for profoundly disabled people who live in an institutional setting. After my close-to-fatal suicide attempt about two and a half years ago, I had to navigate what exactly life looks like after a serious suicide attempt. I consumed an amount of lithium equal to the 50% lethal dose in rats, and an antidepressant that is also a potent anti-emetic (anti-vomiting) drug. I knew I would absorb more of the lithium if I delayed the onset of (inevitable) severe vomiting.
I was hospitalized for only 16 days. The attending physician treating me thought I should go to a residential treatment program, but I was supposed to be at an academic conference and I begged to be realized in time to go. The head of the clinic evaluated the situation and decided to release me. I was discharged within hours of my flight to Europe. After the conference, I was enrolled in a partial hospitalization day program. The official length of the program was 8 weeks; I was probably enrolled for 4 months. My psychiatrist met with me nearly every day.
We tried a lot of medications, but for quite some time I was not permitted to take lithium. This was unfortunate, because lithium is probably the single most effective drug I take. I have cycled through almost every atypical antipsychotic: Seroquel, Abilify, Vraylar, Zyprexa, Saphris, Geodon… I’m sure I’ve forgotten something, it’s more than I can keep track of. I tried Depakote and Lamictal. Nothing has the same effect as lithium. Ironically, lithium also has a specific anti-suicide effect.
I continued to be suicidal throughout and beyond the partial program. I am lucky that my psychiatrist works well with me.
Chronic suicidality is probably more common than people realize. It doesn’t appear in the media. It’s taboo. You fear to acknowledge it exists somewhere. When we talk about improving mental health services, let’s give a little more attention to the people for whom posting a status update with the s-word in it is reason to panic and report it to Facebook headquarters.
Hawton, K., Sutton, L., Haw, C., Sinclair, J., & Harriss, L. (2005). Suicide and Attempted Suicide in Bipolar Disorder: A Systematic Review of Risk Factors. The Journal of Clinical Psychiatry, 66(6), 693–704. https://doi.org/10.4088/JCP.v66n0604
Recently, on Twitter, I confessed that I had not been able to complete reading NeuroTribes (a very interesting book, and also a lengthy one). The other person insisted that a PhD student should be able to read a book and accused me of lacking academic integrity — basically, that I am lazy and don’t deserve my PhD.
I’m here to say that attitude is inherently ableist. But to give the benefit of the doubt, perhaps most people don’t know that bipolar disorder actually can affect your ability to read. I learned to read early as a child — I was a prolific consumer of text, and I had a college reading level in elementary school (this is called hyperlexia). But after being medicated for bipolar disorder, my ability to sustain focus and momentum while reading a long document has been very limited.
Lithium is probably the biggest offender. It kind of affects how you see words on the page — like a pseudo-dyslexia, the words seem kind of blurry and distorted. It can be impossible to read full books. I can still read journal articles because they generally have a defined structure and an abstract. I can also read poetry, which I enjoy. I recommend seeking out these kinds of texts if reading is something you struggle with.
Most of all, I want you to know that this is common, you are not alone in having an acquired inability to read and you still deserve your career, whatever that may be. It’s not a matter of “intellectual thoroughness”; it’s part of a disability, and it’s more common than you think.
I also find it difficult to watch videos, TV, or movies. The information conveyed through video media covers many modalities — sound (music), speech, visuals, movement (spatial), and the overall plot you’re supposed to be following. Sitting for the length of a movie is hard, but it’s also just hard to follow so many things at once. My brain gets overwhelmed with too much information of different kinds to process (evidence of poor sensory integration, a symptom of autism). But it helps to reduce the overload by using captions (combining speech with visuals, thus reducing the number of information modalities) or watching something animated, which compresses the demands of visual and spatial information greatly.