Why would this happen? How could I get worse while getting treatment?
Years ago when I started this blog, every time I had a symptom flare-up, I’d ask myself these questions over and over again sure that if I thought about them hard enough it would all make sense.
Unfortunately, when you have an illness which science has only recently begun to understand, you rarely get the satisfaction of knowing why you’ve gotten sick and what exactly will work to get you better. Sure, well-established, proven guidelines for diagnosing and treating PANS exist (though they didn’t when I started), but all too often, I relapsed without knowing why and had no objective test to prove how sick I was; I’d lose my entire personality, but the autoimmune markers you might expect in someone suffering from brain inflammation never showed up.
In all these years, I never had concrete, mainstream evidence to show that an autoimmune condition was affecting my brain…
Until now that we’ve found an antibody.
After my last major relapse in 2017, and the resulting monthly IVIG treatments, I was sure PANS could never come back. Indeed, it left me alone for long enough that I did a year of grad school without it bothering me. But ironically, I was so scared of repeating what I went through two years ago that when it happened this summer, I didn’t see it until it was too late—and until we found an antibody.
In June, something in me snapped.
I began having crying spells over nothing along with intense suicidal thoughts, and then later I’d be giddy and nearly manic. And then I’d find myself inexplicably angry and agitated. I knew something was off, but I chalked it up to my new headache medicine—of course I blew off the prior week’s full-body rash as nothing sinister at all.
This doesn’t feel like PANS, I tried to convince myself. It can’t be PANS if I’m on IVIG and steroids.
However, within a couple of weeks, even after stopping the medication in question, my cognition declined. I couldn’t remember everyday words and resorted to pantomiming, as if I were a foreigner who barely knew English. I walked into rooms or opened my computer and then forgot what I was doing. I lost reasoning abilities and couldn’t connect all the dots to solve problems.
This only happens to me with PANS, I mused to myself. But it doesn’t quite feel like PANS because I’m not having panic attacks.
I blamed my apparent mental breakdown on the fact that, coincidentally, my other illness myalgic encephalomyelitis (ME) had gotten worse during the same timeframe. I was homebound and could no longer walk down the driveway. I couldn’t manage hardly any mental work without feeling like I had the flu for days afterwards. The severity of my ME left me feeling like there were fewer and fewer reasons to continue living, because what I was doing didn’t feel like living—it was barely existing, and being stuck in a body that was perpetually sick and in pain.
Who, in my situation, wouldn’t feel completely devastated and hopeless? Who said brain inflammation was always the cause? But mostly, I didn’t want to even entertain the possibility that I could have a PANS relapse while on the aggressive treatments of monthly IVIG and high-dose IV steroids. I knew there was only one other treatment my doctor would offer if those failed, and it scared me.
And if you’re trying your hardest not to see PANS, whether you’re the doctor or the patient, you won’t see it even when you’ve got the defining symptoms screaming at you: food restriction, OCD, mood swings, suicidal thoughts, anxiety, and cognitive impairment.
Once I hit rock-bottom, I was desperate for anything that might stop the suffering, so I let my psychiatrist increase the anti-psychotic that had always made me feel like a zombie at higher doses. We reasoned that the IVIG and steroids were dealing with the inflammation component, so maybe I needed something extra to help me out. Indeed, after the higher dose of Seroquel, the suicidal thoughts almost completely stopped the next morning, and I felt like myself.
It couldn’t have been PANS, I falsely assured myself. Seroquel wouldn’t have worked this time. It must be something else.
As it turns out, I was completely wrong and also completely right to blame my decline on “something else.”
Until recently, I’d convinced myself that whatever happened this summer was behind me because my mood has stabilized, and all my other ME symptoms have improved with a cocktail of natural supplements; I no longer feel like I have the flu all the time. Most days, my psych meds keep me stable enough to work a part-time job from home that I love. I’m also writing a book. And most shockingly, I’ve found someone I’m actually somewhat interested in dating. On the surface, it sounds like I’m doing great.
But my “normalcy” ends here.
Seven hours of my desk job over the course of two days last week has left me so little energy that even five days later I have to spend most of my time lying down. I still have meltdowns sometimes because I have no idea how to start a multi-step task. I forget how to spell simple words or write the wrong word entirely. I get ill from walking more than two-hundred feet at once. If I lift more than ten pounds, I wake up in unbelievable pain all over my body the next day. If I listen to books or music for too long, even softly, my ears ring and all sound becomes painful for hours. And then there are the occasional days when I’m suicidal and afraid I’ll hurt myself if I’m left alone.
The truth is I’m not well, and I want my life back.
Indeed, my neurologist told me what I feared most:
“That’s a Strep rash,” she said right away at my visit after seeing the picture from June. “What antibiotic are you on?”
“None,” I said, suddenly putting the pieces together where I didn’t want them to fit. “But I’m okay mentally right now.”
She raised an eyebrow and scanned the notes I’d brought. “Your handwriting’s gotten worse… And you’ve lost weight.”
All of a sudden, I realized that I, an alleged PANS veteran—one who has met dozens and dozens of others like me and claimed to have learned from them—I had made a beginner’s mistake:
If you’ve ever had PANDAS/PANS and get severe psychiatric symptoms, you’d better check for Strep no matter how unlikely it seems—even if you don’t have tonsils like me.
I felt like I’d betrayed myself. What would’ve happened if we caught the infection right away? Would I have been able to continue grad school instead of being stuck at home?
I’d just begun to forgive myself and make peace with my mistake, thinking that going back on antibiotics would put this unfortunate chapter behind me. I didn’t think much would come from the plethora of blood tests my doctor ordered, but then one morning I got a phone call from her nurse:
“You need Rituxan. Your GAD-65 antibodies came back extremely high.”
“What?” I stammered. “But I’m… I mean—I’m already on IVIG.”
“The Rituxan is the only thing that will knock out those antibodies.”
After I hung up the phone, I sat there on the edge of my bed like a stone as the seriousness of my situation fell onto me. Could this be PANS plus some kind of GAD-65 autoimmune encephalitis, perhaps triggered by Strep? GAD-65 doesn’t respond as well to IVIG or steroids as my symptoms had in the past. If I didn’t treat this, it may only be a matter of time before I got back to how sick I was earlier this summer—or worse.
In that moment, I realized that no matter how much I tried to fool myself into thinking everything was fine, and no matter how well my psych meds were working for now, there was an antibody wreaking havoc on me—and it could be the reason I keep having to increase my anti-psychotic. I finally have that strong, objective test showing I’m unwell, and there’s no denying such concrete evidence.
But what is a GAD-65 antibody?
GAD stands for Glutamic Acid Decarboxylase, which is an enzyme related to converting glutamate to GABA. Interestingly, GABA dysfunction is associated with bipolar disorder, and this GAD-65 antibody could prove that mine is indeed immune-related, as we’ve suspected all along. In addition to GAD-65 autoimmune encephalitis (inflammation of the brain), the antibody can also cause Type 1 Diabetes, dysautonomia, Stiff Person Syndrome, and encephalomyelitis. Or, in plain English:
There’s a solid possibility the GAD-65 antibody is attacking my entire nervous system in addition to my brain.
The profound fatigue, post-exertional malaise, sensory sensitivities, loss of appetite, cognitive problems, and dysautonomia that have to this point been labeled “ME” may be related to this antibody. Reducing the GAD-65 antibodies with Rituxan could give me back my life.
No one has ever studied whether some people with ME actually have some kind of GAD-65 autoimmune encephalomyelitis. ME is currently considered incurable and untreatable. The implications of GAD-65 being a possible cause for some, and Rituxan a treatment, could be groundbreaking.
Sometimes, what you fear most is exactly what you need.
As it turns out, this summer’s apparent PANS relapse, and the resulting GAD-65 test, just might be the ticket to getting a treatment that will help the ME symptoms that have impacted every single hour of my life for nearly two years.
However, in some ways, this GAD-65 antibody has brought more questions than answers: Which, if any, of my symptoms is it actually causing? What is its relation to my PANS? Why, last winter, was it only at a low level in my CSF but not in my blood? Have I had this antibody in other PANS relapses? Did Lyme or Strep trigger it? Did it only appear when the ME started? And most importantly, will reducing the antibody with Rituxan lead to tangible improvement?
There are so many unknowns and no guarantees.
However, just as I’ve always done in treating PANS, I have to base my decisions on a combination of existing research, empiricism, intuition, and my doctors’ clinical experience. It’s all brought me this far and pulled me out of the darkest places, so I’m telling myself I have every reason to be hopeful that this will work for me once again.