Jakobstad, June 27, 2015

To continue the football (= soccer) analogy I started at the end of my former post, now there is something of a midfield battle going on, with neither me nor my opponent finding any opening passes. 0-0, thus, but I feel like time is on my side here.

If I ever had the slightest doubt that what I feel in my body during the treatment really could be due to a herxheimer reaction, that doubt is gone now. My up-to-then worst day (two days ago) was followed by an even worse day (yesterday). My whole body was in an inflammatory state, and suddenly I had huge neurological problems in the right part of my body – wandering pain, sudden numbness and “electric shocks” down through my leg as well as up behind my ear. It was simply fascinating – even if that word usually is used in more positive contexts.

A rational explanation to what I experienced could surely be hurriedly suggested. The reason would then be that I had subconsciously compensated for my left-side problems the day before yesterday – strained my right side in order “to help” – resulting in yesterday’s problems.

I can immediately calm down possible know-it-alls by reporting that I’ve overcompensated in the suggested way many times in life, but never ever have I experienced something similar to what I did yesterday. It was simply a neurological chaos taking place particularly in one side of the body, in a way that just can’t be explained as a result of strain. Believe me – I conduct an empirical research in my own body.

Counter-attacking, I drew upon every form of detox and medication I could possibly think of, and by evening it all started to ease out. I still feel a bit sick, but it’s getting better all the time.

Since I couldn’t do much more than ride it all out, I took the opportunity to follow up on the SSRI phenomenon I wrote about earlier. I had grown successively more curious, since so many struck by lyme disease had contacted me reporting similar experiences – in short 1) acute illness, 2) the diagnosis depression, 3) prescribed SSRIs, 4) a severe worsening of the illness during the so called break-in period.

A day of couch-conducted research, it was, and I found something highly interesting.

It has earlier been assumed that depression is due to an insufficient amount of signal substance in the brain, and that SSRIs – limiting the reabsorption of serotonine into the presynaptic cells – show good results since the use of these medicines results in an increased amount of signal substance.

More and more, researchers have started questioning whether this is the whole truth. The hypothesis that depression could be caused by inflammation of the brain has been brought forward, and that SSRIs might have effect due to anti-inflammatory properties.

The first research paper regarding this idea was presented a little over three years ago. The results suggest that the hypotesis might be true – results in test tubes (in vitro, lat., literally “in glass”) show that SSRIs at a dosage equivalent to the dosage usually prescribed by doctors seem to have a significant anti-inflammatory effect.
(The abstract at the link above shows a rough brush picture, the full report I read lies behind login and needs to be access either by user account credits or by payment.)

What I – as well as the research team – found even more fascinating was that lower doses had a contrary effect – that is, they promoted inflammation. It doesn’t stop here: the lower doses triggered the microglial cells – the most important part of the immune defense regarding the central nervous system – into starting producing… that’s right, cytokines.

A person struck by lyme disease has far to much cytokines to start with – the body is kind of in a constant inflammatory state. SSRIs have a break-in period, it can take up to many weeks before the accumulation of the active ingredient is large enough in the body to be able to produce the desired anti-inflammatory effect. Up until then, the SSRIs – according to the research in question – just makes the lyme disease symptoms worse.

Not only, then, is lyme disease so often misdiagnosed, but the medication commonly prescribed makes it all even worse. This is another strong reason as to why the lyme disease awareness amongst doctors has to be increased.

Helsinki, June 14, 2015

Even if I aim for the future, I’d still like to look back for a while. It helps me process everything that’s been happening in the past, and at the same time it paints a picture of how a single person’s life can be infected by lyme.

When my acute symptoms surfaced in Fall 2000 (of which I wrote earlier), I was prescribed antidepressants by my doctor. It was an SSRI-type medicine, with the active ingredient being sertraline. SSRIs are well known to have a break-in period during which the symptoms are not eased, but accentuated. It’s common to talk about 2-3 weeks being needed to turn the negative trend around.

My break-in period was nothing like 2-3 weeks, it was almost two months long. It was one of the worst experiences in my life. Harsh anxiety attacks that several times brought me to the emergency room at the local hospital. I thought my life was in danger. In the ER, EKG and enzyme tests were taken, to check heart rate irregularities and possible traces of a heart attack. Nothing was found.

In addition to the anxiety attacks I had severe arrhythmia, skipped beats. I’ve always had a slow heart rate (about 45 beats per minute, falling to under 40 bpm when my ability of absorbing oxygen increases through exercise). “Skipped heartbeats“, or ventricular extrasystoles, are somewhat simplified two heartbeats too close to each other, resulting in a prolonged time until the thereupon following heartbeat occurs.

At a heart rate of 45 bpm, the heart beats every 1 1/3 second. When two beats are triggered close to each other, there will be up to 2.5 seconds before the next heartbeat takes place. A lot goes through the mind in 2.5 seconds – it is an enormously long time to wait.

Furthermore, my head was completely loaded – that’s the best way I can come up with to describe it. As if the brain was a beehive, a head completely occupied with itself. All external impulses – somebody speaking, music playing, sudden sounds, bright sunlight – were too much. I couldn’t take in anything at all, as if the brain was a vessel filled to the rim with water and every drip that fell into the vessel just spilled over the sides.

And tremors, dizziness, sweating, a neck that didn’t seem to have the strength to carry the head up. It was two very long months. The single thing pulling me through was my wife Ia never taking my condition lightly, and still managing to anchor me in a pitch-black, stormy everyday life.

One can probably have reactions against SSRIs like the ones I described here. Lately, I have nevertheless started to ponder what I went through. I know many who uses these medicines. Several have no break-in periods worth mentioning, others go down into a valley before the journey upwards starts. None of these friends and acquaintances seem to have been in quite the condition I experienced only due to SSRIs.

I have thought this medicine to be particularly taxing particularly for me, and that I have a thin wall between my body and my soul. At the same time, these symptoms match the physical and mental collapse that many struck by lyme experience at the outburst of the disease. Maybe it isn’t a question of one or the other, maybe it was both. Now, in retro-perspective, I believe that lyme was at least a part of the physical and mental chaos I went through.

Helsinki, June 8, 2015

Tomorrow, on Monday, another antibiotics is added to my medication. I will continue to recieve IV-antibiotics as well, every other day from now on. Now I enter the phase of which I’ve been most afraid. Now all the medicines are thrown into the mix.

When the spirochete (the spiral-shaped bacteria) dies in the body, it is through the destruction of its cell wall. Then endotoxins enter the blood stream, which the body experiences as an attack and treats like an inflammation. If the release of endotoxins is large-scaled enough, the human defense mechanism is overloaded. Then something called a Herxheimer reaction occurs. That’s when you start feel not better, but much worse than before.

The Herxheimer reaction (or herx, in daily speech) can be everything from almost neglible to something that makes the patient brutally ill. Some lyme patients produce almost no herx symptoms at all, others are feeling terribly sick. For natural reasons, I wish I belong to the first category, but I have mentally prepared myself for a rough week.

The lyme bacteria is a chameleon that can disguise itself through mimicking symptoms of other diseases, thus confusing the doctors and making it much harder for them to come up with the right diagnosis. When one listens to different patients’ history of disease, their initial symptoms can vary quite a lot.

Late stage symptoms is a different story. When the disease has harassed the body long enough, the common symptoms have appeared. It would all be som much easier if one could look 10 years into the future. Then proper treatment could be started at a stage where the bug simply hasn’t had enough time to cause so much devastating damage.

Now we are practically forced to look at it all in retro perspective, and a lot of people are indeed being misdiagnosed when their first symptoms occur. When my symptoms appeared, I didn’t give borrelia burgdorferi a single tought.

I ruled out my first symptoms as being caused by other factors. When I started taking antidepressants in fall 2000, I thought I would die – I went to the hospital emergency room several times due to irregular hearbeats and panic attacks. The EKG:s showed nothing out of the ordinary. SSRI antidepressants have a breaking-in period during which it is common that the patient feels worse during the first weeks or so.

I felt terrible for a period of six weeks, until it finally eased off. My wife saved me. She tirelessly sat by my side, ensuring me that I would make it, that I would cut through. I did, and came to the conclusion that my breaking-in period just was an unusually long and heavy one.

But the irregular heartbeats didn’t disappear. In my case, I had premature ventricular contractions (PVC) – for many periods as much as one PVC every tenth beat. As my pulse always has been slow, and I excercised a lot during that winter season (which lowered my pulse to about 36 beats per minute), the doctors explained that PVC:s are experienced more often in individuals with a slow heartbeat. I believed them, and carried on.

My next symptom was dizziness. This was explained to present itself due to neck tension, and I started to schedule regular appointments with naprapaths and physiotherapists. The treatments eased the symptoms, but only temporarily. At the transition into year 2001, there were as you can see many signs pointing towards an underlying problem, but neither I myself nor the doctors grasped that just yet.