“People who experience a single random seizure, for instance, are 50 times more likely to become epileptic than someone who has never had one”
Given that epilepsy is diagnosed and treated based on the presence of recurrent seizures, this seems like a tautology - the set of “at least one seizure” contains the set of “at least two seizures”
Like saying “playing at least one game of basketball was associated with a greatly increased chance of playing more than one basketball game in a lifetime, compared to those who had never played”
The phrasing might sound bad from a math perspective, but they're trying to convey something important about the nature of seizures. Seizures act more like a learned skill than a typical illness. The first one primes the brain, and repeated seizures reinforce the pattern, making it easier to trigger.
Model A: First seizure causes subsequent seizures.
Model B: Factor X causes many seizures in a sequence that, as sequences usually do, begins with the first.
Any reason they prefer A over B? Maybe there is some evidence of learning, or a statistical fact that is true of seizures causing seizures but not of factor X causing them independently?
What I'm about to say is just hypothetical, I know basically nothing about medicine.
Suppose that seizures at one point didn't have an influence on the probability of seizures later. Then, that seems to me like it would mean that seizures were a kind of independent point process?
Like, suppose there's a model where, depending on a person's genetics, age, and, idk, let's say diet, predicts a given rate of seizures, and also that this rate varies continuously with age.
In such a model, I don't think we would tend to see something where a person has no seizures until a certain point in their life, and then subsequently begins to have them at roughly a given rate for some period of time, but it would seem compatible with the "seizures causing seizures" idea.
Note: I am not claiming that this is what the data actually shows. I have no idea.
But, on the other hand, if there were some other invisible property which can at some random point change from state A to state B, and in state B seizures are more common, but seizures don't influence whether in state A or in state B, I'm not sure you could distinguish that from the "seizures cause more seizures" idea?
But, if the causal influence wasn't just "have they ever had a seizure", but instead all seizures had an impact on chance of seizure in the near future, then I think that would have statistical effects?
tl;dr: I don't know what I'm talking about, but I suspect you could at least in principle distinguish the two models using some statistical properties.
This is an interesting point. It's pretty common for people to start getting migraines after a head injury (concussion etc). Apparently the genetic component might already be present, but the disease can be dormant until "activated". Perhaps this, too, could be "unlearnt" somehow.
Not just might sound bad. It sounds like utter garbage in support of a theory rather than evidence. Bad mathematical reasoning here really does negate the the claim as anything more than "I wonder if ..." Could be true. Let's find out. Turning it around the probability that you have one and only one seizure could be exactly the same as the probability that you have a first seizure and it is NOT epilepsy. Those could well be different ways of saying precisely the same thing.
This can explained by following the reference to the study:
> Two large-scale randomized trials provided definitive estimates of the risk of recurrence after an untreated first unprovoked, seizure. These are the multicenter study from Italy, FIR.S.T (First Seizure Trial Group, 1993) and the European-wide Multicenter Epilepsy and Single Seizure study or MESS, which included both first seizures and newly recognized epilepsy (Marson et al., 2005). Based on 193 patients randomized to deferred treatment only in the event of a second seizure (i.e., initially untreated), the FIR.S.T study reported recurrence risks of 18%, 28%, 41%, and 51% at 3, 6, 12, and 24 months after the initial seizure. In the MESS study, 408 patients with a first unprovoked seizure were randomized to the deferred treatment group. Their risk of recurrence at 6 months, 2, 5, and 8 years after randomization was 26%, 39%, 51%, and 52%. On average, the observational studies, taken as a whole, provide an estimate of the 2-year recurrence risk in the range of 40%, depending on aspects of the study design (Berg & Shinnar, 1991).
> Both of the randomized trials, especially the second, demonstrate a pattern seen in virtually all of the long-term observational studies of first seizures. Specifically, the risk of a recurrence is highest during the period immediately after the initial seizure. The rate, at which first recurrences occur, drops off with increasing time since the first seizure. Across a number of studies with prolonged follow-up periods, 80–90% of individuals who recur do so within 2 years of the initial seizure (Annegers et al., 1986; Hopkins et al., 1988; Boulloche et al., 1989; Hauser et al., 1990; Shinnar et al., 1996).
> the risk of a recurrence is highest during the period immediately after the initial seizure.
This still isn’t helpful in determining whether the seizure itself makes another seizure more likely, or whether this just means that whatever caused the first seizure is still present.
If there is an external factor that triggered the initial seizure, presumably the closer you are in time to the presence of that factor, the more likely it is that another will be triggered by the same factor.
“ In healthy adults, magnesium sits inside the NMDA receptors, preventing them from being triggered by weak signals that may stimulate your nerve cells unnecessarily. When your magnesium levels are low, fewer NMDA receptors are blocked. This means they are prone to being stimulated more often than necessary.”
Some people claim life changing quality of life improvements on the right type and dosage of magnesia supplement. It could all be placebo. I don't know why it's so common here.
I'm not going to comment on epilepsy because I'm not a physician or a medical researcher. To me, epilepsy seems too powerful and independently energised by local neuronal activity to be overridden by a voluntary thought directed at the vagus nerve.
The examples the author gives of experienced meditators being able to influence what in non-practitioners are autonomic systems, makes sense, given that there is evidence for example of Tibetan monks surviving freezing temperatures. The investigations into that phenomenon show the physiological mechanism is to burn a particular type of fat. How do the monks access that physiology? The meditation switches it on. How does that work? That's the interesting part. It takes many years to learn and decades to gain the skills, but can be stated in one simple sentence. They use visualisation.
I learned to suppress sneezing after much practice. I don't have the language to describe the technique, but I go almost to the point of sneezing, doing the inhale, and then I sort of meditate. I neither try hard to stop the sneeze or do anything active - I just let my mind go blank, and set my expectations that the sneeze is going to fade away. And it does.
Is suppress sneezing something unusual to be learned? I always thought that you can just not sneeze... I remember as a kid, when I noticed a sneeze was coming, I just decided that it was too much work, for whatever reason. Maybe I didn't want to find tissue, or maybe I didn't want to make noise.
The ideal education would begin with a few years of language learning and ear wiggling, to make sure all of the early childhood acquisition advantages were taken before they expire.
One anecdata point: I cannot easily suppress sneezing, at least not always. Delaying it for a second, for example when I am holding a cup of hot coffee and I want to put in on a table quickly before I sneeze, is sometimes possible, but I have to admit that sometimes I cannot even do that.
Ancedote, I didn't feel addicted to a drug. I would go a day or few without having it.
This was until someone claimed I was addicted. As soon as I heard that, I did research to learn if I was actually addicted to the drug. Like a switch, I stopped having multi day breaks. Multi day breaks wasn't what addicts do.
I'm off everything now, but I do wonder if simply learning about addiction triggered my brain to have the suggested symptoms.
Similarly, I think the massive emphasis on how difficult it is to quit smoking ("it's more addictive than cocaine!") has the side effect of making it much more difficult to quit.
I was diagnosed with epilepsy as a teenager, after a single tonic–clonic seizure and a few lesser seizures. Shortly thereafter, I was placed on high doses of phenytoin, which seemingly controlled the seizures (but had various common side effects, including depression and the potential for long term harm to the cerebellum).
Prior to being on the drug, and even a few times while they were giving it to me but tinkering with the dosage, I experienced something like Glover described - it felt like I could feel seizures coming, but somehow exert will over them. I had several instances where I felt like I would have a seizure but then... did not, after focusing on it. But I didn't stay un-drugged long enough to experiment further.
I trudged along for years on the drug. It felt like I was in a haze.
One day, in my 20s, since I had no insurance and no established doctor (I had moved not long before), I ran out of the drug. It was not easy to get more quickly. I decided to try detoxing to see what happened.
Detoxing off phenytoin, I had been told, was reckless, and should require careful supervision by a physician. I was in my 20s though, and did it quickly and fully - I went cold turkey.
I had no seizures. I did, several more times, experience something like the "aura" (as it was called) - but always I seemed to "will it away." Eventually, after some months, I never felt it again.
I had always assumed that I'd just "grown out" of the disorder while taking the drug, some puberty or aging related phenomenon had simply "fixed" it, and that the rapid detox made the quazi-seizure events return (rapid detox off phenytoin can be known to create seizures, even in patients who otherwise would not need it to control a seizure disorder). I'm intrigued, but still quite skeptical, of the the notion that this is something I might potentially have accidentally enacted by sheer force of will.
There might be lessons to learn here for psychological illnesses. Depression, anxiety, whatever. If something as severe and physically real as epilepsy can be avoided by rewiring the trigger, why not more fluffy conditions?
The OP author is a neuroscientist and the article has a particular, appropriate focus reflecting that.
A word some commenters might be searching for, which the article does not use, is etiology. 'Etiology' has connotations of "the murkier beginnings of a disease" -- at least as often applied to "the etiology of a mental illness."
There are clinical programs for addressing "early psychosis" which certainly assume some causes of disease progression (or worsening) can be addressed. I don't believe they are all about adapting to some inevitable.
“ People who experience a single random seizure, for instance, are 50 times more likely to become epileptic than someone who has never had one.1 Like Philip’s raven, the same stimuli that preceded the first fit—such as anxiety or a particular musical passage—more readily trigger future episodes. And the more often seizures occur, the stronger and more pervasive the underlying neural network may become, potentially inducing more widespread or more violent attacks.”
This article is a dumpster fire, and based on fundamentally obsolete and harmful beliefs. Yes people that ever have a seizure are more likely to have epilepsy. This says nothing about why, and what follows is all poorly or non researched editorializing. None of what is said here has even weak evidence. Seizures are an objective physiologic phenomenon we can measure. While there are a wide variety of non-specific predispositions to an episode including stress, no one has the authority to claim the above. Furthermore a large class of epileptic seizures are provoked by imageable, physical brain damage and another large portion have no provocation, this isn’t some middle school angst. It also seems to riff off the obsolete notion that epilepsy was mostly due to mental illness/craziness back when those were equivocated.
The idea that medicine is an objective science that we've fully "solved" is much more harmful.
There are a number of symptoms that we can group into "conditions," yet have a murky etiology.
That's not to say there isn't snake oil out there. There's certainly a ton of that as well. But medical problems aren't always a simple "solve for x" - there is a TON that we still don't know about how the human body works.
I don’t understand what point you are making by saying that seizures are an objectively measurable thing.
Are you suggesting “and therefore it can’t be influenced by the specific thoughts a person has”?
I don’t see a reason that something which we (at least so far) can’t objectively measure, but which the patient can report on, couldn’t have an impact on something which we can objectively measure.
I also don’t understand what you are talking about when you mention middle school angst?
It seems like you have the impression that the article is blaming people for having seizures or something like that? But that isn’t at all the impression I get from it.
His entire point seems very narrow minded. We could fill a dictionary full of all the measurable medical issues that stress can cause. We know that things like a smell can trigger memories in the brain completely involuntarily. So to act as if a memory of something that was happening during a previous seizure couldn't be a catalyst for a future one seems naive to me.
Given that epilepsy is diagnosed and treated based on the presence of recurrent seizures, this seems like a tautology - the set of “at least one seizure” contains the set of “at least two seizures”
Like saying “playing at least one game of basketball was associated with a greatly increased chance of playing more than one basketball game in a lifetime, compared to those who had never played”