PhDwannabe

Can we hear about the professionals yet? Both Cap'n Refsmmat and I were eager to peruse some of their work.

I don't think it's generally appropriate to make diagnoses at a distance. Nor is it really appropriate--or sensible, or helpful--to attempt to make them based on two sentences of self-reported information about an individual which indeed appears to have been... er... interrupted. Nonetheless, as a general point of clarity for the purposes of unasked-for instruction: First and foremost, panic attack-like experiences which appear to be rooted in particular traumatic events are most consistent with PTSD, particularly when they involve dissociate or hallucinatory (in PTSD, we usually call them "re-experiencing" to distinguish them from more general psychoticism) experiences (which panic attacks in Panic Disorder typically do not.) That said, we can't really tease apart a lot of diagnostic nuances with two cut-off lines of text, so don't take that as saying anything too specific about the OP. You're generally on-target in your account of the development of panic disorder, in that it's propagated by avoidance, and often spreads to broad sets of situations or contexts (we would refer to this as "generalization.") Beta blockers are sometimes prescribed for different sorts of anxiety conditions, although they're more commonly used in social anxiety or (this is of course not a full "disorder," just a phenomenon) performance anxiety. Beta blockers are not anxioloytics in a direct sense, they just interrupt the effects of catecholamines on the heart. Thus, the hormones of the stress response don't cause your heart to pound, and your brain doesn't have the kind of internal feedback to tell it to freak out. Far more common for panic disorder are benzodiazapines like Xanax or Ativan--they're big club-to-the-head anxiolytics. Essentially booze in pill form (no joke, they actually hit some of the same GABA receptors). You're also right that they should be combined with CBT; although I'd go a step further and say that CBT ought to just be the first-line treatment. CBT for anxiety disorders of nearly any kind has pretty terrific outcomes. Benzos, as well, are a rather imperfect long-term solution, for many of the reasons you can imagine. Particularly for panic, CBT also just plain works better (that is, gets more people panic-free.) Nonetheless, the forms of CBT used in Panic Disorder are often quite heavily behavioral, and less cognitive, in terms of the "flavor" of their interventions, so I wouldn't necessarily couch their active mechanisms in the terms you used. Sometimes the sort of thought-disputing tactics you mention are not even used for PD, and "exposure" interventions, which simply involve a gradual extinction of the fear, are efficacious just about exclusively. But the cognitive stuff is often very useful, too (I tend to be more of a cognitivist, so you won't find me trashing it at all). Denise, to you specifically, it does sound like you're having a hard time with some things, despite being cut off a bit there in describing them. Unfortunately, it's not likely that anybody here will be able to do much for you, either in terms of "diagnosing" what's going on for you, or really offering any substantial help beyond what a friend or family member might provide (not that that isn't important too). I'm a graduate student in clinical psychology, and I can tell you that psychotherapy for anxiety disorders is really pretty effective much of the time, and it can be very helpful for depression as well (although I'll also warn you that there are some people on the forums who like to loudly insist otherwise, and they may chime in here). If you want, you can send me a private message. I certainly can't do therapy with you, but I can usually help you find someone nearby who can, if you had some interest in that. I wish you luck, either way.

Can we hear about the professionals yet? Both Cap'n Refsmmat and I were eager to peruse some of their work.

I imagine these professionals might be psychology professionals. Since I have graduate-level training in that area, I'd enjoy hearing what they have to say as well. Do you have references of some kind I might be able to peruse?

Sure, that's kind of the question. Metaphysically, I'm a physicalist--I think the brain is just made out of stuff like everything else is, and its interesting functionality is a property of the stuff it's made of. Eventually, I imagine, we'll recreate it, or perhaps create something better or different than it. It's just sort of an engineering problem which we'll figure out eventually. From a naive perspective, a lot of people imagine AI in a way that's a bit anthropomorphic, but there are lots of ways a machine (or indeed, "being") might be intelligent that is different than the way the 3lb blob of goop contained within members of h. sapiens produces intelligence. So maybe we won't be able to recreate human intelligence, but we'll still create a creature that's intelligent in some fashion. To be honest, we might end up creating something so different (and perhaps even more advanced) than ourselves that we'd even have trouble recognizing what we've made. The best way we'd even have to do that, at this point, is still somewhat imperfect and controversial. There are lots of interesting arguments to be had and read in metaphysics, philosophy of mind, consciousness studies, or AI that deal with whether or not this might be possible, and how. But I tend to think we'll settle the question of whether or not we can do it when we do it.

That's a topic of some pretty substantial philosophical debate.

Well, that's sort of a subtle issue, to be honest. "Stimulant" gets validly used (both colloquially and scientifically) to describe either the immediate neurological effects or the final behavioral effects of a drug. So, caffeine, which tends to increase alertness and wakefulness and, to some extent, cognitive ability, can more or less get called a stimulant because of what its behavioral effects are. Something like methylphenidate (Ritalin) is also properly called a stimulant (often a "psychostimulant") even though we use it to treat kids who are hyperactive. "Why would we give a stimulant to hyperactive kids?" many an intro psych student wonders aloud. Well, because methylphenidate's dopamine agonism increases activity in the prefrontal cortex--that's what makes it a stimulant: it increases that activity. Its final behavioral effect is often "calming" because the PFC areas it stimulates are involved in behavioral inhibition, which allows the kiddo in question to more easily stop himself from, say, getting up from his desk and running around his classroom. Though it's a little imprecise, in psych and medicine, "stimulant" does indeed often get used to describe either neurological or behavioral stimulation. Ain't that the truth.

I'd prefer not to promote the spread of information like: ...which is just thrown down and passed off as credible without any kind of scientific support. Have a question? Ask a question. Have an assertion? Discuss your evidence. Without it, I'm just making random claims. Horseback riding cures asthma! Because I said so!

I'm not sure you're really getting the sense of the word "context" as I'm trying to convey it. Suppose you were at a party--a room full of people quietly chatting about, I dunno, various science topics. And then suppose the door opened and a person, just as they're crossing the threshold, without introduction or explanation, began shouting about the "Best and natural acne treatment." No announcement that acne advice is quickly forthcoming. No invitation to debate about acne advice. Indeed, no clear sense of for what purpose anything is being said. Is there anything about that scene that would seem... odd to you?

Well, it should indeed make you wonder: it's terribly unreliable. Part of Loftus' work was to show how easily processes like hypnosis--which was sometimes touted as being able to "recover" memory--could just as easily "implant" false memories that had never happened.

Pretty far out of the scope of practice for a psychiatric nurse, which should've been your first clue. Making claims that are essentially nondisprovable should've been your second. A couple of decades of cognitive science is more than enough to crank this through the garbage disposal. In short, it's easily demonstrable that human memory does not function like a hard drive, and that recall is actually substantially comprised of what we'd usually refer to as "imagination." If this were not so, memory would not be so tragically easy to manipulate. Suppose I read out a list of words like bed, pillow, nap, rest, sheets, mattress, snooze, dream, etc. A few minutes later, I read out another list, and ask you to tell me whether these words showed up on the first list, or if they're new (this is what we call a "recognition" task.) The list might go something like this: car, bed, dog, streetlight, rest, sleep, doctor, sheets, dream. People do pretty well picking out the ones from the first list. They also do pretty well picking out "sleep," which wasn't on the first list, but they believe they heard a minute ago as vehemently as they do any of the other words. Why? Because their brain was never recording the words, and they were never really stored--in our now-familiar hard drive sense--in memory. The brain was recording a sort of cheat: "a bunch of words about sleep." We've replicated this a million times. I did it with intro psych students semester after semester (the experimental paradigm is a bit more complex than this, but I've given you the basics) and it always works out wonderfully. If you want more information, look up the work of Beth Loftus. Her research systematically destroyed the "recovered memory" movement of the '80s and showed us a lot about how our efficient cognitive trickery functions to get us through the day without actually recording a whole hell of a lot of specifics.

Is, um, there a question in here somewhere? Something to discuss? Or just weirdly contextless and unsolicited medical advice?

I couldn't agree more.

I'm a grad-level PTSD researcher. As described, this is not anywhere close to PTSD.

Long life though I might hope to live, I hope I don't make it to see Peak Chalk. The survivors will envy the dead!

This is not anything anywhere near attachment disorders, and the post immediately above takes information from a scientifically unsound self-help book that won't really get us anywhere. Neither is it really a syndrome, of sorts (in that it's not really some kind of cluster of symptoms that hang together in the absence of some clear pathophysiological process). It's just a phenomenon--something that happens. It's kind of mundane enough that it doesn't really have some sort of widely used clinical description or term. A wider variety of food tastes good when you're hungry; it just is what it is. There's plenty of behavioral terminology we could employ to describe contingencies that might alter the reinforcement value of a reinforcer, but it's not the descriptor you're looking for.

OK, let me make sure I've got this. You wanted a neurological explanation for a phenomenon that essentially isn't neurologically verified. Someone suggests--astoundingly--that increased blood flow to the brain upon lying down would "generate new thoughts" and insight in some clinically recognizable and significant manner. You agree with this, and to support it, you copy/paste stuff from an awkwardly translated advertisement for some Lithuanian quack medical device--which, mind you, doesn't have anything to do with what we're talking about--that some interested party named Boris is busy wallpapering all over the internet. I'm going to go ahead and register myself as thus far sort of uncompelled by this particular line of reasoning.

Is this satire? I really want to believe that this is some sort of humorous allusion to something out of Galen or Hippocrates I'm just not erudite enough to recognize. If this--gods preserve us--actually isn't satire, I'm just going to go ahead and clear this up: This is not in the neighborhood of the area of the general realm of how cerebral blood flow affects cognition. This explanation is absolutely, categorically, 170%, not right. It is not capable of existing on the same planet as right. It is parsecs away from right. I cannot emphasize enough how far from plausible this is.

I am indeed getting kind of a ghostly feeling.

No, it, um, isn't.

No. And no.

There likely isn't one, because he wasn't correct. Empirical science has not borne out the vast majority of the specific assumptions of his clinical methods, many of which have been long-abandoned, or maintained in practice by only small groups of clinicians.

Vincent, I don't know why you're typing in Courier, but it hurts the eyes. No, it cannot be demonstrated that At least, not empirically. There are plausible and relevant causal agents here that are not amenable to direct experimentation. This is as much a philosophy of mind issue as it is a neurobiological one. Wikipedia's the best place to start and the worst place to end. Drug treatment outcome studies have a worrisome habit of waving the flag of success when treatment differences reach statistical significance. Statistical significance is not clinical significance. Effect sizes, which are roundly ignored in popular reports of these studies, are frequently disappointing. Go read some of them and look at the effect size statistics in their results sections. If you're unfamiliar with this thing called "effect size," go back to your friend Wikipedia. Plenty of evidence for this. Why don't you look at the article he provided? While I continue to maintain that the story is extremely complex and really quite poorly explained by mere serotonin differences, that bare fact as stated is an empirically measurable, and empirically measured, one.

Actually, there is a fair amount of accumulating evidence that the serotonin hypothesis is vastly oversimplified, and what we are seeing in what are admittedly fairly low-effect size results associating low serotonin levels and depression is really one branch of a far more complex process which has largely yet to be observed. This guy's blog post is relatively informative on the matter for the, well, between-layperson-and-scientist, and has a lot of good links if you'd like to see some of the empirical work. People tend to take it for granted that this bit of science is settled, and that certainty is often unreconciled with this fact that, well, drugs that agonize monoamines like serotonin don't even work that well. Their clinical effects are modest at best, and often barely make it above rates of improvement seen in placebo control conditions. At any rate, neurotransmitter explanations get you relatively little in terms of the whole story anyway, since neurochemical interactions are a grand mediator of all behavior, cognition, emotion--essentially everything we do and experience. To refer to neurotransmitter deficits or excesses as causal--as the start of the story, as it were--is problematic for about a million reasons on its own.

What exactly is your question?