"Please stop bleeding, please stop bleeding. Oh God please stop bleeding."

The clinical psychology module this year has us looking at numerous mental disorders from three different angles: Aetiology (causes), symptoms and treatments. I'm no expert in this area yet, but I'm hoping that I'll soon be pretty up on my anxiety disorders by the end of this semester. They fascinate me, no thanks to the class itself mind you.

You see; something I have done very little of during my course is learn how to help people through their problems. It seems utterly bizarre to me that a course so focussed on human foibles should ignore treatment so completely. At the most, I'd learned the principals underlying Cognitive Behavioural Therapy (CBT). The lack of detailed training is a heavy burden when friends go through anything from "Aaaaah stress aaaaaah" to "all moisture in my body spent the last 5 hours escaping through my eyes." It is a delight, therefore, to poke my nose into a well written chapter on panic disorder in a book written by Nolen-Hoeksema (2008).

The chapter itself has given me a brilliant background insight into the aetiology, symptoms and treatments; but pretty much all of the journal articles it links to are not part of Abertay's subscription. It's a fairly common problem students encounter, when their university has full access to "Nymphomaniac tradesmen's annual crafting guild review" but completely ignores "Annual review of clinical psychology".

I mean really? "What should we sign up for? What about this clearly relevant journal?" - "Don't be a fool. Our students will only learn if we make it almost impossible for them to do so!" It's a problem glossed over whenever the vast distribution of knowledge is alluded to in political or humanitarian statements; that to view, analyse, review, trade or collaborate you must pay a hefty fee to a third party website or 7. My personal example here is that Craske & Waters (2005) wrote a mass review of almost every study to do with anxiety disorders; making their paper the single most important thing I could look at to help me with my assessments. A free version doesn't exist, so I will either have to pay $20, or (as will happen) use less valuable / relevant sources. By definition my actual research becomes sub-standard. People who get their work published under the same restraints must realise their knowledge is massively restrained. Gah.

Balancing invisible ducks.

Let's do this. Anxiety disorders have for different types of symptoms: Somatic (physical), emotional, cognitive and behavioural. Generally, anxiety is a sort of broken fear response. It hosts many of the same responses, but suffers from a number of flaws. That is to say, the response is disproportionate to whatever danger may exist. Usually there is no actual realistic concern that could explain the anxious response anyway. On top of all that, whilst fear responses subside when the danger has gone on its merry way, anxiety remains. 

Panic disorder is a diagnosis given to individuals who have panic attacks on a regular basis and so begin to structure their lives and behaviour around the fear of another striking. Panic attacks are more common than one would think. King, Gullone and Tonge (1993) found that 40% of young adults tended to have panic attacks when they were feeling under pressure. Panic attacks are pretty rough. I've never had one and hope that doesn't change. If a combination of heart palpitations, pounding heartbeat, numbness, chills/hot flushes, sweating, trembling, choking sensation and chest pain / nausea doesn't sound bad enough; there is also a crippling sense of  'unreality'.

How crap does 'unreality' sound? The sense that your body is out of your control and doing horrible things against your will that seem out of all proportion. It's the much more ominous version of watching yourself strip off and run wildly through Asda whilst you stare out of your eye-sockets, aghast. The final symptom listed is a fear of dying. It's probably worth mentioning that people suffering from panic attacks tend not to actually die.

Today is the day for watermarked stock images, I reckon.

Panic attacks are usually brought on by specific situations or events, in which case they are usually part of a phobic reaction. They are brought on by intense stress and so are isolated events that, although pretty shocking, are nothing to get overly worried about. It is when the panic attacks come out of the blue during normal, calm, day to day activities that individuals begin to get concerned. The lack of obvious cause doesn't exactly help a person get over the wretched experience, and having them frequently is no fun. No fun at all. As mentioned above, the diagnosis of 'panic disorder' is given to people like this, who begin to let fear of another attack enter their routine. (Watch this space. I've ordered the Diagnostic and statistical manual of mental disorders - DSM-IV-TR - which gives the actual conditions of diagnosis for this sort of thing. I'll write up an official definition once it arrives).

In individuals suffering from panic disorder, attacks can come at pretty different intervals. They might have many within a short period then go for months before having any again, or they might have regular attacks once or twice every week. Sufferers generally begin to believe they have deathly illnesses (which is fair enough, considering what they have to go through). Due to the seemingly random nature of the attacks and the previously mentioned unreality, sufferers can feel that they are going crazy or losing control of their bodies. This sort of thing, in certain people, leads them to hide their symptoms through an odd sense of shame. The isolation makes things worse and makes them demoralised and depressed (remember folks: talking helps).

Caske and Waters (2005 - See?! THESE buggers turn up everywhere and say something wise) reckoned that 7% of all people experienced panic attacks each year, and 3-4% of the human race will actually pick up panic disorder for some of their lives. Really? 3-4%? I suppose it'd be pretty hard to stand in a room with 30ish people and have them all be perfectly calm individuals; but that's a sign of our society. All people? I'm not convinced; Australians are pretty laid back.

Just ask Hugh.

People are more likely to obtain the disorder between adolescence and their mid-thirties. Ehlers (1995) performed a study in which he noted 92% of individuals who had it would continue to have symptoms for at least a year beyond the initial attacks; and for those whose symptoms went away, in 41% of cases it'd fly right back again. Alcoholism, depression and agoraphobia can develop from the condition, but you'll see later why I reckon this statistics lean painfully towards individuals who were given drug treatment at the expense of actual therapy.

Craske and Waters....again.... reviewed family histories of panic disorder patients. About 10% of first-degree relatives also had the disorder, as opposed to the 2% in relatives of non-sufferers. Hettema, Neale and Kendler (2001) added further support to the 'hey, there's probably something genetic about this' viewpoint by taking from twin studies that 30-40% of all variation in rates was down to genetics. (Twin studies are fairly straight forward. Monozygotic / identical twins share 100% of their genes; dizygotic twins only share 50%. For conditions which have a genetic contributor, the concordance rate should be higher in identical twins that in non-identical twins for this reason. It gets more complex, but that's the basic principal). So, there is a general predisposition to panic disorder or anxiety?

Donald Klein happened upon the finding that antidepressant medicine reduced the frequency of panic attacks, back in 1964. Most of these drugs affect the regulation of the neurotransmitter norepinephrine in the brain, and so his logical conclusion was that the fluctuations of that chemical might be the root cause of panic. Over the intervening years, evidence has built up which suggests that is indeed the case. There is poor regulation of norepinephrine in sufferers of panic disorder, especially in the locus ceruleus in the brain stem. A man I would not like to shake hands with, Redmond (1985), found that shooting electricity through that area in monkeys’ brains caused them to react in panic. He also showed that cutting it out entirely created fearless monkeys.

Additional research finds that altering the level of norepinephrine (again, especially in the locus ceruleus) causes panic attacks (Charley et al. 2000). Yohimbine alters it but no other neurotransmitters. When people with panic disorder take this, they tend to have a panic attack right on the spot! Oddly, then, other drugs which alter the activity of norepinephrine have been shown to alleviate the symptoms (Charley again). Hmmm.

Serotonin, GABA and CCK have also been found to have some affect on panic disorder (Bell and Nutt, 1998). Drugs that alter the functioning of serotonin systems seem to be useful in reducing panic attacks. Certain theories have suggested panic disorder is all down to high levels of the chemical in key brain areas, but others have argued that it’s due to low levels! It makes sense that acute panic attacks are affected differently by serotonin than longer lasting anxious fear of the next attack.  Increasing serotonin levels in the periaqueductal gray area of the brain stem reduce panic-like responses, whilst increasing them in the amygdale increases anxiety, and especially anticipatory anxiety (Graeff et al. 1996). I have literally no idea what or where the periaqueductal gray is. Let's Google it. One mo...

http://en.wikipedia.org/wiki/Periaqueductal_gray

There you go. Magic.

As women with panic disorder have reported an increase in symptoms during their pre-menstrual periods and the postpartum period, it might be that progesterone increases vulnerability to panic symptoms (Yonkers, 2001). Progesterone affects both serotonin and GABA systems, fluctuating around could mess them around a bit, and if changes in level leads to increased susceptibility to panic then it could well be a valid problem. To make things worse, increases in progesterone can induce chronic hyperventilation which may be enough in itself to start off a panic attack. The amount of times I’ve written the word panic is getting to me...

Gorman, Papp and Coplan (1995) suggested a kindling model of panic, in which poor regulation of neurotransmitters associated with panic (especially in the locus ceruleus) kick of a panic attack, and in turn ‘kindle’ a lowering of the threshold for chronic anxiety in the limbic system, which both creates more panic attacks, and increases the chances of poor regulation back in the locus ceruleus. Bugger. (The limbic system is believed to have a lot to do with general anxiety). 

What do you know? I actually found a diagram.

People who have panic disorder can reliably be made to have a panic attack with fairly simple techniques, begging the question of why those without panic disorder cannot be led into it so easily. If we can answer that, we can discern what is different between the statuses. Inhaling a small amount of carbon dioxide or hyperventilating, ingesting caffeine or taking sodium lactate (similar to lactic acid) lead into attack around 50% of the time (Craske and Barlow, 2001. Rapee et al. 1992). The methods have one thing in common, they illicit the fight or flight response to some degree. Due to their crap regulation of norepinephrine or serotonin, those with panic disorder can be tricked into the response without there being a fear-source present. Something unmentioned here is the added ease of testing. I could slip you some sodium lactate or ask you to hyperventilate. If that leads you into a panic attack then it could be that you're working with panic disorder. 

So, many people with panic disorder seem to have a biological vulnerability to it, in the form of poor norepinephrine (and other neurotransmitter) regulation. Cognitive theorists wisely point out that psychological issues should probably be considered too. Craske and Barlow (2001) told us that people prone to attacks pay very close attention to their bodily sensations as a matter of course. Combined with a general pessimistic outlook, this leads to their misinterpreting the signals as negative, which leads to CATASTROPHIC SNOWBALLING THINKING! Getting baselessly worked up increases both physiological and psychological arousal (I wish we had another word instead of arousal to use in this context. It's far too associated with happyfun time by this juncture that most research of this type sounds like the Kama sutra). 

That arousal (-.-) in the sympathetic nervous system and the mind is seen as verification that they were right to be getting worked up. This downward spiral leads straight to a full on panic attack if some logic can't be slotted in. After the first attack, the person becomes hypervigilant for any weird symptoms, keeping him/her in a state of constant arousal (oh ffs...), which facilitates anxiety increases in itself. McNally (1999a) dubbed the belief that bodily symptoms will have negativity consequences as 'anxiety sensitivity'. Seems like the best way to stop yourself having a panic attack, is to convince yourself everything is fine. Successfully believe that you're ok, and you will be. How nifty is that?

Sanderson, Rapee and Barlow (1989) performed an utterly incredible study using the notion of self-efficacy. If you haven't encountered the term before, look it up in the context of Bandura's studies. Self-efficacy is our perceived ability to deal with the problems we are faced with. High self-efficacy means that you believe you are in control of your situation. Low self-efficacy means that you no longer believe you can cope with the problems in your life (this is similar to the idea of internal/external locus of control. Rotter, 1954). Having high self-efficacy is generally the best way to go. The Royal College of Surgeons found that giving patients control over their own morphine intake caused them to use less than would otherwise have been administered, and actually had many of them recover faster. Bandura (some sodding date) showed that participants could deal with larger and longer electric shocks if they felt they could control the length. It's pretty amazing stuff, is efficacy.

Puts my 'control' blog post in a new context.

So S, R and B had two groups of people with panic disorder enter different rooms and attach breathing masks to their mouths. The air they breathed through it had slightly enriched carbon dioxide content. If you're paying attention, you'd know that breathing carbon dioxide can quickly start a panic attack, and these participants were told that openly. The second group were told that a knob on the side of their equipment could regulate the amount of carbon dioxide they were breathing. In actual fact it had no effect. By the end of the experiment, 80% of the first group had had a panic attack; only 20% of the second group had. That's pretty cool, in my book.

Not strictly relevant, but the 'self-efficacy' image results were boring.

The vulnerability-stress model of panic disorder is a mix between the biological and the cognitive stuff we looked at above. It summarises the aetiology: People have some level of biological vulnerability that provokes a hypersensitive fight or flight response. Due to this, much milder stimuli can cause the response and the physiological characteristics associated with it. Despite this, panic attacks only become frequent if the people also engage in CATASTROPHIC SNOWBALLING THINKING about their bodily sensations.

So: Biological sensitivity (poor regulation of neurotransmitters, lowered limbic system threshold, over-sensitive fight or flight) - Catastrophic thinking - Panic attack - Hypervigilance for signs of panic (constant arousal) - Increased probability of a second attack. As this circle completes itself, some sufferers begin to associate the attacks and general anxiety with situations, places, people that realistically have little to do with it. Avoiding those stimuli can lead to agoraphobia.

So, on that dire note. Come back next time for treatment information.