Here's a bone for you more psychology-based people.
Is Social Anxiety Disorder just "shyness"? Well, yes and no, but, more importantly, no.
Anxiety is a good thing. It allows us to adapt to our environment and modify behaviors appropriately. It motivates us to accomplish tasks and also increases our cognitive skills, such as enhancing memory of certain things and focusing our attention. It is only when anxiety becomes inappropriate (or hyperactivity of this state) that this becomes termed a disorder. The effects of anxiety disorders can be quite pervasive, interfere with several aspects of life, and often can become crippling to the sufferer. My previous posts on the septo-hippocampal system are very relevant to this post.
Anxiety disorders are not on a single "anxiety axis" but are multi-dimensional in nature (figure below). Anxiety, in a broad sense, is an exaggeration of uncertainty within the world. You can't just have "normal anxiety" or "irregular anxiety" (this may be the case within a specific class of the disorder, but on the whole, there are several different classes -- I hope you get my point).
(after the jump is a short clip describing social anxiety)
For my own sake, I won't be citing references. If you are interested in where something comes from, let me know, and I'll get you the relevant material.
This is by no means a comprehensive view of anxiety, as it is a highly complicated disorder.
Anxiety disorders are a multi-dimension disorder
Psychology of Social Anxiety
Anxiety can manifest itself cognitively in several forms. I will emphasize Social Anxiety Disorder (SAnD, not to be confused with Seasonal Affective Disorder, or SAD), but this largely can apply to other states of anxiety, with other aspects of uncertainty and ambiguity rather than social (or person-person) situations.
Social anxiety (or social phobia, but phobia is not the correct term) is the excessive fear of how one will be perceived by others. These fears include: being judged, acting in a way that will cause embarrassment and humiliation, and/or not performing satisfactorily in others' views (relates to judgment). Often, the person will put up a "front" to try and "impress" others, while believing that they cannot live up to this standard in all actuality.
It is thought that these individuals often accentuate the negative feedback (e.g. criticism, whether it be constructive or otherwise), while ignoring any positive feedback (e.g. compliments) they may receive. These individuals will become conditioned to certain situations in which they have experienced these negative states and will try to avoid them (e.g. social situations). These individuals genuinely want social interactions, relationships, and connections; however, they just do not know how to approach them in such a way to overcome their extreme anxious feelings. After all, humans are social by nature.
In extreme cases, this can manifest into agoraphobia, which is often the case when a person has extreme physiological reactions (i.e. severe panic attacks). This often will lead to the person sequestering themselves in a safe environment (house).
Social anxiety also encompass physiological states of the body. These physiological states come through the sympathetic nervous system, resulting in sweating, heart racing, palms become clamy, hyperventilation (some, of course, may be absent from other individuals). Because of these symptoms, minor passive avoidance behaviors are expressed through being quite reserved in conversation or interactions, crossing of the arms to "keep close" or to avoid hand shaking (fear of embarrassment), often appearing to be busy to avoid being asked to do a specific favor or task that may potentially lead to negative consequences, or just leaving the situation in general. Beta-blockers are a useful drug to help manage the physiological symptoms but do not help with the cognitive (thoughts) of SAnD. In this case, usually anxiolytics or anti-depressants are prescribed (see below for more details).
Some of these symptoms can be overcome by Cognitive-Behavioral Therapy and some cannot. These individuals will always have a higher anxiety level in certain situations, but the key is to find a way to manage this anxiety, despite giving more weight to negative evidence.
This portion will relate to anxiety (normal and irregular) in general. From a neuroscience perspective, not much is known about the underlying neural correlates of specific classes of anxiety disorders. We have drugs to manage them but rarely do we know how they work or what circuits/brain regions they affect.
The septo-hippocampus is thought to be a region that detects conflict between the 'real world' and the 'expected world', which nicely maps onto the problems associated with anxiety disorders. This area is also responsible for modifying motor programs/behaviors in an appropriate way to accommodate such new information. Another role of the hippocampus is to form associative memories. These memories take the form of associating a stimulus "A" with another "B". These can be associations between a specific context or situation and a reaction/outcome (such that a link is "bridged" in this area (maybe, also depending on the temporal discontinuity) between, in this case, a social situation in context "X" with having a panic attack or having overwhelming feelings of extreme self-conscientiousness, embarrassment, disappointment, high symapthetic arousal, etc...), which is ultimately weighted more heavily than other positive factors that may have occurred here. Here, is also where another neural locus comes into play.
The amygdala is an almond-shaped region that is in front of the hippocampus (right image). This region is largely thought to play a role in the perception of fear and has dense connections with the parahippocampal region, prefrontal cortex, striatum, insula, and several other loci. This area may, too, play a role in fear conditioning, whereby a neutral stimulus (shaking of a hand) is associated with an aversive stimulus (feelings of embarrassment or disappointment). In g eneral, one can think of this area as playing a major role in the processing of fear, while also connecting to other neuroanatomical regions that "weigh in" on this fear and anything that is associated with this fear and how it is perceived by the person (e.g. with the frontal cortex, insula, hippocampus...)
Treatment & Chemistry:
The treatment of anxiety disorders is interesting, to say the least. The main source should always be Cognitive-Behavioral Therapy (CBT), which, in short, is examining your cognitive thoughts and attempting to modify the way you think about specific actions/situations/thoughts and modifying your behavior through this analysis.
Often in conjunction with CBT, individuals are often prescribed drugs with anxiolytic effects. It appears that anti-depressant, like SSRIs (Selective-Serotonin Reuptake Inhibitors), SNRIs (Selective-Serotonin/Norepinephrine Reuptake Inhibitors), MAOIs (Monoamine Oxidase Inhibitors), and others are very well at balancing dysregulation of the neurotransmitter systems (serotonin, serotonin/norepinephrine, monoamines). These drugs are all used to help regulate the balance of these neurotransmitters by making them more available for receptor binding. In the case of SSRIs and SNRIs, these block the re-uptake mechanism that clears them from the synaptic cleft; blocking the re-uptake allows them to be available longer and to bind to their respective receptors more often and for longer. MAOIs work on monoamines, which are normally broken down by monoamine oxidase; if this enzyme is inhibited, the monoamines are available longer in the synaptic cleft to bind more frequently.
Very interestingly, these anti-depressants / anti-anxiety medications affect adult neurogenesis (birth of new neurons in the brain), which occurs within the hippocampus.... hmm... it all comes together, eh? See Functional Neurogenesis blog for a new paper that was published in Nature describing a possible connection between everything (stress, depression, neurogenesis).
In addition, other anxiolytics, such as barbiturates and benzodiazepines (like Xanax), among others, work on the GABA system, specifically the GABA(A) receptor, by increasing the frequency of ion channels on this receptor opening. GABA is often inhibitory, and, increasing the opening of these channels leads to an influx of chloride ions, hyperpolarizing the neuron, and making it less likely to fire a signal, there by "dampening" the circuitry. If you have hyperactivity in a system, one way to combat it is through dampening the circuit.
Just a quick overview of the psychology. neuroscience, and chemical treatment involved.
*I am actually thinking 'What will they think of this?' as I write this!
Referring websites & articles:
Canteras, N., Resstel, L., Bertoglio, L., Carobrez, A. P., & Guimarães, F. (2010). Neuroanatomy of anxiety. Current topics in behavioral neurosciences, 2, 77.
McNaughton, N. (1997). Cognitive dysfunction resulting from hippocampal hyperactivity--a possible cause of anxiety disorder? Pharmacology Biochemistry and Behavior, 56(4), 603-611.