By at August 1, 2012 | 11:25 pm | Print


I was 28 when I finally realized I wasn’t immortal. I was walking across a parking lot to see a concert on a hot, sunny day when I suddenly became lightheaded, got the chills, my peripheral vision went dark, and I felt like I was going to pass out. I thought for sure I was having a stroke, but I wasn’t. A month later I’m sitting in my dining room doing nothing important and out of the blue I felt like someone just reached into my chest, grabbed my heart and began squeezing tightly for 30 minutes. I thought for sure I was having a heart attack, but again, I wasn’t. A subsequent trip to the ER and a 2-day stay in the hospital for testing resulted in an “I’m sorry, sir, you’re so healthy I can’t even tell you to take an aspirin” response from my doctor. Needless to say, I was frustrated. More importantly, I was scared. The next few months brought on more occurrences of either head, chest, or a combination of both problems. Patterns started to develop. I’d get the head problems when I’d go out on days that were both hot and sunny and I wasn’t wearing sun glasses. I’d get the head problems in stores with very high ceilings. Walgreens, Target, and Home Depot were often avoided. Chest problems seemed to occur late at night when I was laying in bed trying to fall sleep. The last straw was when I was afraid to walk into a Walgreens to get my son medicine one evening.  I decided to find a doctor that could help.

The result: being diagnosed with General Anxiety Disorder(GAD)

The solution: Try two classes of medicine that are used to help treat the disorder: SSRIs and benzodiazepines

So what are they and how do they work? To understand how both classes of medicine work, it is first important to understand how neurons work. Neurons are nerve cells and are used to transmit information throughout the body.  This communication works by one end of a neuron, the axon terminal,  sending electrical and chemical signals to the receiving end of another neuron, the dendrite. For a neuron to send a signal, the sending end of one neuron releases a chemical neurotransmitter into an intracellular gap(space) between the sending and receiving neuron called the synaptic cleft. From here, the chemical can migrate and chemically bind to receptors on the dendrite. The dendrite then reacts in specific ways depending on what receptors have been ‘activated’.  If enough receptors are activated, then the message can continue to be sent to other neurons.  Altering the amount of neurotransmitter available to bind to the receiving neuron, either directly or indirectly, is the basis for how these two types of medicine work.

SSRI – Selective Serotonin Re-uptake Inhibitor

SSRIs are used to treat a variety of symptoms but depression and anxiety are the most common disorders they are prescribed for. It is believed that low levels of serotonin can cause symptoms of depression and anxiety, therefore the goal is to increase these levels being transmitted to the neurons.  SSRIs do not, however, increase the level of serotonin that the body manufacturers. To take the nerve cell discussion from above one step farther, the nerve cell that sends the serotonin into the synaptic cleft also has the ability to reabsorb(re-uptake) excess serotonin that is left in the synaptic cleft that has not bound itself to the the dendrite’s receptor. This is may done for efficiency, allowing the body to conserve resources manufacturing more serotonin when some of it could be reused.  This re-uptake is controlled by a protein called a serotonin transporter. In short, an SSRI blocks this transporter from doing it’s job of getting the serotonin back into the sending(presynaptic) nerve cell. The “selective” part of the acronym comes from the fact that a nerve cell can send and re-uptake other neurotransmitters besides serotonin but SSRIs only block the re-uptake of serotonin. As a result of the nerve cell not being able to re-uptake the serotonin, the serotonin is left in the synaptic cleft  and therefore has the chance to find more binding sites on the dendrite to bind to.  This process, in effect, simulates an increase in serotonin, and as a result may alleviate the anxiety. Some common brands belonging to this group of medicines are Prozac, Celexa, Paxil, and Lexapro, which is what I was prescribed.


This class is also used to treat symptoms such as depression and anxiety but the mechanism of action is different than an SSRI. Benzodiazepines act by slowing down the neurotransmitter   system, acting as a sedative.  As stated in the SSRI discussion, neurons can send and receive more than one chemical to produce different effects on the body. One of these chemical/receptor pairs are the GABA neurotransmitter and the GABAA  receptors, the latter of which are located on the dendrite.  The binding of GABA to GABAA  is what indirectly causes the inhibitory effect. GABAA  receptors also have their own receptors and specifically have a receptor that benzodiazepine molecules can bind to. So, we now have a receptor-on-a-receptor, and when this benzodiazepine receptor becomes bound, it has the effect of making the GABAA  receptors more easily bound to by the GABA neurotransmitter, thus increasing the inhibitory effect on the body.

So, given a choice, which group might you try first? We’ll now look at the benefits and drawbacks that I’ve experienced with both groups.

SSRI – Lexapro

I must say that up until, and for quite some time after my of diagnosis, I was in the mindset that I could  overcome anything that had to do with problems involving my head without the use of medicine. I guess you could say I was ‘mentally macho’.  So when the doctor prescribed Lexapro, one of the most common and recent SSRIs, I wasn’t very receptive to the idea. Most bothersome to me is the fact that with most, if not all SSRIs, you are supposed to take them daily. Not only was I against taking the pill, but I’ve never been good with routines in general. For years I had worked at home and my alarm clock was usually one of my co-workers calling to discuss a job we were working on.  My work hours and daily routine were very inconsistent. This made it difficult to remember to take the pill consistently but for the most part I succeeded for the first few months. The near-term side effects started coming in right away. There are something like 20+ side-effects if you read literature on it, but I will just describe what I personally went through. The first couple weeks were hard to sleep. I would get this anxious, tingling feeling somewhere in my brain at what felt like the brain stem area. It would cause me to move my jaw around a lot like I was expecting it to pop.  In addition, every night when I was just about to fall asleep I’d get shocked awake as if I had a dream that someone smashed a window right near my head. Fortunately both of these problems completely went away after a couple weeks of taking the medicine and never returned. Another common side effect I experienced was having a severely delayed orgasm during intercourse. I was living with my girlfriend at the time and we were regularly intimate. I had the problem fairly consistently while I was taking Lexapro. This was a big source of frustration but I put up with it. While I haven’t experienced it myself, I have known people taking SSRIs that have not been able to have an orgasm at all. This is another common side effect and the few people I have known that have experienced this were women. Not surprisingly, all of them eventually tried other medications for their problems.

Most importantly, Lexapro worked. For months I didn’t have any chest pains or head issues at all when taking it daily. Once in a while I’d forget to take it for a couple days and when I’d remember I’d decide to stop taking it altogether to see if the anxiety would come back. More often than not the symptoms would return after 1-2 months. I’d start taking it again and the symptoms would disappear . I was at least convinced that the medicine was doing what I couldn’t do on my own.

Benzodiazepines – Xanax

After a couple years of taking Lexapro I chose to stop taking it and just deal with the chest and head issues. My reasoning was that I never did actually pass out, have a stroke, or have a heart attack. The more those episodes occurred the more I was able to deal with them because I was convinced I’d be fine in 5 minutes. After that year I started noticing a pattern of pain in my testicles whenever I’d drive to Chicago on business. Once I’d arrive in Chicago at a job site I’d notice my testicular pain would go away but my chest pain became more frequent. I decided to go to a different doctor and explain my symptoms and my history with Lexapro. The doctor prescribed me a low dose of Xanax to take whenever I thought I was going to be put into a situation where an anxiety attack may occur. Before I began my next drive to Chicago I took my prescribed dose and had no pain whatsoever in my testicles the entire trip. Once I got to the job site, not a single chest pain occurred. Once again I was humbled by the power of medicine.

So what are the benefits and drawbacks of Xanax? The benefit for me is being able to take the pill on an as-needed basis. Since I know what situations would potentially cause me to have an anxiety attack I could take a pill to prevent it from happening. That is the main benefit to me.  The cost savings by not taking a pill daily is notable as well. In fact, I’m still using the first Xanax prescription I was given over 2 years ago. The drawbacks are that I still occasionally get unexpected anxiety attacks, usually in the form of chest pain late at night that I wasn’t expecting. It’s tolerable, and ½ my recommended dose usually makes them go away within 10 minutes. The other drawback is that Xanax makes me rather tired due to it’s sedative effects.  It’s not something I’d want to take if I had a job where I drove a lot or had to take it on a daily basis. Lexapro never seemed to have any sedative effects and I also had no problem drinking alcohol with Lexapro even though you’re warned not to. I haven’t been in a situation where I’ve combined alcohol and Xanax but I’ve been told by enough close friends that it is definitely a bad combination. If you’re still with me on the way Xanax works as previously noted,  it may make sense why alcohol and Xanax don’t mix. Alcohol, like Xanax, also binds to the GABA(as well as others) receptor. By combining the two, the sedative effects are amplified. One interesting note is that in the 12 years I’ve dealt with this problem I’ve never had an anxiety attack of any sort after I’ve had a few drinks in my system. I suppose alcohol was doing the job of Xanax in those circumstances. The idea to take away here is that if you’re a frequent drinker then an SSRI may be a better choice for you.



Fundamentals of Anatomy and Physiology, 9E, Chapter 12. Martini / Nath

“Depression (major depression)”



“How Drugs Affect Neurotransmitters – Alcohol”


“How Drugs Affect Neurotransmitters – benzodiazepines”


benzodiazepine Fact Sheet


Written by: Robert Emmons



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