I expected that for the first couple of days I would feel the muscle-twitching anxiety that came when I missed a dose, but it was not so bad, and I had hopes that I might taper off quickly. On the third day, however, I began to find it difficult to focus and was unable to sit at my desk for more than a half-hour at a time. I was agitated, restless and hyperaware of sounds. When I read, sentences seemed to run into one another on the page, and I realized that this was not just because of difficulty focusing my mind but also my eyes. By early evening on that day, I felt so jittery and anxious that I decided I needed more medication. Somewhere, I recalled, a couple of years earlier I stashed a blister pack of 37.5-milligram capsules, a sample my doctor had passed on to me. But where? Although I could have split open a 75-milligram capsule, in my anxious state I became bent on finding those 37.5’s. An hour or more later, after manically scavenging through everything in the apartment, I found them — six remaining in the blister pack. I took one and felt as if I could now go on. I felt relieved to have them. I would stay with my reduced dosage as long as I could, but they would be my backup if I found that I absolutely needed them.

Over the next several days they came in handy, especially at night, when I would wake up feeling dizzy, almost seasick, disoriented and in a heavy sweat, the pillow soaked. One night, awake and not eager to go back to lying restlessly in bed, I went online, typed in “Effexor withdrawal” and found bulletin boards full of pained, plaintive and sometimes angry posters who had quit taking their medication and were suffering a broad but surprisingly consistent range of symptoms: dry mouth, muscle twitching, sleeplessness, fatigue, dizziness, stomach cramps, nightmares, blurred vision, tinnitus, anxiety and, weirdest of all, what were referred to as “brain zaps” or “brain shivers.” While there were those who went off with few or no symptoms at all, others reported taking months to feel physically readjusted. In the face of those symptoms, many despaired, gave up and returned to the drugs.

By the end of the second week, I felt confident that I could continue on 75 milligrams a day. But then my symptoms became more physical: the chills at night and the cold sweats continued. I felt tingling in my shoulders and hands, spasms in my legs. These came and went, seemingly with no reason. And then one night as I lay back to go to sleep, I felt a quick spasm in my head as if an electrical current had suddenly been sent through a circuit somewhere inside my brain. Two more followed in quick succession. With each came a wave of nausea. I sat up. They seemed to disappear. They returned. I realized these were the brain zaps, and over the next few weeks they would come, with no distinguishable pattern, several times a day.

Image Credit... Horacio Salinas for The New York Times

Coping with the ever-changing and seemingly capricious symptoms was beginning to exhaust me. I couldn’t stick to any sleep schedule. I couldn’t think clearly. I was becoming unfocused, agitated and unable to sit long enough to read or work. The stress of anxiety and sleeplessness that I’d almost forgotten seemed to be returning. And that scared me.

Was my depression returning, or could getting off this drug actually cause so many and various symptoms? I spoke with neuroscientists, research psychiatrists and practicing therapists. All of them knew of the difficulties some people had in getting off not only Effexor but other antidepressants as well. They also all agreed that most of these symptoms were caused by a deficiency of serotonin.

What was happening was this: When I started taking Effexor, the drug began inhibiting my brain cells’ process of reabsorbing “excess” serotonin — that is, the serotonin that had gone unused in sending signals across the synapses from one neuron to another. This was the purpose of taking the drug — to increase the amount of serotonin my cells had to work with and therefore, in theory, enable me to cope with my stress and depression. I say “in theory” because even 20 years since the introduction of drugs like these, every researcher with whom I spoke was cautious about presuming a direct relationship between increased serotonin levels in neural synapses and a decrease in depression. First, no one has ever measured the amount of serotonin in the synapses between anyone’s brain cells. No one knows what constitutes a low, high or even standard level. Second, for reasons unknown, only a little better than half the people treated with antidepressants respond to them. Third, studies have shown that placebos have only a slightly lesser rate of effectiveness than the drugs. Fourth, serotonin levels are affected by many things — exercise, light, sleep, diet and even time of day. And finally, serotonin has so much influence on chemistry and functions in so many places in the body and brain relating to mood, sleep, sexual desire, appetite and body temperature that to say that it acts in any one particular way is impossible.