Stuttering, GABA, and Benzodiazepines

In the last post, we discussed the neurochemistry of the brain and its effect on stuttering. In particular, the neurotransmitter GABA acts as an inhibitor and reduces the effect of the neurotransmitter, dopamine, which has been implicated in stuttering.

In this post, we discuss various drugs that may enhance the action of GABA. There are basically three mechanisms to accomplish this:

      • The amount of GABA in the synapse between two neurons may be enhanced
      • The reuptake of GABA into the presynaptic neuron may be inhibited, thus
         maintaining the level of GABA in the synapse
      • The binding of GABA onto the post-synaptic neuron may be encouraged.

Benzodiazepines (BZs) are drugs that encourage the binding of GABA onto post-synaptic reeptors. The mechanism involved is that BZs themselves bind to BZ receptors on the neuron. BZ and GABA receptors exist together in an interactive complex. In effect, the binding of BZ facilitates the binding of whatever GABA is in the synapse (one of the puzzles of neurology is that there are BZ binding sites on neurons but BZ is not a naturally occurring chemical in the brain). And when GABA binds to a neuron, as shown in the diagram of the previous post, it inhibits the action of dopamine in the motor neuron section of the brain, hence improving fluency. Examples of BZ drugs are Valium, Ativan, and Xanax.

While BZs may reduce the incidence of stuttering through the mechanism cited above, they also have side effects such as the reduction of anxiety and sleep inducing properties. While the former may be beneficial for a stutterer since stuttering is partially a mind problem (see the post on the Mind-Body Problem), the later property is a liability. In addition, with continuous use a dependence and tolerance may be built up for the drug. So BZs should be used selectively and sporadically for situations when the individual expects to be in an anxiety producing situation such as speaking before an audience or engaging in a job interview. In such situations, the effect of the BZ should be to improve fluency and not have much of a sleep inducing effect because of the high initial state of anxiety.

Some stutterers using BZs have also reported that it heightens the level of their articulateness. Thoughts, ideas, and words seem to flow more smoothly. This phenomenon may be explained in two ways. First, greater fluency enables one's speech to keep up with one's thoughts, so there is a closer temporal match between thoughts and speech. Secondly, a study conducted in a nursing home indicated that patients given low dosages of a BZ became more lucid in that they were able to communicate in a more coherent manner. The speculation was that administration of the drug reduces "brain noise." So "brain noise" because of excessive dopaminergic activity may be what stutterers have in the motor neuron section of the brain as well as elsewhere in the brain, which may adversely affect articulateness as well as fluency.

In the next post, we will discuss pagoclone and stuttering.