Riley postulates two “loops” of speech, an inner or medial system and an outer or lateral system.9 The lateral system is preserved in stuttering and can be activated through singing, rhythmic speech, etc., but the inner loop, as mediated by the striatum and influenced by dopamine, remains impaired. Once a person who stutters initiates speech, he or she often avoids taking a breath as the whole system must again be jump-started. The low striatal metabolism may be the common-state phenomenon underlying this timing.
DSM-IV diagnostic criteria for stuttering
- Disturbance in normal fluency and time patterning of speech (inappropriate for the individual’s age), characterized by frequent occurrences of one or more of the following:
- Sound and syllable repetitions
- Sound prolongations
- Interjections
- Broken words (e.g., pauses within a word)
- Audible or silent blocking (filled or unfilled pauses in speech)
- Circumlocutions (word substitutions to avoid problematic words)
- Words produced with an excess of physical tension
- Monosyllabic whole-word repetitions (e.g., “I-I-I-I see him”)
- Sound and syllable repetitions
- The disturbance in fluency interferes with academic or occupational achievement or with social communications
- If a speech-motor or sensory deficit is present, the speech difficulties are in excess of those usually associated with these problems.
Coding note: If a speech-motor or sensory deficit or a neurological condition is present, code the condition on Axis III.
The dopamine hypothesis of stuttering
Stuttering is likely related to abnormal elevations of cerebral dopamine activity. Stimulant medications, which increase dopamine activity, have been shown to increase stuttering symptoms.10 As will be reviewed later, dopamine antagonist medications have been shown to improve the symptoms of stuttering. Also, the striatal hypometabolism in stuttering seen in PET imaging may be a result of a hyperdopaminergic state.
To investigate this dopamine hypothesis of stuttering, Wu et al measured presynaptic dopamine levels in individuals who stutter.11 These were found to have 50% to 200% higher levels of dopamine activity than did the controls. Dopamine is inhibitory to striatal metabolism, providing an explanation for the striatal hypometabolism seen in stuttering. Also, risperidone was found to increase striatal metabolism in those whose stuttering improved on this medication.12
Evaluating the patient
One should begin with a comprehensive psychiatric history. Because many patients began stuttering in childhood and have had difficulty dealing with their disorder, other psychiatric disorders such as social phobia may be present. Moreover, other medical etiologies (e.g., stroke) may cause a speech disorder that resembles stuttering.
Stuttering involves abnormalities in fluency as well as tic motions and cognitive avoidances. Inquiries should be made as to the patient’s fluency of speech during work, during introductions, speaking in front of an audience, with family, etc.; the level of stuttering can vary depending on the particular environment.
Stuttering fluency can be rated through an objective scale known as the Riley SSI-3.13 This scale measures the duration of each stuttering event, the percentage of syllables stuttered versus syllables spoken, the severity of associated tic motions, and a global score of the aforementioned components. Because most psychiatrists cannot routinely perform this scale to assess the patient’s progress, it is best to partner with a speech-language pathologist who can also assist the patient through speech therapy.
Nonetheless, you may assess the progress of treatment by relying on your own “ear,” the patient’s own assessment, and the input of a significant other or family member.
In addition to considering DSM-IV criteria, comprehensive treatment should address all aspects of this disorder, including not only the fluency enhancement but improvement in social avoidances and cognitive restructuring. Be aware that stuttering waxes and wanes over time. You should expect to see some “dips” in efficacy during the course of therapy. A longitudinal assessment over several months is needed to determine if the stuttering treatment is efficacious.
What we’ve learned about drug therapy
Many medications have been tried to treat stuttering but few have shown efficacy in well-controlled trials. Most pharmacologic studies did not include a placebo control or employ objective measures of stuttering severity, nor did they provide multiple baseline and treatment measures.
The critical new knowledge is this: Medications that lower dopamine activity have shown replicated efficacy in improving stuttering. The benzodiazepines have been shown to reduce anxiety short-term but have not been shown to improve fluency in stuttering. Limited studies of serotonergic antidepressants suggest a possible role in reducing the social anxiety of stuttering but have not been shown in well-controlled trials to improve stuttering fluency directly.
Multiple studies of haloperidol in the 1970s showed that this medication improved fluency in individuals who stutter. Long-term compliance with this medication, however, was poor given its dysphoric side effects, sexual dysfunction, extrapyramidal concerns, and risks of tardive dyskinesia. Limited research with calcium-channel-blocking medications (e.g., verapamil, nimodipine) showed limited efficacy in stuttering.14,15 Calcium-channel blockers, however, may exert a mild antidopamine effect.