Alleviation of Developmental Stuttering Following Deep Brain Stimulation of the Ventral Intermediate Nucleus of the Thalamus

To the Editor: Stuttering is a disorder of speech fluency characterized by prolongations, repetitions, and blocks. Developmental stuttering has an early onset, and acquired stuttering typically occurs later in life and is often secondary to neurological injury. While the full etiological nature of stuttering is still unclear, a growing body of evidence suggests that the basal ganglia provide internal timing cues to signal the next motor pattern in a sequence and are thus implicated in the dysfunction in stuttering. Further evidence stems from the clinical observation that extrapyramidal movement disorders, such as Parkinson's disease, can exacerbate developmental stuttering or cause acquired stuttering (1). Previous reports describe the use of deep brain stimulation (DBS) to improve acquired stuttering (2). To our knowledge, this is the first report of alleviation of developmental stuttering using DBS.

A 64-year-old woman developed an essential tremor in her right upper extremity at the age of 18 that gradually worsened over decades and was refractory to medical treatment. The patient also had a history of severe developmental stuttering since she was 5 years old that was characterized by significant blocks and prolongations. The combination of developmental stuttering and essential tremor was severe enough to cause impairment of daily functioning, avoidant behavior, and anxiety. The patient received extensive speech therapy in her youth with no improvement of dysfluency. At age 62, a deep brain stimulator was implanted in the left ventral intermediate nucleus of the thalamus to treat her essential tremor. The stereotactic coordinates of the deepest midpoint contact were 11.4 mm left, 4.2 mm posterior, and 0 mm inferior to the anterior commissure-posterior commissure midpoint. The patient experienced complete resolution of her tremor and decreased frequency and duration of her stuttering immediately after DBS. Subsequent adjustment of the stimulation parameters to achieve optimal tremor control maintained this improvement in fluency. The final settings of the device were case positive, lead 2 negative, 2.40 mA, pulse width set at 104 μs, and frequency at 184 Hz.

This direct manipulation lends support to previous reports of the importance of the basal ganglia and other subcortical structures in the mechanism of stuttering. While the ventral intermediate nucleus of the thalamus is not formally part of the basal ganglia, the thalamus receives input from pathways of the basal ganglia for subsequent cortical modulation. Thus, stimulation of the ventral intermediate nucleus of the thalamus may shift the balance of the pathways to alleviate the aberrant timing responsible for developmental stuttering. Because of the limited data regarding DBS on developmental stuttering, further research is necessary to elucidate its potential role as a treatment strategy. Since coexisting essential tremor in stuttering is unique, generalizability to other patients may be limited.