Advances in Our Understanding of Adult Neurogenic Stuttering

By Luc De Nil, Ph.D., and Catherine Theys, M.Sc. (Summer 2012)

When we think of stuttering, we normally think of developmental stuttering that has its onset during a child’s early developmental years. However, since the first published case study in the early 1800’s, researchers and clinicians have been aware that stuttering or stuttering-like disfluencies also can occur in persons after they have experienced neurological trauma or disease1. Since then, many patients have been described in the literature documenting how neurogenic (or acquired) stuttering can manifest itself at an adult age. However, little is known about the incidence or prevalence of neurogenic stuttering, and few systematic studies have investigated the characteristics of neurogenic stuttering that are common to these patients. Even fewer have used brain imaging to identify the neural mechanisms underlying the onset of stuttering in adults.

Stroke and traumatic brain injury are the two most commonly reported causes of neurogenic stuttering but it also has been observed as a result of neurodegenerative diseases (e.g., Parkinson Disease), and other conditions such as epilepsy, brain tumors and drug use1. Because most studies on neurogenic stuttering report on single patients, and these may not necessarily represent what is typically seen in neurogenic stuttering, we conducted a multi-facetted study on a large group of patients in an attempt to shed more light on their speech fluency disorder. These studies were done at the University of Leuven in Belgium as part of the doctoral degree completed by the second author.

In an attempt to gain a better understanding of the prevalence of neurogenic stuttering in the clinical setting, we first conducted a survey study of speech-language pathologists who were asked to respond to a series of questions on the occurrence and characteristics of neurogenic stuttering in their patients2. Information was obtained on 58 patients with neurogenic stuttering following various neurological disorders, most often stroke. The findings indicated that neurogenic stuttering is not an uncommon disorder and, indeed, that many clinicians had worked with such patients. Furthermore, the data suggested that patients with neurogenic stuttering are not a homogeneous group but may differ in terms of lesion site and speech characteristics in part based on the underlying neurological disease.

In a second phase of the project, a systematic, prospective study on stroke-induced stuttering was completed. This study was limited to stroke patients because they constitute the largest etiological group among patients with neurogenic stuttering. It consisted of three consecutive parts. First, data on the incidence and prevalence were obtained by repeatedly screening 319 stroke patients for speech dysfluencies in the first year following their stroke3. If screening indicated potential stuttering, a more extensive test battery was administered. As a result, 17 of the 319 patients were diagnosed with neurogenic stuttering, resulting in a 5.3% incidence among stroke patients. The stuttering persisted in at least 2.5% of these patients for more than six months following the stroke. In a second part of the study, the behavioral speech characteristics and the co-occurring speech and language disorders associated with neurogenic stuttering were investigated4. Aphasia and dysarthria were diagnosed as frequently co-occurring communication disorders, while apraxia was diagnosed much less frequently. While patients with co-occurring aphasia presented with a significantly higher frequency of stuttering, dysarthria or cognitive problems did not lead to more severe stuttering.

In a final part of the study, we investigated the localization of brain lesions that were most likely associated with the diagnosis of neurogenic stuttering in stroke4. This was done by comparing the brain lesions of 20 patients with stroke-induced stuttering to those of 17 stroke patients without stuttering. We showed that 9 left-hemisphere areas were significantly associated with the presence of neurogenic stuttering. These areas were largely overlapping with the cortico-basal ganglia-cortical network comprising the inferior frontal cortex, superior temporal cortex, intraparietal cortex, basal ganglia and their white matter interconnections through the superior longitudinal fasciculus and internal capsule. Our results showed that stroke-induced neurogenic stuttering is not associated with neural dysfunction in one particular brain area but may occur following one or more lesions throughout the cortico-basal ganglia-cortical network, and that neurogenic stuttering in stroke patients likely results from disintegration in a neural network necessary for fluent speech, not unlike that observed in developmental stuttering.

As a result of our studies on neurogenic stuttering, we now have a better understanding of the incidence and prevalence of neurogenic stuttering, the stuttering characteristics associated with this condition, as well as the influence of co-occurring disorders. Most importantly, we have started to investigate the neural correlates associated with neurogenic stuttering following stroke. Many questions still remain and need further systematic studies in this and other patient populations. Finally, it is important that we expand these studies to investigate issues of differential diagnosis with co-occurring speech and language deficiencies (e.g., word-finding problems), and to provide clinical treatment guidelines for optimal management of neurogenic stuttering. Luc De Nil, Ph.D., is a professor at the University of Toronto and a visiting professor at the University of Leuven. Catherine Theys, M.Sc., is a doctoral candidate at the University of Leuven.

REFERENCES

1 De Nil, L.F., Rochon, E., Jokel, R. Adult-onset neurogenic stuttering. In: McNeil MR, ed. Clinical management of sensorimotor speech disorders, 2 ed. New York: Thieme, 2009:235-248. 2 Theys, C., van Wieringen, A., De Nil, L.F. (2008). A clinician survey of speech and non-speech characteristics of neurogenic stuttering. Journal of Fluency Disorders. Mar;33:1-23. 3 Theys, C., van Wieringen, A., Sunaert, S., Thijs, V., De Nil, L.F. (2011). A one year prospective study of neurogenic stuttering following stroke: incidence and co-occurring disorders. Journal of Communication Disorders;44:678-687. 4 Theys, C., De Nil, L.F., Thijs, V., van Wieringen, A., Sunaert, S. (in press) A crucial role for the cortico-striato-cortical loop in the pathogenesis of stroke-related neurogenic stuttering. Human Brain Mapping.