Stuttering following acquired brain damage: A review of the literature
Introduction
Despite the fact that adult onset of stuttering behavior in previously fluent speakers has been discussed in the literature for more than 100 years, it remains unclear whether acquired stuttering is a distinct disorder or an epiphenomenon of other motor speech disorders such as apraxia of speech. Furthermore, conclusions regarding the nature of the underlying mechanisms of acquired stuttering remain speculative. A not insignificant factor contributing to the uncertainty surrounding acquired stuttering is the range of neurologic conditions that have been correlated with the syndrome: it has been reported in cases of single lesion strokes (e.g., Helm-Estabrooks, Yeo, Geschwind, Freedman, & Weinstein, 1986), multiple lesion strokes (e.g., Grant et al., 1999, Helm et al., 1978), traumatic brain injury (TBI) (e.g., Helm-Estabrooks and Hotz, 1998, Lebrun et al., 1990, Ludlow et al., 1987), seizure disorder (e.g., Lebrun, 1991, Sechi et al., 2006), Parkinson's syndrome (Canter, 1971, Koller, 1983), dialysis dementia (Rosenbek, McNeil, Lemme, Prescott, & Alfrey, 1978), and senile dementia (Quinn & Andrews, 1977). Additionally, various pharmacological agents have been reported to cause stuttering in individuals with no previous history of the disorder (see Brady, 1998 for review). In most of these cases, normal speech patterns returned after the drug was discontinued. A curious case of transient acquired stuttering in a young man with severe, chronic anorexia nervosa resulting in a significant hypoglycemic state was reported by Byrne, Byrne, & Zibin, 1993. All-in-all, given the many conditions that might give rise to acquired stuttering, one might well ask why it occurs so infrequently that it is deemed a phenomenon worthy of formal report. Indeed, the relatively rarity of acquired stuttering, itself, is in need of explanation.
Equally challenging with regard to acquired stuttering is the characterization of the speech output disorder. Few case reports provide comprehensive descriptions of the speech patterns that are labeled as “stuttering.” An exception is the report by Jokel, De Nil, and Sharpe (2007) who systematically assessed the speech characteristics of 12 individuals with neurogenic stuttering secondary to either TBI or stroke. These investigators assessed their cases in relation to the six principal characteristics of neurogenic stuttering often referred to in the neurogenic stuttering literature (see for example, Helm-Estabrooks, 1999, Ringo and Dietrich, 1995, Rosenbek et al., 1978). These characteristics, which are generally understood as distinguishing acute onset, neurogenic stuttering from developmental stuttering, are as follows.
Six Features of Neurogenic Stuttering
- 1.
Dysfluencies occur on grammatical words at a similar rate of occurrence as substantive words,
- 2.
Repetitions, prolongations, and blocks occur in all positions of words,
- 3.
There is a consistency in stuttering behavior across speech tasks.
- 4.
The speaker does not appear overly anxious about the stuttering behavior,
- 5.
Secondary symptoms such as facial grimacing, fist clenching, and eye blinking are rarely observed,
- 6.
An adaptation effect is not observed,
After examining their 12 cases vis a vis the extent to which their behaviors did or did not conform to these six oft-cited features of acquired neurogenic stuttering, Jokel et al. (2007) concluded that their cases did not comprise a homogeneous group. Van Borsel and Taillieu (2001) presented taped speech samples of acquired and developmental stuttering” to a panel of experienced professionals who regularly treated individuals with fluency disorders. The raters were asked to judge the severity of the dysfluency disorder, decide whether the disorder was consistent with the diagnosis of stuttering, and finally determine whether the disorder was neurogenic or developmental. Raters misidentified individuals with acquired stuttering as having developmental stuttering as often as they correctly identified individuals with developmental stuttering as having that form of dysfluency.
It would appear that sufficient level of uncertainty has been raised about the validity of the “six features of neurogenic stuttering” that they should be collectively regarded as a “rule of thumb” rather than pathognomonic indicators of neurogenic stuttering. In other words, if an individual with a history of a documented neurologic event shows all six behaviors associated with neurogenic, acquired stuttering, then that diagnosis can be made with greater certainty than If the individual does not display all these behaviors.
In this paper we review the literature related to neurogenic stuttering, discuss the complicated task of differential diagnosis and explore possible neuropathological correlates.
Section snippets
Acquired stuttering vis-à-vis aphasia and motor speech disorder
A review of the published cases of acquired neurogenic stuttering shows that many cases can be grouped into two categories, i.e., those whose stuttering was associated with aphasia and those whose stuttering was associated with a motor speech condition. Most of the cases have involved a relatively young group of individuals who developed dysfluent speech following a stroke or traumatic brain injury.
Luchsinger and Arnold (1965) described neurogenic stuttering as being either a core aspect of
Neuropathological correlates of acquired neurogenic stuttering
Arguably, the most complex aspect of acquired neurogenic stuttering is the issue of its neuropathological correlates. A review of case reports with lesion information shows that various areas within the neuraxis have been implicated in this disorder. It would appear that acquired stuttering is not correlated with a lesion in one discrete area of the nervous system. Instead, it appears that lesions causing acquired stuttering have been located in all lobes of the both cerebral hemispheres and
Acknowledgments
The preparation of this chapter was supported by NIH grants P30DC005207, R21DC007165, and R01DC009045. We would like to thank Martin Albert, William Milberg, Lorraine Obler, and Rossie Clark-Cotton for their insightful comments about this case. We thank Ellen McCracken for editorial assistance.
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2020, World NeurosurgeryCitation Excerpt :Head trauma is a known cause of persistent neurogenic stuttering. Additional causes of neurogenic acquired stuttering include strokes, neurodegenerative disorders, and brain neoplasm.5,6,21,22 A case series was conducted of veterans with persistent stuttering for over 15 years from penetrating missile wounds to the head.5
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2019, Journal of Fluency DisordersCitation Excerpt :In this study, based on the symptomatology, three different subgroups of PWNS were found. A concluding hypothesis could be that, because of the co-morbid symptomatology and varying etiology (Lundgren et al., 2010; De Nil et al., 2017; Theys et al., 2011), NS can be “located” in different levels in the hierarchy, as well as in the transfer of information between the lower and higher level loops in the HSFC model, rather than exclusively in any one loop. In typical speakers, 75.5% of clusters and in adults with DS, 75% of the clusters were found to consist of two disfluency units (Bona, 2018; Robb et al., 2009).
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2018, Medical Clinics of North AmericaCitation Excerpt :Acquired stuttering presents later than developmental stuttering, most commonly secondary to neurologic event such as stroke or traumatic brain injury, with a smaller percentage being psychogenic in origin. Acquired stuttering can arise from damage to nearly any part of the brain,36 and most who develop fluency issues as a result of neurologic event also had concomitant speech disorders such as aphasia, dysarthria, or apraxia of speech. Reports of acquired fluency disorders attributed to medication side effect found fluency returned after the medication was discontinued.37