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Article Excerpt
This study is part of a larger project aimed at exploring the speech, language, cognitive, psychosocial, and medical characteristics of adult neurogenic stuttering. In the present article, speech disfluency patterns in adults with neurogenic stuttering in two diagnostic groups, traumatic brain injury and stroke, were compared. The results revealed that people with neurogenic stuttering do not present as a homogeneous group but that they may present with different speech disfluency characteristics, as well as etiology-dependent self-perceptions. It is anticipated that the observations in the present article ultimately will lead to a greater understanding of the neural mechanisms underlying speech fluency and will result in more effective diagnostic and interventional approaches.
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Neurogenic stuttering is a condition in which previously fluent individuals gradually or suddenly become clinically disfluent after experiencing a head injury (Ardila, Rosselli, Surloff, & Buttermore, 1999), stroke (Grant, Biousse, Cook, & Newman, 1999), or other form of brain damage (Lebrun, Retif, & Kaiser, 1983). Typically, this disorder occurs in adults, but individual case studies of suspected acquired stuttering in young children also have been reported (Nass, Schreter, & Heier, 1994).
It has been reported frequently that the disfluency patterns seen in neurogenic acquired stuttering tend to differ from those typical of developmental stuttering. For instance, while developmental stuttering is characterized by disfluencies that occur primarily on initial sounds or syllables, some have argued that disfluencies in neurogenic stuttering may occur at initial, as well as medial and final positions in the word or syllable (Canter 1971; Lebrun, Leleux, Rousseau, & Devreux, 1983).
Furthermore, neurogenic stuttering has been associated with more diffuse distribution of disfluencies across words of various grammatical classes compared to developmental stuttering as well as a low incidence of secondary behaviors (Canter, 1971; Helm-Estabrooks, 1993; Helm-Estabrooks & Hotz, 1998; Ringo & Dietrich, 1995). In a recent publication, Manning (2001, p. 171) listed six speech features that are useful in differentiating neurogenic from developmental stuttering:
1. Disfluencies occur on functor and content words equally;
2. No anxiety about disfluencies;
3. Stuttered moments are not restricted to initial syllables;
4. Secondary behaviors occur rarely;
5. No adaptation effect; and
6. Disfluencies occur on all speech tasks.
This view of two distinct speech fluency disorders has been challenged by some, who have argued that it may be difficult to differentiate between the two types of stuttering based on verbal output alone (Van Borsel & Taillieu, 2000). In addition, it is apparent that any characterization of neurogenic stuttering based on behavioral characteristics needs to take into consideration the etiology of the neurogenic disorder (Helm-Estabrooks, 1993). Although accurate incidence of neurogenic stuttering is lacking, a number of survey studies (Market, Montague, Buffalo, & Drummond, 1990; Stewart & Rowley, 1996), as well as a review of published case studies and other reports in the literature, suggest that neurogenic stuttering is most frequently observed following the occurrence of stroke or head injury. Therefore, in this article we will focus primarily on neurogenic stuttering following these two neurological conditions.
Neurogenic stuttering following a stroke may occur in isolation (Helm-Estabrooks, Yeo, Geschwind, Freedman, & Weinstein, 1986) or be accompanied by aphasia and/or apraxia of speech (Knopman et al., 1983; Lebrun, Leleux, & Retif, 1987; Mazzucchi, Moretti, Carpeggiani, & Parma, 1981). The clinical manifestation of disfluencies may result from a single lesion (e.g., Grant et al., 1999), or from a number of coexisting lesions (e.g., Thacker & De Nil, 1996). Several brain sites have been implicated, including subcortical regions such as thalamus and brainstem (Abe, Yokoyama, & Yorifuji, 1993; Van Borsel & Taillieu, 2000), basal ganglia (Nass et al., 1994), and cerebellum (Van Borsel & Taillieu, 2000), as well as cortical regions including temporal and parietal lobe (Ardila & Lopez, 1986; Bijleveld, Lebrun, & Van Dongen, 1994; Helm-Estabrooks et al., 1986), supplementary motor area (Van Borsel, Van Lierde, Cauwenberge, Guldermont, & Van Orshoven, 2001), and frontal cortex (Van Borsel & Taillieu, 2000). The relationship between the appearance of neurogenic stuttering and lesion lateralization also has been of some interest to researchers. For instance, Rosenbeck, Messert, Collins, and Wertz, (1978) presented data from seven male neurogenic stuttering patients, six of whom were right-handed, whereas one was left-handed. Five of the patients presented with mostly left frontal and/or temporal lesions (including the left-handed patient), one patient had right parietal involvement, and the remaining patient showed bilateral diffuse lesion localization. In general, the onset of neurogenic stuttering in stroke can be associated with either unilateral (mostly left) or bilateral lesions.
With respect to the type of disfluencies, the patients reported by Rosenbek et al. (1978) demonstrated predominantly sound or syllable repetitions within monosyllabic words (15-65%). Some prolongations (0-47%) and phrase repetitions (0-26%) were also reported. Several other studies reported sound repetition and blocking associated with left-sided strokes alone (Bijleveld et al., 1994; Grant et al., 1999). A male patient with a stroke in the left mesiofrontal cortex with disfluencies on word-initial sounds and fluent on repetition and reading aloud was described by Ackerman, Hertrich, Ziegler, Bitzer, and Bien (1996). Van Borsel and colleagues (2001) reported a similar case of a 69-year-old male but for whom disfluencies were not limited to the initial sounds, but included medial and final sounds.
While neurogenic stuttering often is associated with left lateralized stroke, several reports have documented the occurrence of stuttering following a right hemisphere lesion. Prolongations and repetitions of sounds in a patient with right-sided parietal stroke were reported by Rosenbeck et al. (1978) and by Grant et al. (1999). Word and phrase repetition and, to a lesser degree, sound and syllable repetition after a right-sided stroke were reported by Horner and Massey (1983). Their patient's spontaneous speech was more disfluent compared to tasks involving oral reading or repetition. A patient reported by Rosenbeck et al. on the other hand showed no task-related variations in speech fluency. Fleet and Heilman (1985) described a case of a right-handed woman with a right-sided stroke who stuttered in the absence of aphasia. She had a family history of developmental stuttering (father and brother) but had never stuttered herself until the stroke. Another right-handed male patient with a right-sided stroke who demonstrated disfluencies in all positions and on all grammatical classes was reported by Ardila and Lopez (1986). Their patient presented with phoneme and syllable repetition and, to a lesser extent, word and phrase reiteration. It is evident that acquired stuttering is not limited to left hemisphere lesions but can also be induced by damage to cortical areas in the right hemisphere.
In addition to cortical lesions, several studies have found that acquired stuttering can occur in patients with strokes in subcortical brain regions. Ciabarra, Elkind, Roberts, and Marshall (2000) recently described three stuttering patients with various subcortical lesions. Rapid speech and repetition of every syllable was described in a male patient with lesion in the pontine region. Prolongations of consonants and occasional repetition of initial syllables were described in a female patient with lesion in the left putamen extending to the caudate and corona radiata. The third patient, a female with a small subcortical lesion in the left corona radiata, putamen, and subinsular areas presented with repetition of initial syllables and occasional prolongation of initial sounds. Two earlier studies described two patients with callosal infarction that resulted in initial syllable repetition (Hagiwara, Takeda, Saito, Shimizu, & Bando, 2000; Tsumoto, Nishioka, Nakakita, Hayashi, & Maeshima, 1999). Acquired stuttering has also been reported with lesions to the striatum (Carluer et al., 2000) and the paramedian thalami and midbrain (Abe et al., 1993).
In addition to stroke, neurogenic stuttering also has been reported following head injury. In one of the few studies that also included neuroradiological imaging, Ludlow, Rosenberg, Salazar, Grafman, and Smutok (1987), reported stuttering in 10 veterans with penetrating missile wounds sustained during the Vietnam War. Computed tomography scans of their patients revealed left hemisphere damage in four participants, right hemisphere lesions in five others, and bilateral lesions in the remaining participant. Interestingly, in comparison with a control group of head-injured patients who did not experience speech disfluencies, neurogenic stuttering patients in their study were more likely to show lesions in the corpus callosum and the basal ganglia (caudate and lentiform nuclei). Palilalic speech and dysprosodia were observed in all patients. Although a detailed analysis of speech disfluencies was not provided, Ludlow et al. described their subjects' speech as "shot from a gun, with intermittent and unpredictable bursts of rapid and unintelligible speech, uncontrolled repetitions or prolongations, and long silences without struggle" (p. 62). All patients reportedly had significant deficits on tasks involving motor control, such as rapid hand movements and oral/speech movements.
A somewhat more detailed account of speech characteristics of neurogenic stuttering due to right parietal damage after a missile wound has been provided by Lebrun, Bijleveld, and Rousseau (1990). They presented a case of a 58-year-old man with persistent stuttering whose main disfluencies included long blocks at the beginning of words that lasted several seconds, and were accompanied by secondary behaviors. In addition, initial sound and syllable repetitions and sound prolongations were observed. Generally, function and content words were affected to a comparable degree. The sounds [TEXT NOT REPRODUCIBLE IN ASCII] and [TEXT NOT REPRODUCIBLE IN ASCII] were found to be particularly troublesome.
Very little is known about disfluencies following other types of head injury, such as those resulting from a motor vehicle accident or physical trauma to the head. Helm-Estabrooks and Hotz (1998) presented a case of a 30-year-old woman who sustained a head injury and became disfluent as a result of an automobile accident. The patient's magnetic resonance imaging (MRI) showed a right frontal/parietal lesion. Stuttering was reported as one of the behavioral signs of impaired functioning. However, it was never established whether the disfluencies were the result of the brain damage (neurogenic) or of the stress related to the accident itself (psychogenic).
A single case of a 55-year-old male patient with a head injury associated with a brief loss of consciousness was described by Ardila and colleagues, (1999). Sound and syllable repetitions in this patient corresponded to a mixture of stuttering and palilalia. In addition to speech disfluency, their patient displayed a tendency for word iterations when writing (paligraphia). Four years after his head injury, paligraphia had disappeared but severe palilalia and stuttering persisted, though only...
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