لکنت زبان اکتسابی در یک پسر بچه 16 ساله

This case study describes a 16-year-old boy who started to stutter after a rotavirus infection followed by signs suggestive of a cerebellar encephalitis. It illustrates the fact that acquired stuttering can be observed in younger children and that it may be difficult to distinguish neurogenic from psychogenic forms of acquired stuttering in some cases. This is especially true following a disease that is not commonly associated with acquired stuttering. Speech, language and medical results of our patient are reported in detail. Similarities with previously reported cases and comparisons to (speech) characteristics of psychogenic and neurogenic stuttering will be discussed.

Acquired stuttering is a disorder characterized by stuttering-like disfluencies which appear gradually or suddenly in mostly adult patients who have no previous history of stuttering. It rarely occurs in children (e.g. Nass et al., 1994 and Yeoh et al., 2006) and contrasts with developmental stuttering which normally has its onset between the age of 2 and 6 years (Bloodstein, 1995). Acquired stuttering can be differentiated in a neurogenic and a psychogenic form. Neurogenic stuttering typically occurs in adults following stroke, traumatic brain injury or neurodegenerative disease (De Nil et al., 2008 and Theys et al., 2008). It has also been described following epilepsy (Michel et al., 2004), encephalitis (Chen & Peng, 1993), use of medication (Movsessian, 2005), anorexia (Byrne, Byrne, & Zibin, 1993) and other disorders that might affect brain function. In contrast, psychogenic stuttering most likely appears as a consequence of an emotional or psychological trauma (De Nil et al., 2008) and has been characterized as a conversion reaction (Mahr & Leith, 1992). It often co-occurs with nonorganic somatic complaints, which may raise a suspicion of neurologic disease and thus complicate the differential diagnosis between neurogenic and psychogenic stuttering (Roth, Aronson, & Davis, 1989). In this paper we present the case of a 16-year-old boy who started to stutter following a rotavirus infection, accompanied by signs suggestive of a cerebellar encephalitis. This case illustrates the fact that acquired stuttering can be observed in younger children and that it may be difficult to distinguish neurogenic from psychogenic forms of acquired stuttering in some cases, especially following a disease that is not commonly associated with acquired stuttering.

The current case description represents an atypical patient with acquired stuttering. Not only the age at the onset of the stuttering is unusual, but also reports of stuttering after cerebellar involvement and after encephalitis are infrequent. Although psychological involvement cannot be totally excluded, a neurological explanation of the symptoms seems likely and multiple analogies with previously described case studies are present. We therefore believe that D.'s problems are of neurogenic origin but that the presentation of his problems might have been exacerbated by environmental stressors. As is illustrated by this case, the potential role of the cerebellum in the neural control of speech fluency deserves further study. Previous brain imaging studies (De Nil et al., 2001 and Fox et al., 2000) have highlighted the potential importance of cerebellar involvement in developmental stuttering. This hypothesis is further supported by the current case study which confirms that cerebellar dysfunction also may result in stuttering behavior in older children and adults. This suggests that it may be of interest to investigate the presence of speech disfluencies in persons with ataxic dysarthria and other cerebellar syndromes, and to correlate the presence and severity of stuttering behavior with data from functional and structural cerebellar imaging. Whatever the cause of the acquired stuttering, it is clear from D.'s case as well as from other case reports that intensive speech therapy in these patients may assist in, if not be required for, recovery of speech fluency.