Abstract
Objective: To investigate laryngeal function and phonatory disturbance in children with traumatic brain injury (TBI), using both perceptual and instrumental techniques.
Design and participants: The performance of 16 individuals with moderate to severe TBI acquired in childhood and 16 nonneurologically impaired control subjects was compared on a battery of perceptual (Frenchay Dysarthria Assessment, speech sample analysis) and instrumental (Aerophone II, laryngograph) assessments.
Results and conclusions: As a group, the children with TBI demonstrated normal, or only minimally impaired laryngeal function, when compared with the control group, which contrasts with the significant laryngeal impairment noted in adults after TBI. Several reasons for the different findings in relation to laryngeal function in adults and children after TBI are postulated: (1) differing types of injury usually incurred by adults and children may result in a relatively decreased degree of neurologic impairment in these children, (2) differences in recovery potential between adults and children, and (3) the pediatric larynx is still developing, hence it may be better able to compensate for any impairment incurred.
It has been suggested by several authors that impaired phonatory aspects of speech production may affect speech intelligibility.1-3 Inadequate laryngeal control may result in unpredictable phonatory changes leading to sudden breaks in voicing, pitch, and intensity, hence potentially reducing intelligibility. Excess stress for context, and decreased pitch variation may reduce, or create ambiguity, in the information conveyed to listeners. Impaired laryngeal timing can interfere with the articulatory function of the larynx, resulting in a reduced ability to achieve voiced/voiceless contrasts, leading to poor differentiation of voiced cognates (t/d, k/g) and a possible reduction in intelligibility.
Apart from a few case studies,4-7 there is a paucity of research concerning the status of laryngeal function in children after traumatic brain injury (TBI), and the effects of the impairment, if any, on speech intelligibility. Daniel-Whitney5 identified severe laryngeal dysfunction in a severely dysarthric child with TBI, whereas Murdoch and Horton6 and Theodoros and colleagues7 noted moderately impaired laryngeal function in the children they examined. Cahill and colleagues investigated the speech of three children with TBI, and found that two of the three cases demonstrated mild to moderate laryngeal dysfunction.
Laryngeal dysfunction has frequently been reported in the speech of adults after TBI.8-15 However, there are conflicting reports of the most prominent deviant features observed in this population. In their study of the speech of adults with severe closed head injury (CHI), Vogel and von Cramon14 noted that in the early stages of recovery the subjects' voices were mainly breathy, weak, and whispery, but in the later stages of recovery mild signs of spastic dysphonia emerged. Theodoros and colleagues15 identified hoarseness, harshness, and intermittent breathiness as being significantly more apparent in the speech of a group of adults after severe CHI compared with the control group. These authors identified a predominantly hyperfunctional pattern of laryngeal activity in their CHI subjects, which was consistent with the findings of other authors.14,16 Several case study reports of adults after TBI have identified weak, breathy phonation in some subjects,11,12 suggesting hypofunctional laryngeal activity, whereas a strain-strangled vocal quality, suggestive of hyperfunctional laryngeal functioning, has been observed by others.17 Neither Vogel and von Cramon14 nor Theodoros et al.15 identified a significant degree of strain-strangled vocal quality in their CHI subjects.
This variation in laryngeal dysfunction subsequent to TBI is not unexpected, given that the mechanism of brain injury in TBI commonly results in a variety of lesions in the brain. Speech and phonation are complex motor acts involving simultaneous activation and control of many muscles,18 and as such, impairment in laryngeal function may result from damage at various levels of the central nervous system.19 Varying forms of dysphonia (hyperfunctional, hypofunctional, or incoordinated laryngeal function) may result from bilateral damage to the upper motor neurones, lesions in specific lower motor neurones, damage to the extrapyramidal system and its connections, or lesions of the cerebellum and its pathways. In addition, following TBI it is quite possible that multifocal lesions are present within the central or peripheral nervous system, which could result in the presentation of varying types and degrees of dysphonia. Although pure forms of dysphonia may present in isolation after TBI, some individuals may present with mixed forms of phonatory disturbance (e.g., spastic ataxic, flaccid-ataxic) resulting from diffuse or multifocal lesions that may occur in various locations within the nervous system subsequent to TBI.
Because of the dearth of research into the nature and severity of the speech disorder that may result after TBI in childhood there has been a reliance on data from the adult population to describe the laryngeal and phonatory dysfunction that may occur in these children. However, it should not be assumed that the underlying physiologic impairment in laryngeal dysfunction is similar in children and adults. The laryngeal structures undergo marked changes between the ages of 5 and 12 years. These changes include a lowering of the position of the larynx in the neck, an increase in the overall length of the vocal folds, and changes in the ratio of the membranous and cartilaginous portions of the vocal folds.20,21 Therefore, neurologic damage affecting the laryngeal mechanism may result in different outcomes in children and adults, resulting from the pliability of the developing larynx. Additionally, there may be different mechanisms of neurologic damage in children and adults. Consequently, there is a need for greater understanding of the nature of the physiologic functioning of laryngeal mechanism in children with dysarthria subsequent to TBI, so that more satisfactory strategies for the treatment of acquired childhood dysphonia can be developed.
The aim of the present study, therefore, was to investigate laryngeal function and phonatory disturbance in a group of children with TBI, using both perceptual and instrumental techniques.