Introduction

The following exercise is a case study of a 39-year-old man (‘AB’) who was studied by Grunwell and Huskins (Reference Grunwell and Huskins1979). AB suffered a cerebrovascular accident in December 1972 which resulted in dysarthria and other neurological sequelae. The case study is presented in five sections: primer on acquired dysarthria; client history and clinical presentation; speech evaluation; focus on mixed dysarthria; and assessment issues.

Primer on acquired dysarthria

‘Acquired dysarthria’ is a collective term for a group of motor speech disorders which are caused by damage to the central and/or peripheral nervous systems. Typically, these disorders have their onset in adulthood, although acquired dysarthria may also arise in childhood. The perceptual anomalies that occur in acquired dysarthria reflect impairments in one or more speech production subsystems, namely, articulation, resonation, phonation, respiration and prosody. Acquired dysarthria may minimally disrupt speech intelligibility. Alternatively, the disorder may compromise speech production to such an extent that the client is severely unintelligible and must use an alternative means of communication.

The incidence and prevalence of acquired dysarthria in the general population is largely unknown. To understand the epidemiology of this motor speech disorder, it is necessary to examine its incidence and prevalence in relation to specific clinical populations. Adults who sustain a cerebrovascular accident or stroke are most at risk of acquired dysarthria. Using the Registry of the Canadian Stroke Network's database, Flowers et al. (Reference Flowers, Silver, Fang, Rochon and Martino2013) estimated the incidence of dysarthria in a sample of 221 patients with acute ischaemic stroke to be 42%. Another significant cause of acquired dysarthria in children and adults is traumatic brain injury (TBI). Safaz et al. (Reference Safaz, Alaca, Yasar, Tok and Yilmaz2008) reported the presence of dysarthria in 30.2% of 116 persons with TBI who were followed at a single centre in the five-year period between 2000 and 2006. Aside from stroke and TBI, other neurological disorders associated with acquired dysarthria include multiple sclerosis, Parkinson's disease, and motor neurone disease (also known as amyotrophic lateral sclerosis). The incidence and prevalence of acquired dysarthria in several of these disorders has also been investigated. Danesh-Sani et al. (Reference Danesh-Sani, Rahimdoost, Soltani, Ghiyasi, Haghdoost and Sabzali-Zanjankhah2013) reported the presence of dysarthria in 42.1% of 500 patients aged 11 to 69 years with multiple sclerosis. Perez-Lloret et al. (Reference Perez-Lloret, Nègre-Pagès, Ojero-Senard, Damier, Destée, Tison, Merello and Rascol2012) estimated the prevalence of dysarthria in 419 patients with Parkinson's disease to be 51%.

All aspects of speech production may be compromised in dysarthria. In terms of articu-lation, a speaker with dysarthria may produce weak and distorted consonant and vowel sounds. Problems with resonation may arise on account of mistiming of the closure of the velopharyngeal port. A breathy voice may reflect inadequate glottal valving of the pulmonary airstream during phonation. A speaker with dysarthria may produce short, truncated utterances on account of impaired respiration. In terms of prosody, a speaker with dysarthria may place stress on the wrong syllables within words, and the wrong words within sentences. Each of these speech production difficulties are related to neuromuscular deficits which affect the range, speed, force and timing of movements of the articulators and other organs of speech.

Dysarthria may occur in isolation in clients. However, it is often the case that it is found alongside dysphagia and other neurogenic communication disorders, principally aphasia and apraxia of speech. In their study of 221 clients with acute ischaemic stroke, Flowers et al. (Reference Flowers, Silver, Fang, Rochon and Martino2013) found that the highest co-occurrence of any two impairments was 28% for the presence of dysphagia and dysarthria. Dysarthria in combination with dysphagia and aphasia was present in 10% of these clients. A combination of dysarthria, sialorrhoea (drooling) and dysphagia was present in 136 (33%) of 419 patients with Parkinson's disease examined by Perez-Lloret et al. (Reference Perez-Lloret, Nègre-Pagès, Ojero-Senard, Damier, Destée, Tison, Merello and Rascol2012). These additional disorders are significant in that they can make a differential diagnosis of dysarthria difficult (particularly if apraxia of speech is present), and they provide additional obstacles to the successful rehabilitation of clients.

Client history and clinical presentation

AB is 39 years old. In December 1972, he had a cerebrovascular accident (an intracerebral haematoma). He has a history of hypertension. Following his CVA, he presented with right-sided weakness. He displayed right upper and lower facial weakness, some dysphasia, dysphonia and dysarthria of brainstem origin. AB's wife reported that his speech had been somewhat nasal and difficult to understand prior to his CVA. In January 1974, AB's speech musculature was examined. It was found to be bilaterally affected, with greater impairment on the right. There was spastic weakness of the lips and tongue. The palate was atrophied and foreshortened. The palatal impairment was attributed to flaccid weakness. All articulatory movements, but especially those involving the palate, were impaired. AB was given a speech diagnosis of mixed dysarthria owing to the presence of both bulbar and suprabulbar signs.

Speech evaluation

AB's speech production underwent a comprehensive assessment. The slow movement of the articulators contributed to a general slow speaking rate. There was articulatory imprecision in the production of consonants and vowels which was related to slowness of movement and weakness of articulation. AB frequently failed to reach target positions. This resulted in errors of vowel quality and the use of a fricative stricture in place of a stop. In terms of phonation, AB displayed a breathy voice. The loudness of the voice did not vary. There was also a lack of pitch variation, and the pitch of the voice was abnormally high. AB exhibited audible nasal emission, which was evident on a spectrogram as a high frequency noise trace. Excessive nasal resonance was evident during voiced segments.

The interaction of these deviant features reduced the intelligibility of AB's speech. AB's uneconomical use of air meant that he was only able to speak in short phrases. His slow rate of articulatory movements also contributed to the restricted length of his utterances. The lack of variation in pitch and loudness and poor breath control compromised the use of stress, rhythm and intonation. Breathy voice and excessive nasal resonance limited AB's ability to produce qualitative distinctions between vowels. A reduction in intra-oral air pressure compromised consonant production, particularly plosives and fricatives.

Focus on mixed dysarthria

AB's speech disorder was diagnosed as a mixed flaccid-spastic dysarthria. Individual deviant speech parameters could be attributed to spasticity and/or flaccidity. AB's slow rate of speech and articulatory imprecision could be attributed to spasticity which limits the range, force and speed of articulatory movements. Poor adduction and abduction of the vocal folds, manifested in a breathy voice and audible inspiration, was suggestive of a flaccid condition of the vocal folds. However, an indirect laryngoscopy was not performed and so this impression could not be confirmed. AB's breathiness might also be explained by spasticity. A spastic condition of the vocal folds, manifested in extreme tension of the folds and their reduced elasticity, could also explain AB's problems with high monopitch and monoloudness.

AB's palatal abnormality, which is responsible for his nasal emission and hypernasality, can be attributed to the combined effects of spasticity and flaccidity. The effect of spasticity on the palate is to produce a tendency towards downward movement. Flaccidity makes the palate too weak to counteract this movement. Because a flaccid weakness of the palate tended to predominate in AB, he had an incompetent velopharyngeal sphincter. AB's spasticity was exacerbated by the increased muscular effort needed to counteract the effects of his weak and fatiguing speech musculature. His general body tension rose as he made more effort to speak. As he made more effort to speak, the imbalance created by the asymmetrical nature of his spasticity was also exaggerated. The effect of these factors was heard as increasing inefficiency and weakening of articulations, the loss of control over coordination of breathing and phonation leading to increasing air wastage, and continuous nasal escape related to a breakdown of control over velopharyngeal valving.

Assessment issues

The assessment of AB's speech focused on the functioning of speech production subsystems and the impact of deviant speech parameters on AB's intelligibility. The functioning of physiological mechanisms such as phonation and respiration and the impact of impairment of these mechanisms on speaker intelligibility correspond to the ‘body’ and ‘activity’ levels of the International Classification of Functioning, Disability and Health (ICF; World Health Organization, 2001). Lowit (Reference Lowit and Cummings2014: 400) states that ‘[a]t the body level, the functioning of the various speech subsystems, i.e. respiratory, laryngeal, and velopharyngeal function and oral musculature are investigated. In terms of the activity level, a variety of data elicitation methods are available to assess intelligibility, ranging from evaluations of single words and phrases to reading passages and spontaneous speech.’ The evaluation of these levels typically proceeds by means of published assessment protocols such as the Frenchay Dysarthria Assessment-2 (FDA-2; Enderby and Palmer, Reference Enderby and Palmer2008), which examines speech production under the following 11 sections: reflex; respiration; lips; jaws; palate; larynx; tongue; intelligibility; rate; sensation; and associated factors.

Today, dysarthria assessment is as likely to consider the impact of this speech disorder on an individual's participation in daily activities (the third level of the ICF framework) as it is on a speaker's intelligibility. During an assessment of dysarthria, it is at least as important for clinicians to consider the impact of dysarthria on an individual's self-esteem, quality of life and social participation as it is to assess the effect of respiratory, phonatory and articulatory impairments on a client's intelligibility. The need for assessment of the impact of dysarthria on a client's psychological wellbeing and participation could not be clearer. Piacentini et al. (Reference Piacentini, Mauri, Cattaneo, Gilardone, Montesano and Schindler2014) reported that dysarthria-related quality of life is significantly compromised in patients with multiple sclerosis and dysarthria, while Skolarus et al. (Reference Skolarus, Burke, Brown and Freedman2014) found that dysarthria is a predictor of participation restrictions in stroke survivors. A number of clinical tools have been validated for the purpose of assessing impact and participation, not all of which are designed specifically for clients with dysarthria. (The reader is referred to Lowit (Reference Lowit and Cummings2014) for a list of scales for the assessment of the psychosocial effects of communication disorders.)