Of these, 70 individuals were diagnosed with flaccid, mixed flaccid-spastic, ataxic, hypokinetic, or spastic dysarthria and therefore were included in this analysis.
In particular, measurements taken from the superior surface of the tongue revealed stiffness values that were highest for the flaccid and flaccid-spastic dysarthria groups and lowest for the hypokinetic and spastic dysarthria groups.
Orofacial stiffness measures were predicted to be lower than normal in individuals with flaccid, mixed flaccid-spastic, and possibly ataxic dysarthrias and higher than normal in those with hypokinetic and spastic dysarthrias [3,39,51-52].
Specifically, spastic dysarthria, or pseudobulbar palsy, results from bilateral alterations to the upper motor neuron, both to the pyramidal and the extrapyramidal tract.
Traditionally, the differential diagnosis between apraxia of speech and spastic dysarthria is based on perceptual parameters, on aspects of neuroanatomical lesions and on physiological parameters that reflect the movements of speech mechanism.
Three groups of subjects were selected: 4 patients diagnosed with spastic dysarthria (age range: 14-49 years, [bar.
To select participants with spastic dysarthria, the medical criteria used were the location of the lesion and the presence of neuromuscular disorders associated with this pathology.
Specifically, the variables related to the sequencing of articulatory syllabic movements (PTKavr and PTKavp) allow distinguishing between apraxia of speech and spastic dysarthria from normal.
It was expected that this variable would allow distinguishing between spastic dysarthria and normal even if it did not allow distinguishing between apraxia of speech and normal.
In conclusion, the nature of the differences found between the apraxia of speech and spastic dysarthria groups for those variables that best reflect motor planning processes (PTKavr, PTKavp, F2rate) could corroborate the existence of two distinct levels of motor control, planning and programming, as proposed by van der Merwe's (1997) sensorimotor model.