Thirty-second speech samples were studied of at least 30 patients in each of 7 discrete neurologic groups, each patient unequivocally diagnosed as being a representative of his diagnostic group. Three judges independently rated each of these samples on each of 38 dimensions of speech and voice using a 7-point scale of severity.
Computer analysis based on the means of the three ratings on each patient on each dimension yielded results leading to these conclusions: (1) Speech indeed follows neuroanatomy and neurophysiology. There are multiple types or patterns of dysarthria, each mirroring a different kind of abnormality of motor functioning. (2) These patterns of dysarthria can be differentiated; they sound different. They consist of definitive groupings of certain dimensions of speech and voice, deviant to distinctive degrees. (3) Five types of dysarthria were delineated: flaccid dysarthria (in bulbar palsy), spastic dysarthria (in pseudobulbar palsy), ataxic dysarthria (in cerebellar disorders), hypokinetic dysarthria (in parkinsonism), and hyperkinetic dysarthria (in dystonia and chorea). Also, a mixed dysarthria combining elements of flaccid and spastic dysarthrias was identified in amyotrophic lateral sclerosis. (4) Observed occurrence of a single dimension uniquely in a given neurologic disease and distinctive co-occurrence of several dimensions can aid diagnostically in identification of neurologic disorders.
Correlation matrices were used to demonstrate co-occurrence of deviant speech dimensions observed. Application of this technique led to the emergence of eight distinctive clusters of dysfunction. Each of seven neurologic disorders studied had its own unique group or pattern of clusters. However, any one cluster emerged in and was shared by more than one disorder. Inspection of the dimensions present in a cluster permitted giving the cluster a logically determined name based usually on the defective physiology responsible for the cluster. Knowledge of the neuromuscular characteristics of each disorder led to deductions concerning the neuromuscular substrate for each cluster. Intercluster correlations yielded clues concerning co-occurrence of certain neuromuscular defects. Further inspection led to identification of the probable neuromuscular bases of individual deviant speech dimensions. These conclusions may serve as hypotheses for more accurate physiologic and neurophysiologic measurements to further delineate the problems of dysarthria.
To identify behaviors which might distinguish developmental apraxia of speech from “functional” articulation disorders, 30 children with moderate to severe defective articulation but with normal intelligence, hearing, and language abilities and with no apparent organic pathologic condition and a group of matched control subjects were given a battery of speech and nonspeech tests. Pediatric neurologic examinations were completed for the subjects with defective articulation. Speech data were analyzed according to type of articulation error and by a method of distinctive-feature categorization. Highly significant differences were found between control and defective articulation subjects. A rationale was established for division of the defective articulation group on the basis of their performance on isolated volitional oral movement tasks. Combinations of variables that emerged as statistically significant differentiating predictors between these two subgroups of subjects with defective articulation were neurologic ratings, two- and three-feature errors, distortions, prolongations and repetitions, additions, one-place errors, and omissions. These behavioral differences support the conclusion that an identifiable developmental apraxia of speech exists in some children with defective articulation.
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