The syndromes of developmental dysphasia and their remediation are outlined in the selected proceedings of the Fourth International Child Neurology Congress held in Jerusalem, Israel March 16-20, 1986. Six dysphasic syndromes are identified through the combined psycholinguistic/ aphasiology model: 1) Verbal dyspraxia, 2) phonological production deficit, 3) verbal auditory agnosia, 4) phonologic-syntactic deficit, 5) lexical-syntactic deficit, and 6) semantic pragmatic deficit. In subtypes 1 and 2 impairment is in the expressive system with comprehension relatively intact. Verbal dyspraxia is a severe expressive disorder in which the child is extremely nonfluent and may be mute. Phonological production deficit is characterized by fluency but nonetheless unintelligibility. In both syndromes the production of consonants is more difficult than of vowels. Apraxia of speech and developmental misarticulation are terms sometimes applied to these expressive dysphasias. All dyspraxic dysphasias are difficult to treat and many require speech and language therapy beyond the preschool years. Many need to be introduced to a visual-manual system such as reading and writing at an early age, and some severe cases require formal sign language in conjunction with verbalization. Subtype 3 verbal auditory agnosia, commonly called word deafness, is an inability to decode spoken language at the level of phonology. Despite normal peripheral hearing the individual is unable to derive any meaning from the sounds he or she hears. These children comprehend virtually nothing and are essentially mute. Naming an object, drawing a picture of the object, and naming the picture with a printed label facilitates vocabulary building and the labels can then be used to make requests. Subtype 4 is a mixed receptive expressive deficit and results in telegraphic speech with omission of prepositions, verbs, and the endings on nouns and verbs. The use of gestures, communication boards and written words to supplement oral language are encouraged. In dysphasia subtype 5, lexical syntactic deficit, syntax or the arrangement of words is immature and comprehension of abstract language may be poor. Language is dysfluent with multiple hesitations, false starts and self-corrections. The syndrome is seen in both autistic and nonautistic children. Dysphasia subtype 6, semantic pragmatic deficits with hyperverbal or loquacious speech but their communicative intent and semantic content are limited and superficial. Jargon, neologisms, paraphasias, and circumlocutions are common. Speech is quite rapid and “cluttered”. The subtyping of dysphasic children permits the design of specific interventions for the particular language needs of the children in each group. [1]

COMMENT. These attempts to subtype dysphasic children are helpful in the definition of pathogenesis and brain localization and they allow the development of specific intervention strategies. The neurologic bases of developmental dysphasias are probably multiple. Some syndromes may result from genetic abnormalities in brain development while early focal or multifocal acquired brain pathology may be responsible for others. The differentiation of developmental and acquired aphasias in young children may be difficult and subtle cerebral abnormalities may be uncovered by the MRI in children who have otherwise normal neurologic findings. The authors of this article hypothesize that in the course of providing sound therapeutic intervention at an early age they may be able to enhance brain reorganization through the development of alternative pathways. For example, providing dysphasic children of subtype verbal auditory agnosia with a visual language system may promote a bypass of areas of auditory dysfunction and enable the children to acquire verbal language that would have been inaccessible through the auditory channel alone. Failure to show improvement after intensive remediation may be explained by bilateral brain abnormalities that prohibit reorganization. Autistic children who exhibit severe social attentional and behavioral deficits have the most guarded prognosis.