To date there have been few reports on dysarthria acquired in childhood, especially studies regarding articulation. The present report focuses on the case of a 5-year-old girl who suffered pseudobulbar palsy after cerebral infarction due to Moya Moya disease at the age of 4 years. She developed severe dysarthria with slight bilateral spastic paresis and right facial paresis. Lesions of bilateral frontal lobes were detected by MRI-CT. Angiography demonstrated the vascular shadow typical of Moya Moya disease in both cerebral hemispheres.
    After cerebral infarction, the subject's intelligence and linguistic ability were impaired and her behavior became restless. She could speak vowels and a few distorted consonants : only ⁄h⁄⁄k⁄⁄g⁄⁄N⁄⁄j⁄. Her articulation was characterized by hypernasality, harsh voice, articulatory inaccuracy of consonants, low vocal pitch slow rate of speech, and prosodic insufficiency, similar to adult cases.
    Analyses of the sound spectrogram and phonolaryngogram of her articulation revealed prolonged duration of each syllable and transfer of consonants to vowels, depression or disappearance of high frequencies over second formants, and abnormal pitch and intensity at beginnings and endings.
    Although she manifested anarthria for two months after onset, her dysarthria has improved qradually during the three years since she started speech therapy.

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     This report bears on the four-year long diachronic observation of a case of acquired palilalia caused by an intracerebral hemorrhage due to head trauma. It was approximately seven months after his trauma that the patient began exhibiting striking palilalia behavior along with echolalia and a global deterioration of mental activities. Palilalia was still present two years later in spite of some degree of general improvement. A particularity of this patient was that palilalia occurred in response to relatively complex questions whereas it was hardly present in response to simpler ones. Contrary to observations made in other cases of palilalia, instrumental sound analyses revealed that articulation speed, although somewhat fast, did not keep increasing as palilalic uterances went on, and that vocal intensity remained within normal ranges, i. e., did not decrease from the onset of a given palilalic utterance to its end. CT-scan and MRI imaging showed the brain lesion to be nearly restricted to the cortex of the right frontal convexity and its underlying white matter. It is suggested that palilalia is, in certain cases, caused by a disturbance of higher motor speech controlmechanisms.

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