Prosodic changes in aphasic speech: timing.

Controversy remains about the impairment of prosody in aphasia, particularly with regard to speech timing. This paper addresses this topic through an analysis of timing in four sets of a common morphological paradigm. The paradigm consisted of a basic form (stem) and two longer derived forms (e.g. zip, zipper, zippering). Normally, vowel durations are shorter in longer derived forms (e.g. zippering) than in the stem (e.g. zip), due to a process called 'initial shortening'. Twelve patients with aphasia (four each Broca, Wernicke, and Anomic), and 11 age-matched healthy adults were assessed. Structural (CT) and functional brain imaging (PET) were available for all patients. While all groups showed initial shortening between the stem and the derived forms, the patients with Broca's aphasia presented an inverse pattern between the two derived forms (longer initial vowel in 'zippering' than 'zipper'), and the patients with Wernicke's aphasia produced significantly longer vowel durations overall than the healthy participants. The results are related to radiological information regarding the location of structural and functional brain damage and relative preservation and loss of prosodic features in cerebral damage.

Study on the pathogenic mechanism of Broca's and Wernicke's aphasia.

OBJECTIVE: To study the mechanisms of aphasia by observing cerebral blood flow and metabolism changes in language functional areas of the brain using imaging, in order to develop a language rehabilitation plan for aphasia patients. METHODS: Fifty-eight patients who suffered from Broca's or Wernicke's aphasia secondly to cerebral infarction were evaluated using the Western aphasia battery and Frenchay dysarthria assessment. CT and MRI were obtained to identify the location of lesions, and the language areas were analysed with magnetic resonance spectroscopy (MRS) and perfusion-weighted imaging (PWI). The results were compared with those of the contralateral hemisphere. RESULTS: Of the 58 patients, there were 23 Broca's aphasia patients, 29 Wernicke's aphasia patients and six other aphasia types. We excluded five patients accompanied by dysarthria, six patients with other aphasia types and 14 patients with much more disease lesions. Finally, we analysed the remaining 12 Broca's aphasia and 21 Wernicke's aphasia patients by MRS and PWI. MRS shows that the N-acetylaspartate, choline and creatine of the Broca's or Wernicke's area were reduced than those of the contralateral hemisphere, while PWI results show that the damaged Broca's or Wernicke's areas were in a hypoperfusion state. CONCLUSIONS: Broca's or Wernicke's area of aphasia patients exhibits hypoperfusion and hypometabolism, indicating that they might be the mechanisms of Broca's or Wernicke's aphasia.

Cerebral glucose metabolism in Wernicke's, Broca's, and conduction aphasia.

Cerebral glucose metabolism was evaluated in patients with either Wernicke's (N = 7), Broca's (N = 11), or conduction (N = 10) aphasia using 18F-2-fluoro-2-deoxy-D-glucose with positron emission tomography. The three aphasic syndromes differed in the degree of left-to-right frontal metabolic asymmetry, with Broca's aphasia showing severe asymmetry and Wernicke's aphasia mild-to-moderate metabolic asymmetry, while patients with conduction aphasia were metabolically symmetric. On the other hand, the three syndromes showed the same degree of metabolic decline in the left temporal region. The parietal region appeared to separate conduction aphasia from both Broca's and Wernicke's aphasias. Common aphasic features in the three syndromes appear to be due to common changes in the temporal region, while unique features were associated with frontal and parietal metabolic differences.