Background: In clinic, primary progressive aphasia is a dementia syndrome with the only or prominent characteristic of progressive decline in language function. In advanced stage, deficit of cognitive capability and loss of daily living ability would turn up while memory ability would be relatively preserved. The risk factors of primary progressive aphasia might include poor language ability in childhood and speech center involved by brain trauma. Objective: To report the intrac erebral image features of 1 case of primary progressive aphasia so as to disclose the general lesion area of the disease, the changes of intracerebral blood volume and metabolism, and connecting fibers among the language domains. Design: Case-report. Setting: Department of Intervention, Hongqi Hospi tal, Mudanjiang Medical College, Hei Longjiang Province. Participants: 1 case of patien t with primary progressive aphasia, male, 56 years old and with senior high school culture, was in business before the onset of disease. He had "progressive decline in language ability for 3 years" as the main complaint and was diagnosed in Department of Neurology of Beijing Tiantan Hospital on March 20th, 2004. 3 years before that time, the patient could not tell the name of daily living appliances while his comprehensive ability was generally normal. 2 years before, he could still be in business. 1 year before, his language disorder was aggravated, auditory and comprehensive abilities gradually decreased and the changes of character turned up while he could take care of himself and had no obvious degeneration in memory ability. Neural systemic examination: systolic pressure was 130 mmHg and diastolic pressure was 80 mmHg, with clear consciousness, poor language expression ability, and nomenclatural disability while no abnormity was inspected in other neural systematic examinations. He was assessed as sensory aphasia with normal memory and intelligence according to aphasia assessment measuring scale made by the First Hospital of Beijing Medical University. Methods: First, general magnetic resonance examination was taken to fix the lesion area of the patient. Then, functional magnetic resonance was carried out, which mainly included using magnetic resonance spectroscopy analysis to determine the metabolic rates of N-acetyl-aspartic acid, choline and creatine in the lesion area and then compare them with those in the contralateral corresponding area; Magnetic resonance perfusion imaging was carried out to detect regional cerebral blood volume, regional cerebral blood flow, average pass time and peak time of the contrast medium; Fiber-tracking method was used to track corticospinal tract and the amount of connecting fibers between left Broca and Wernicke areas and then compare them with those in the contralateral corresponding area. Main outcome measures: Detection of the metabolic r ates of N-acetyl-aspartic acid, choline and creatine in lesion area and the contralateral area; Detection of regional cerebral blood volume, regional cerebral blood flow, average pass time and peak time of the contrast medium in lesion area and the contralateral area; Comparison of the amount of connecting fibers between left corticospinal tract and left Broca and Wernicke areas. Results: 1 The results of general magnet ic resonance: there was atrophy in left temporal and frontal lobes, especially significant in temporal pole, which was manifested as widening of cerebral sulcuses and fissures, thinness of cortex, and enlargement of frontal and temporal angles. 2 The results of functional magnetic resonance: N-acetyl-aspartic acid, choline and creatine in left temporal lobe and anterior part of frontal lobe decreased more obviously and regional cerebral blood volume and regional cerebral blood flow in these areas decreased, while average pass time and peak time of the contrast medium in these areas slightly increased as compared with those in the contralateral areas; fraction of anisotropy values and the tracked fasciculus in left corticospinal tract decreased, and the connecting fibers between Broca and Wernicke areas also decreased as compared with those in the contralateral area. Conclusion: The lesion area of primary progressive aphasia is mainly located in left temporal and frontal lobes where low perfusion, low metabolic state and decrease of connecting fibers between Broca and Wernicke areas were shown as compared with those in the contralateral area, which might be the pathogenesis of this case of primary progressive aphasia.