Transcortical sensory aphasia. A case report
1Neurologist in the Xanthi General Hospital
2Psychiatrist in the Xanthi General Hospital
3Pathology Trainee in the Xanthi General Hospital

Transcortical sensory aphasia is characterized by impaired auditory comprehension with fluent speech but poor word content, paraphasia and intact repetition. Good repetition is also present in transcortical motor aphasia in which comprehension is well preserved but speech flow is disturbed. Repetition, the hallmark of transcortical aphasias, is disturbed in Broca’s and Wernicke’s aphasias as well as in conduction aphasia where fluent speech and comprehension are intact. only in subcortical aphasia is repetition well-preserved, characterixed by hypophonia, while fluency and comprehension may vary. Transcortical sensory aphasia does not incur a motor deficit, while transcortical motor aphasia is accompanied by right hemiparesis. Overall, the prognosis of transcortical sensory aphasia is good. The lesion site is syndrome-specific. The lesion is usually located in the language-dominant hemisphere, in the frontal lobe, in the thalamus, the basdal ganglia, in the perfusion area between the middle and posterior cerebral artery, in the perfusion area of the posterior cerebral artery and in the areas surrounding the Sylvian fissure. Aphasia has aslso been reported in a lesion in the non-language dominant hemisphere. The variety in the lesion site is due to the fact that transcortical sensory aphasia can present in a wide spectrum of lesions, with subcategories, in the presence of multiple lesions or even in an unsystematic analysis of aphasic syndromes. The lesion is typically caused by an ischemic infact but also by a haematoma, a tumor, and more rarely by encephalitis or a degenerative disease. We present the case of a right-handed patient who exhibited transcortical sensory aphasia following a recent ischemic infarct to the left parietofrontal lobe. the patient had no motor or sensorial deficit or hemianopia; word fluency with poor content, little paraphasia and intact repetition. He exhibited echolalia, anomia and reading and writing ability. Brain magnetic resonance imaging revealed ischemic microvascular leukoencephalopathy and development of a secondary brain atrophy. The 56-year old patient had a history of poorly-controlled arterial hypertension and sleep apnea. The patient underwent a transcranial and intracranial ultrasound of the carotid arteries, heart echocardiogram and transoesophageal echocardiogram which revealed no vascular stenosis or an obvious cardiac source of embolism. However, a dilatation of the left ventricle and a mild dilatation of the left atrium were established. These findings can be attributed to sleep apnea. Three months later, the patient had still difficulty in finding words, with no paraphasia. The present case of aphasia, which is attributed to a lesion of a slightly different location, reinforces the view that transcortical sensory aphasia could be a symptom of different location, reinforces the view that transcortical sensory aphasia could be a symptom of different lesions or be due to the fact that vascular celebral attacks may include multiple lesions.

Key words: Transcortical, aphasia.