López GJS, Erazo TE, Alegría LMA, Calleja CJM

Language: Spanish
References: 15
Page: 127-131
PDF size: 115.17 Kb.

ABSTRACT

Introduction: Aphasia is a disorder of language, where there is alteration in the production and/or understanding of both oral and written language. It can occur in both child and adult population. Presentation of case: A 70 year-old female presented an event of motor aphasia without hemiparesis after a respiratory arrest. An magnetic resonance imaging showed an acute ischemic lesion in the insular cortex bilaterally. A subsequent study showed no infarcted zone. The patient´s deficit subsided after a couple of days. At the present time the patient has no deficit. Discussion: We present data regarding the clinical syndrome of aphasia without hemiparesis and its anatomic an etiologic associations (embolic stroke at the insular cortex). At histologic examination insular zone may have a role on language production. When the insular region suffers a vascular event it generally involves another region that may add neurologic symptoms or data not corresponding to a pure insular affection. This symptoms include dysarthria, ataxia, aphasia that can be global, transcortical motor or conduction type. On the other hand there are chronic degenerative diseases that involve the insula and course with aphasia. There are few reports of hypoxic episodes that are accompanied with transitory neurologic disorders. Most cases describe a transitory global amnesia, although at special circumstances (mountain climbing) aphasia, motor disorders, and apraxia have been observed. Conclusions: We postulate that the transitory aphasia that the patient presented was due to an episode of focal insular ischemia due to an event of cerebral hypoxia. In transient global amnesia due to temporal dysfunction, magnetic resonance imaging studies have been done pondring diffusion, which shows restricted diffusion of the temporal lobes, which correlates with hypoperfusion in emission computed tomography by individual photons. Conclusion: We postulate that the episode of cerebral hypoxia conditioned insular focal ischemia with transient dysfunction expressed as transient aphasia.

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