Aphasia

Hillis AE. Aphasia: Progress in the last quarter of a century. Neurology 2007;69: 200-213.

This review article surveys the advances in the field, the value of current research, and what has been learned. Aphasia has grown much more complex than that of the Wernicke's and Broca's types. The paper is careful, that is, it is painstakingly nuanced. There are no broad sweeping proclamations. Localization is approximate. Our understanding of aphasia and, moreover, the localization of language, has grown exceedingly complex. Although in medical school, the Wernicke/Broca, receptive/motor, and fluent/dysfluent divide is stressed, the understanding of aphasia is far beyond these easy categories. Without diving in to deeply, a few of the more concrete points are delivered below.

Broca's aphasia, broadly includes "reduced phrase length, impaired melody and articulatory agility, diminished words per minute, and agrammatic sentence production". The different permutations and number of these independent yet intertwined deficits all arise from compromise of blood flow through the superior division of the left middle cerebral artery. The posterior, inferior frontal gyrus is implicated in deficit studies. Aphasias in the Wernicke's spectrum are associated with disruption of blood flow to the inferior division of the left MCA, which supplies the posterior, superior temporal gyrus.

Transcortical aphasias are characterized by intact repitition. Transcortical motor aphasia shares features of Broca's aphasia but with impaired repetition. Associated lesions occur "just anterior or superior to Broca's area, often caused by occlusion of the ACA or "watershed" areas between the ACA and the MCA." Conversely, transcortical sensory aphasia is caused by "lesions surrounding Wernicke's area, in the watershed territories between the MCA and PCA or the PCA territory. Mixed transcortical aphasia is global aphasia with preserved repetition. This syndrome shows dysfunctional cortex surrounding Broca's and Wernicke's areas, "sometimes known as 'isolation of the speech area'".

Conduction aphasia is characterized by phonemic paraphasias.

Pure alexia is usually caused by two lesions, one to the left occipital cortex caused by compromise of the left PCA, and the other to the splenium of the corpus callosum. The splenium lesion disrupts nerve tracts carrying visual information from the right occipital cortex to the left hemisphere language areas. These same two lesions can effect optic aphasia, in which an object cannot be identified by sight but can be identified through tactile cues.

The latter part of the article distinguishes different aphasias by their disrupted cognitive processes. Anecdotal examples of patients with selective aphasias demonstrate the separation of different cognitive functions, and at the same time, their overlap. Consult the article for this to be explained better than I could at this point.