Wernicke aphasia that is caused by stroke usually improves in time, sometimes to the point where the deficits can be detected only by asking the patient to repeat unfamiliar words, to name unusual objects or parts of objects, to spell difficult words, or to write complex self-generated sentences. A more favorable prognosis attends those forms in which some of the elements, for example, reading, are only slightly impaired from the outset.
As discussed earlier, the term Wernicke area has been applied to the posterior part of area 22 in the most lateral part of the planum temporale. As a rule, in Wernicke aphasia the lesion lies in the posterior perisylvian region (comprising posterosuperior temporal, supramarginal, angular, and posterior insular gyri) and is usually a result of embolic occlusion of the inferior (lower) division of the left middle cerebral artery. A hemorrhage confined to the subcortex of the temporoparietal region or involvement of this area by tumor, abscess, herpes encephalitis, or extension of a small putaminal or thalamic hemorrhage may have similar effects but a better prognosis. Any lesion that involves structures deep to the posterior temporal cortex, including stroke, will cause an associated right homonymous quadrantor hemianopia. Usually, there is no weakness of limbs or face for which reason the fluently aphasic patient may be misdiagnosed as psychotic or confused, especially if there is jargon aphasia. According to Kertesz and Benson, persistence of Wernicke aphasia is related to a lesion that involves both the left supramarginal and angular gyri and therefore, elements of Gerstmann syndrome may be evident.
The posterior perisylvian region, therefore, appears to encompass a variety of language functions, and seemingly minor changes in the size and locale of the lesion are associated with important variations in the elements of Wernicke aphasia or lead to conduction aphasia, pure word blindness, or to pure word deafness (see the following text). The interesting theoretical problem is whether all the deficits observed are indicative of a unitary language function that resides in the posterior perisylvian region or, instead, of a series of separate sensorimotor activities whose anatomic pathways happen to be crowded together in a small region of the brain. In view of the multiple ways in which language is learned and deteriorates in disease, the latter hypothesis seems more likely.
This syndrome is caused by destruction of a large part of the language zone, embracing both Broca and Wernicke areas and much of the territory between them. The cause is usually an occlusion of the proximal left middle cerebral artery, but it may be the result of hemorrhage, tumor, abscess or other lesions, and transiently as a postictal effect. Almost invariably, in cases of global aphasia, there is a degree of right hemiplegia, hemianesthesia, and homonymous hemianopia.
All aspects of speech and language are affected. At most, the patient can say only a few words, usually some cliché or habitual phrase, and can imitate single sounds, or only emit a syllable, such as “ah,” or cry, shout, or moan. Many are initially mute. They may understand a few words and phrases, but, because of rapid fatigue and verbal and motor perseveration—they characteristically fail to carry out a series of simple commands or to name a series of objects. They cannot read or write or repeat what is said to them. The patient may participate in common gestures of greeting, show modesty and avoidance reactions, and engage in self-help activities. With the passage of time, some degree of comprehension of language may return, and the clinical picture that is then most likely to emerge is closest to that of a severe Broca aphasia.
Improvement frequently occurs when the underlying cause is cerebral trauma, compression from edema, ictal or postictal paralysis, or a transient metabolic derangement such as hypoglycemia or hyponatremia, which may also worsen the aphasia of an old lesion that had involved language areas.