A new concept in aphasiology was created when Wernicke (1874/1977) described ten patients with different forms of aphasia, and showed that two of the patients had fluent but paraphasic speech with poor comprehension (i.e., sensory aphasia). At autopsy of another patient, a lesion was found in the left posterior temporal lobe. This type of aphasia has been called by many names, including receptive, impressive, sensory, or more generally fluent aphasia. In most of the current classification systems, this type of syndrome is called Wernicke's aphasia. It affects 15%–25% of all patients with aphasia (Laska et al., 2001).

Although the exact boundaries of Wernicke's area are controversial, the typical lesion associated with Wernicke's aphasia is most often located in the posterior temporal area. The middle and superior temporal lobe posterior to the primary auditory cortex are affected in almost all cases. The primary auditory cortex is also often affected, as are the white matter subjacent to the posterior temporal lobe, the angular gyrus, and the supramarginal gyrus. In rare cases, restricted subcortical lesions may result in Wernicke's aphasia and hemiplegia, the latter being uncommon in cases with cortical lesions. Recent studies have not changed these classical views of the clinico-anatomical relations of initial aphasia.

Patients with Wernicke's aphasia are usually older than patients with Broca's aphasia. However, some rare cases of children with acquired fluent aphasia and a posterior temporal lesion have been described (Paquier and Van Dongen, 1991). Ferro and Madureira (1997) have attributed the age difference between patients with fluent aphasia and those with nonfluent aphasia to the higher prevalence of posterior infarcts in older patients. The most common etiological factor in vascular Wernicke's aphasia is cardiac embolus, which more often affects the temporal area, whereas carotid atherosclerotic infarctions are in most cases located in the frontoparietal area (Harrison and Marshall, 1987; Knepper et al., 1989). Coppens (1991), however, points to a higher mortality rate in older patients with stroke, which might cause a selection bias in studies showing a relationship between age and type of aphasia.

The typical clinical signs of Wernicke's aphasia include poor comprehension of spoken and written language and fluent but paraphasic (phonemic and semantic) speech. In some cases, neologistic jargon may occur. Naming is also severely affected, and phonemic or semantic prompting is of no help. Poor repetition distinguishes Wernicke's aphasia from transcortical sensory aphasia. Writing mirrors the speech output. Handwriting is usually well formed, but the text is without content, and jargonagraphia may occur. Because of posterior lesions, hemiparesis is present in rare cases, but visual field defects are more common. Many patients also show signs of anosognosia, especially during the acute stage of the illness. In most cases, the use of gestural communication or pantomime is affected as well.

Patients not traditionally classified as having aphasia may also show language disturbances resembling Wernicke's aphasia, such as patients with schizophrenia, dementia, or semantic dementia, a fluent form of primary progressive aphasia.

Some authors suggest that Wernicke's aphasia is not a uniform entity but includes many variants. Forms of neologistic, semantic, and phonemic jargon and pure word deafness may all be grouped under Wernicke's aphasia. Pure word deafness is a rare disorder characterized by severe difficulties in speech comprehension and repetition with preservation of other language functions, including the comprehension of nonverbal sounds and music (Kirshner, Webb, and Duncan, 1981). However, when Buchman et al. (1986) reviewed 34 published cases, they were unable to find any really pure cases—that is, cases without any other more generalized perceptual disorders that could be classified as acoustic agnosia or mild language disorders such as paraphasia, naming difficulties, and reading and writing disorders. Most of the patients with “pure” word deafness have had bilateral temporal lesions, but some patients with unilateral left hemisphere lesions have been described (Takahashi et al., 1992).

Personality factors may play a role in the clinical expression of aphasia. In some views, jargon aphasia is not solely a linguistic deficit. Rochford (1974) suggested that a pathological arousal mechanism and lack of control were crucial to jargon aphasia. Weinstein and Lyerly (1976) suggested that jargon aphasia could emanate from abnormal adaptation to the aphasic speech disorder. They found a significant difference in premorbid personality between patients with jargon aphasia and those without jargon aphasia. Most of their patients with jargon aphasia had a strong premorbid tendency to deny illness or openly expressed fear of illness, indicating the importance of anosognosic features in jargon aphasia.

Linguistically, patients with Wernicke's aphasia speak with normal fluency and prosody without articulatory distortions. They often provide long and fluent answers (logorrhoea) to simple questions. In fact, patients with Wernicke's aphasia produce an equal number of words as persons without aphasia in spontaneous speech. However, they show less lexical variety, a high proportion of repetitions, and empty speech (Bates et al., 2001). This may give an impression of grammatically correct speech, but the meaning of the utterances is lost because of a high proportion of paraphasias and neologisms (Lecours and Lhermitte, 1983). This type of speech error is called paragrammatism. Patients with Wernicke's aphasia show morphological errors, but less so than patients with Broca's aphasia (Bates et al., 2001). However, there is some evidence that in highly inflected languages such as Finnish, the number of errors is higher on inflected words than on the lexical stems (Niemi, Koivuselkä-Sallinen, and Laine, 1987). At least in spontaneous speech, distorted sentence structure in utterances of patients with Wernicke's aphasia is related to the lexical-semantic difficulties rather than to morphosyntactic problems (Helasvuo, Klippi, and Laakso, 2001). The same has been found in sentence comprehension. Patients with Wernicke's aphasia performed correctly only on sentences that did not require semantic operations (Pinango and Zurif, 2001). According to these findings, the deficit in phonemic hearing does not explain the nature of comprehension problems in patients with Wernicke's aphasia.

Most patients show skill in pragmatic abilities, such as using gaze direction and other nonverbal actions in conversation. Unawareness of one's own speech errors usually occurs initially in Wernicke's aphasia, but some degree of auditory self-monitoring develops after onset, and patients then begin to use various self-repair strategies to manage conversation (Laakso, 1997). In contrast to self-repair sequences in nonaphasic speakers, these sequences are very lengthy and often unsuccessful.

The initial severity of the aphasia is considered the most important single factor in predicting recovery from aphasia. Wernicke's aphasia is usually tantamount to severe aphasia. In a study by Ross and Wertz (2001), of all patients with aphasia, those with Wernicke's aphasia and global aphasia showed the most severe impairment in language functions and communication. These patients showed only limited recovery when measured at the impairment level by the Boston Diagnostic Aphasia Examination (BDAE) and at the disability level by CADL. In addition to initial severity of aphasia, supramarginal and angular gyri involvements seem to relate to poor recovery in comparison with cases without extension to the posterior superior temporal gyrus (Kertesz, Lau, and Polk, 1993).

Patients who have recovered from Wernicke's aphasia have shown a clear increase in activation in the right perisylvian area, suggesting a functional reorganization of the language with the help of the right hemisphere (Weiller et al., 1995). However, Karbe et al. (1998) reported that increased activity in the right hemisphere was present in patients with poor recovery and reflected the large lesions in the left hemisphere. Patients with good recovery showed increased activation in the left hemisphere surrounding the damaged area.

The classification of aphasia depends strongly on the methods used in the assessment. The major diagnostic tests, such as the BDAE, the Western Aphasia Battery (WAB), or the Aachener Aphasie Test (AAT), have slightly different criteria for classification. For example, whereas the WAB assigns all patients to some aphasia classification, up to 70% of patients examined with the BDAE might be designated as having unclassified aphasia. Another issue that confuses classification is the time after onset at which the evaluation is done. Depending on the sample studied, more than half of patients with aphasia will show evolution to another type of aphasia during the first year after the onset of illness (Ross and Wertz, 2001). Patients with initial Wernicke's aphasia will usually evolve to have a conduction or transcortical type of aphasia, and may evolve further to have anomic aphasia (Pashek and Holland, 1988). On the other hand, the condition of elderly patients with initial global aphasia tends to evolve to Wernicke's aphasia during the recovery period, and the condition of younger patients evolves to Broca's aphasia. This could explain why only one-third of patients with fluent aphasia and lesions in Wernicke's area have a persisting aphasia, and only slightly more than half of patients with chronic Wernicke's aphasia have lesions in Wernicke's area (Dronkers, 2000).