Sextus Empiricus (about AD 200) is credited1 with being the first person to use the word “aphasia”, albeit in a philosophical sense. Carl Wernicke's studies on aphasia, published from 1874, are among the classics of clinical neurology. However, Benton and Joynt2 suggest that Johann Schmidt in 1677 gave the first account of paraphasia and alexia. They also observed that:

”Almost all the clinical forms of aphasia—complete motor aphasia, paraphasia, jargon aphasia, agraphia and alexia—had been described before 1800. The unawareness of defect which may accompany paraphasia and jargon aphasia had been noted, as well as the coincidence of aphasia and agraphia...”

After the studies of Gall3 in 1807, and Bouillaud, there were many exponents of a dynamic view of aphasia. Finkelnburg (1870) regarded speech disorders as part of a wider disturbance, which he called lack of symbolic representation. Word blindness and word deafness, described by Bastian, were disorders of perception, independent of speech defects.

Critical to Wernicke's concepts was his anatomical demonstration of anarc of cerebral matter, in which lesions would be associated with aphasia.4 He distinguished three varieties5 that still form the broad foundation of modern nosology.

Sensory aphasia, Wernicke attributed to a lesion of the auditory centre, which abolished “sound-images”, and so prevented the patient from understanding words and from recognising his owns defects of speech.

Destruction of the third frontal convolution caused motor (Broca's) aphasia, with loss of the images for articulated speech.

A lesion that destroyed the pathway between the two centres caused conduction aphasia, leading to misuse of words but no defect of understanding. Moreover, a lesion destroying both centres caused loss of understanding both and expression of speech—total aphasia.

The anatomical substrate lay in an arc in the dominant temporal lobe with linked fibres in the left third frontal convolution with central connections (figure). This was known as Wernicke's arc. He recognised that an auditory centre was in the first temporal convolution (Wernicke's area), and the centre for articulated speech in Broca's area.6

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Wernicke's illustration of the arc, 18744

Broca had described: “aphemia . . .the result of a profound, but accurately circumscribed lesion of the posterior third of the second and third frontal convolutions.” Trousseau in 1864 used the word aphasia7 to replace aphemia.

Later Broca distinguished two main speech disorders: aphemia, and verbal amnesia—in which the patient lost the memory not only of spoken but also of written words—corresponding to Wernicke's receptive or sensory aphasia.

Both Dax8 and Broca had shown that loss of speech was caused by damage to the left half of the brain. But more penetrating analysis was left to Hughlings Jackson9 and others, who asked what was meant by loss of speech. He considered the importance of propositional versus emotional speech. The brain's levels of inhibition and disinhibition influenced the language content

The thesis of a precise anatomical localisation as the basis for focal symptoms proved controversial. Freud10 was critical of the “diagram makers”, thus anticipating Head by 30 years. Freud thought that Wernicke's and Lichtheim's classifications corresponded neither to clinical or pathological facts. He recognised purely verbal, asymbolic, and agnostic varieties of aphasia. Goldstein's later studies11 were founded on Jacksonian concepts. Central, or in Wernicke's terminology—conduction aphasias, were seen as disorders of “inner speech”. He regarded nominal aphasia as more than a loss of words, since, he said, it contained abnormal behaviour that any categorical action was disturbed.

Head (1926) also famously scorned the “diagram-makers” represented by Wernicke and others:

”They failed to appreciate that logical formulae of the intellect do not correspond absolutely to physical events, and that the universe does not exist as an exercise for the human mind . . .”

None the less, Wernicke's arc has proved an invaluable guide to clinical localisation of focal lesions affecting language and speech.