APHASIA

A disorder in the ability to produce or to understand spoken language. It usually results from brain damage caused by an accident, a stroke or invasive surgery; but some accounts include the effects of dementia. Evidence from aphasics provides possible insights into the location of language in the brain, and into the constituent parts of language processing, some of which may be lost by an aphasic and others retained. However, it is dangerous to rely too heavily upon evidence from these atypical subjects. We cannot assume that brain damage has wiped out a given aspect of language processing. Information may have been relocated; or a process may have switched to new (and less efficient) channels than those normally employed.

 Well-established syndromes are associated with damage to the two language-sensitive areas of the brain identified by Broca and Wernicke. It is important to note that the characteristics of each type are merely possible symptoms: the exact effects vary considerably from patient to patient.

Broca’s aphasia is often characterised by agrammatism: an absence of syntactic structure and omission of function words and inflections. Articulation may be poor and speech is generally effortful, with many hesitations. Comprehension appears to be good, but it may be that the patient is using positional, semantic or pragmatic cues to puzzle out meaning, rather than relying upon syntax. Vocabulary is weighted towards concrete nouns, with verbs sometimes under-represented.

 Wernicke’s aphasia is characterised by syntactically complex and well structured speech, containing function words and correct affixation. Speech is apparently effortless, fluent and rapid. Indeed, many of Wernicke’s patients claim not to recognise that they have speech difficulties. But there may be severe problems in retrieving vocabulary, with a reliance on general or inappropriate nouns and verbs. Comprehension may be markedly impaired.

Early accounts of Broca’s aphasia associated it with impaired motor activity which led to difficulty in assembling utterances; while Wernicke’s aphasia was said to reflect impaired access to stored lexical information. However, Broca’s aphasics show signs not just of being unable to use functors appropriately but also of being unable to understand them.

The fact that the symptoms of aphasia vary considerably from patient to patient suggests that the language-sensitive areas of the brain may be differently located in different individuals. Alternatively, particular language functions may be so localised that a great deal depends upon the exact position of the lesion which inflicts the damage. Recent brain imaging data suggests a third possibility: the reason for the vulnerability of the Broca and Wernicke areas is that they constitute a major crossroads for the neural connections which transmit widely distributed linguistic information across the brain.

 Instead of relating type of aphasia to the area of the brain in which damage has occurred, clinicians prefer to analyse symptoms. A first observation might consider the extent to which lexical-semantic processing is impaired, as against grammatical or sentence processing. However, a distinction is still often made between non-fluent aphasia of the Broca type and fluent or expressive aphasia of the Wernicke type.

 Other less-discussed aphasias are:

jargon aphasia, characterised by a large number of nonsense words in the patient’s speech;

conduction aphasia, characterised by an inability to repeat what has just been heard (though comprehension may remain unaffected);

transcortical aphasia, where the best-preserved skill is the ability to repeat words and comprehension is often severely impaired;

anomia, where the main or only symptom is the inability to retrieve words.

Features of these types of aphasia are observed to different degrees in different patients. They suggest that the processing of word form can be separated from the processing of word meaning.

See also: Brain, Brain: localisation, Dementia, Disorder

Further reading: Caplan (1992); Harris and Coltheart (1986); Lesser and Milroy (1993); Obler and Gjerlow (1999)

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