Dysphasia in more detail

Features of dysphasia

Dysphasia can be seen as a disruption in the links between thought and language. The diagnosis is made only after excluding sensory impairment of vision or hearing, perceptual impairment (agnosia), cognitive impairment (memory), impaired movement (apraxia) or thought disturbance as in dementia or schizophrenia. When testing for dysarthria and dysphasia, the patient%u2019s ability to repeat or produce difficult phrases or tongue twisters can be indicative.

People with receptive dysphasia often have language that is fluent with a normal rhythm and articulation but it is meaningless as they fail to comprehend what they are saying.
People with expressive dysphasia are not fluent and have difficulty forming words and sentences. There are grammatical errors and difficulty finding the right word. In severe cases they do not speak spontaneously but they usually understand what is said to them.

Specific types of aphasia are associated with damage to particular cortical regions but in practice distinctions are not always clear. Language is a complex activity involving many cortical and sub-cortical areas and lesions do not dissect clearly demarcated anatomical areas. Generally, expressive dysphasia suggests an anterior lesion while receptive dysphasia suggests a posterior lesion. There are a number of sub types. They are:

* Sensory (Wernicke's) aphasia - lesions are located in the left posterior perisylvian region and primary symptoms are general comprehension deficits, word retrieval deficits and semantic paraphasias. Lesions in this area damage the semantic content of language while leaving the language production function intact. The consequence is a fluent or receptive aphasia in which speech is fluent but lacking in content. Patients lack awareness of their speech difficulties. Semantics is the meaning of words. Semantic paraphrasia is the substitution of a semantically related but incorrect word.
* Production (Broca's) aphasia - lesions are located in the left pre-central areas. This is a non-fluent or expressive aphasia since there are deficits in speech production, prosody and syntactic comprehension. Patients will typically exhibit slow and halting speech but with good semantic content. Comprehension is usually good. Unlike Wernicke%u2019s aphasia, Broca%u2019s patients are aware of their language difficulties. Prosody is the study of the meter of verse. Here it means the rhythm of speech.
* Conduction aphasia - lesions are around the arcuate fasciculus, posterior parietal and temporal regions. Symptoms are naming deficits, inability to repeat non meaningful words and word strings although there is apparently normal speech comprehension and production. Patients are aware of their difficulties.
* Deep dysphasia - lesions are in the temporal lobe especially those mediating phonological processing. Symptoms are word repetition problems and semantic paraphasia (semantically related word substituted when asked to repeat a target word).
* Transcortical sensory aphasia - Lesions are in the junction areas of the temporal, parietal and occipital areas of left hemisphere. Symptoms are impaired comprehension, naming, reading, writing and semantic irrelevancies in speech.
* Transcortical motor aphasia - lesions are located between Broca%u2019s area and supplementary motor area. Symptoms are transient mutism, telegramatic, dysprosodic speech. Telegramatic means omitting unimportant words, as was done when sending a telegram. Dysprosodic speech is monotone.
* Global aphasia - occurs with extensive damage to the left perisylvian region, white matter, basal ganglia and thalamus. Symptoms are extensive and generalised deficits in comprehension, repetition, naming and speech production.