The aphasia may be defined as disorders of language secondary to lesions of the brain.. In most cases there is disorder of the output of speech. In the experience of the author aphasia in spoken speech is invariably accompanied by similar abnormalities in writing. Aphasia in spoken language is of two major types: (1). Non-fluent aphasia, in which few words are produced slowly and with great effort, and sounds are incorrectly articulated. Production of grammatical words is relatively more affected so that sentences tend to, be ungrammatical, e.g., “Weather sunny.”
Fluent aphasia, in the more extreme forms of which the patient produces runs of well -articulated speech, which has the rhythm and melody of normal language and a basically normal grammatical structure, but which tends to convey little information , e.g., “I was at the other one and then I was at this one,” a fluent aphasic’s circumlocutory manner of explaining that he was in another hospital previously. The speech of these patients usually contains many incorrect words, called Literal (or phonemic) paraphysis are substitutions of well-articulated but incorrect .sounds, e.g., “spoot” for “spoon,” and verbal paraphasias are incorrect usages of words, e.g., “knife” for “fork,” or “department” for “hospital.”
In differential diagnosis, one must be wary of describing mutism as aphasia, since even
severe aphasia are usually not mute. Causes of mutism are (1) uncooperativeness, (2) psychiatric disorders, e.g., severe depression or schizophrenia,
- widespread disorders of brain, such as trauma, subarachnoid hemorrhage, or metabolic disorders,
- lesions of mesencephalic and pontine tegmentum, an<| (5) bilateral lesions of the cranial nerves serving the speech organs, their nuclei, or their supranuclear pathways.
Dysarthria should not be confused with aphasia. Dysarthric speech is incorrectly articulated, but if transcribed shows correct grammar and word usage. A helpful clue is that if a patient with disorder in speech rights correctly (or produces correct language on a typewriter), he is almost certainly not aphasic.
A common error is to misdiagnose a fluent aphasia as schizophrenic word-salad. Several clues help to make the differential diagnosis. Fluent aphasia is much more common than schizophrenic word-salad. The schizophrenic speech disorder usually develops in chronic “back ward” schizophrenics. By contrast fluent aphasia may come on abruptly as the result of a stroke in a previously well person. Finally fluent aphasia from vascular disease usually occurs in older people, whereas schizophrenia almost always is manifest before the age of 30.
What Is Aphasia:aphasia Syndromes and Their Localizations.
Broca’s aphasia is the result of a lesion of Broca’s area, i.e., the portion of the frontal lobe just anterior to the face, lip, tongue, and mouth area of the motor cortex. This produces a nonfluent aphasia, and writing is also involved. Comprehension of language is intact. There is nearly always a right hemiplegia. Wernicke’s aphasia results from a lesion of Wernicke’s area, the posterior portion of the superior temporal gyrus. The aphasia is typically fluent. Written language is equally impaired. Comprehension of spoken and written language is severely impaired. Repetition of spoken language is poor. There is usually no hemiplegia, and other elementary neurologic signs are usually lacking.
Conduction aphasia results from a lesion of the parietal operculum, i.e., the region lying above the sylvian fissure. There is fluent aphasia involving speech and writing, with severely impaired repetition but intact comprehension. Elementary neurologic signs are usually absent, with the occasional exception of cortical sensory loss on the opposite side. Anomic aphasia is characterized by fluent aphasia in speech and impairment of written language, but with intact comprehension and repetition. The components of the Gerstmann syndrome (discussed subsequently) are often present. In this syndrome the lesion, if focal, is at the region of the parietotemporal junction, but a similar syndrome is produced in nonfocal widespread disease of the brain, such as is caused by metabolic disease or by large tumors with raised intracranial pressure.
These four syndromes are the most common, and although overlapping forms are common, relatively pure forms are not rare. Certain other sjmdromes are much less common.In isolation of the speech area there is a large lesion involving the cortex and underlying white matter in a C-shaped configuration that spares Broca’s area, Wernicke’s area, and their interconnections, but destroys the cortex and underlying white matter that surround the speech region. These patients either may show little spontaneous speech or may have fluent abnormal speech.
The most striking characteristic of this disorder is that despite an almost total lack of comprehension, the patient can repeat well without dysarthria. This lesion is usually the result of anoxia or of carotid insufficiency. Alexia without agraphia is a syndrome in which the patient speaks and writes normally but cannot comprehend written language. The lesion, almost always the result of infarction in the distribution of the left posterior cerebral artery, consists of destruction of the left visual cortex and the splenium, i.e., the posterior portion, of the corpus callosum. In alexia with agraphia the patient can neither write nor comprehend written language, but other language functions are normal.
Other components of the Gerstmann syndrome (see below) may be present. The lesion involves a portion of the left angular gyrus. A right visual field defect may occur if the lesion extends deeply into the white matter but is often absent. Pure word-deafness describes a syndrome in which there is dense incomprehension of language in the presence of intact hearing , although other language functions are intact. Two types of lesion produce this: either a single lesion lying subcortically in the posterior temporal lobe or bilateral lesions of the middle portion of the first temporal gyrus. Pure agraphia is extremely rare. It has been said that the responsible lesion lies in the posterior portion of the second frontal gyrus, but there are few convincing cases.
