Aphasia is a communication disorder that occurs after language has been developed, usually in adulthood. Not simply a speech disorder, aphasia can affect the ability to comprehend the speech of others, as well as the ability to read and write. In most instances, intelligence per se is not affected.
Aphasia has been known since the time of the ancient Greeks. However, it has been the focus of scientific study only since the mid-nineteenth century. Although aphasia can be caused by a head injury and neurologic conditions, its most common cause is stroke, a disruption of blood flow to the brain, which affects brain metabolism in localized areas of the brain. The onset of aphasia is usually abrupt, and occurs in individuals who have had no previous speech or language problems. Aphasia is at its most severe immediately after the event that causes it. Although its severity commonly diminishes over time through both natural, spontaneous recovery from brain damage and from clinical intervention, individuals who remain aphasic for two or three months after its onset are likely to have some residual aphasia for the rest of their lives. However, positive changes often continue to occur, largely with clinical intervention, for many years. The severity of aphasia is related to a number of factors, including the severity of the condition that brought it about, general overall health, age at onset, and numerous personal characteristics that relate to motivation.
The National Aphasia Association estimates that approximately 25–40% of stroke survivors develop aphasia. There are approximately one million persons in the United States with aphasia, and roughly 100,000 new cases occur each year. There are more people with aphasia than with Parkinson's disease, cerebral palsy, or muscular dystrophy.
Although aphasia occasionally results from damage to subcortical structures such as basal ganglia or the thalamus that has rich interconnections to the cerebral cortex, aphasia is most frequently caused by damage to the cerebral cortex of the brain's left hemisphere. This hemisphere plays a significant role in the processing of language skills. However, in about half of left-handed individuals (and a few right-handed persons), this pattern of dominance for language is reversed, making right-hemisphere damage the cause of aphasia in this small minority. Because the left side of the brain controls movement on the right side of the body (and vice versa), paralysis affecting the side of the body opposite the side of brain damage is a frequent co-existing problem. This condition is called hemiplegia and can affect walking, using one's arm, or both. If the arm used for writing is paralyzed, it poses an additional burden on the diminished writing abilities of some aphasic individuals. If paralysis affects the many muscles involved in speaking, such as the muscles of the tongue, this condition is called dysarthria. Dysarthria often co-occurs with aphasia.
There are a few more problems that can result from the same brain injury that produces aphasia, and complicate its presentation. Most notable among them are the problems collectively called apraxia, which influences one's ability to program movement. Apraxic difficulties make voluntary movements difficult and hard to initiate. Apraxia of speech results in difficulty initiating speech and in making speech sounds consistently. It frequently co-occurs with both dysarthria and aphasia. Finally, sensory problems such as visual field deficits (specifically, hemianopsia) and changes in (or absence of) sensation in arms, legs, and tongue commonly occur with aphasia.
There are neurological disorders other than aphasia that also manifest difficulty with language. This makes it important to note what aphasia is not. Traumatic brain injury and dementias such as Alzheimer's disease are excellent examples. Although brain injury is a cause of aphasia, most head injuries produce widespread brain damage and result in other neuropsychological and cognitive disorders. These disorders often create language that is disturbed in output and form, but are typically the linguistic consequences of cognitive disturbances. In Alzheimer's disease, the situation is much the same. Language spoken by individuals with Alzheimer's reflect their cognitive problems, and, as such, differ from the language retrieval problems typically designated as aphasia. In
short, if the damage that results in language problems is general and produces additional intellectual problems, then aphasia is a correct diagnosis. In the absence of other significant intellectual problems, then the language disorder is probably localized to the brain's language processing areas and is properly termed aphasia.
Finally, aphasia is not conventionally used to refer to the developmental language learning problems encountered by some atypically developing children. However, when children who have been previously developing language normally have a stroke or some other type of localized brain damage, then the aphasia diagnosis is appropriate.
Aphasia manifests different language symptoms and syndromes as a result of where in the language-dominant hemisphere the damage has occurred. The advent of neuroimaging has improved the ability to localize the area of brain damage. Nevertheless, the different general patterns of language strengths and weaknesses, as well as unexpected dissociations in language function, can explain how normal language is processed in the brain, as well as provide insights into intervention for aphasia.
Aphasic individuals almost uniformly have some difficulty in using the substantive words of their native language. Most experts in aphasia recognize that aphasia varies along two major dimensions: auditory comprehension ability and fluency of speech output. In reality, aphasic behaviors vary greatly from individual to individual, and fluctuate in a given individual as a result of fatigue and other factors. In addition, largely in relationship to lesion size, aphasias differ in overall severity.
|
|
Author Info: Audrey L. Holland PhD, The Gale Group Inc., Gale, Detroit, Gale Encyclopedia of Neurological Disorders, 2005 |