What are aphasia and dysphasia?

Causes and Symptoms

Dysphasias are usually associated with cerebrovascular accident (CVA), or stroke, involving the middle cerebral artery or one of its many branches. Language disorders
may arise, however, from a variety of injuries and diseases: vascular, neoplastic, traumatic, degenerative, metabolic, or infectious.

Dysphasia results from dysfunction in the left cerebral hemisphere, most commonly in the frontotemporal region of the brain and particularly around the insula. Most language disorders are attributable to acute processes that either resolve or cause a chronic residual deficit, while others result from degenerative disorders that cause the dysfunction to be progressive.

Dysphasias have been classified both anatomically and functionally. Other classifications are linguistic and describe the fluency, volume, or quantity of speech. Pure forms of any language dysfunction, however, are very rare. Expressive dysphasias are primarily characterized by expressive deficits, but a verbal comprehension deficit may be present. Receptive dysphasias have expressive deficits. Transcortical dysphasias involve the ability to repeat and to recite. Speech is fluent but with striking paraphrases. The individual is unable to read and write, and comprehension is impaired.

Transcortical dysphasias are caused by hypoxia
(oxygen deficiency) from prolonged hypotension (low blood pressure), carbon monoxide poisoning, or other mechanisms that destroy the border zone between the anterior, middle, and posterior cerebral arteries. Blood supply is marginal in this region. Hypoxia in this area may occasionally isolate the posterior speech areas or all the speech areas from the remainder of the cortex, although both areas remain intact. The sensory and motor speech areas are, therefore, functional, but connections with other sensory or motor areas are impaired. Information from the remaining areas of the cortex cannot be transmitted to be transformed into language.

Aphasias can be classified into Broca’s, Wernicke’s, anomic, or global aphasias. Aphasia reflects damage to one or more of the brain’s primary language centers, which, in most persons, are located in the left hemisphere. Broca’s area lies next to the region of the motor cortex that controls the muscles necessary for speech, and presumably coordinates their movement. Wernicke’s area, which helps control the content of speech and affects its auditory and visual comprehension, lies between Heschl’s gyrus, the primary receiver of auditory stimuli, and the angular gyrus, a “way station” between the auditory and visual regions. Connecting Wernicke’s and Broca’s areas is a large nerve bundle, the arcuate fasciculus, which also helps control the content of speech and enables repetition.

The left hemisphere is dominant for language in all right-handed people and in the majority of left-handed people. When a stroke occurs in the dominant hemisphere, the patient may experience dysphasia or aphasia. Language disorders involve the expression and comprehension of written or spoken words. When the lesion involves Wernicke’s area of the brain, the patient experiences receptive aphasia; neither the sounds of speech nor its meaning can be distinguished, and comprehension of both written and spoken language is impaired. The lesion causing expressive aphasia affects Broca’s area, the motor area for speech. The patient has difficulty speaking and writing. Aphasias may be classified as either nonfluent or fluent. In nonfluent aphasia, the patient speaks very little and produces speech slowly and with obvious effort. In fluent aphasia, the patient may speak, but the phrases have little meaning because of impaired comprehension. Conduction aphasia is a type of
fluent aphasia in which the lesion is in the pathway between Broca’s and Wernicke’s areas. Most aphasias are mixed, with some impairment of both expression and understanding. A massive lesion may result in global aphasia, in which virtually all language function is lost.

Stroke is the most common cause of aphasia. Associated findings usually include decreased level of consciousness, right-sided hemiparesis, and paresthesia. Another communication problem experienced by many stroke patients is dysarthria, or slurred speech. Dysarthria results from a disturbance in muscular control and produces impairment of pronunciation, articulation, and phonation. Dysarthria does not result in any disturbance of language function itself. However, an occasional stroke patient may be unfortunate enough to have both aphasia and dysarthria.

A transient ischemic attack (TIA) can produce any type of aphasia. Usually, the aphasia occurs suddenly and resolves within twenty-four hours of the TIA. Brain abscess may result in any type of aphasia. Usually, the aphasia develops insidiously and may be accompanied by hemiparesis, ataxia, facial weakness, and signs of increased intracranial pressure. A brain tumor may cause anomic aphasia, which may be an early sign of the condition. Encephalitis
(brain inflammation) usually produces transient aphasia. Its earlier signs include fever, headache, and vomiting. Accompanying the aphasia may be convulsions, confusion, stupor or coma, hemiparesis, asymmetrical deep tendon reflexes, positive Babinski’s reflex, ataxia, myoclonus, nystagmus, ocular palsies, and facial weakness. Head trauma may cause any type of aphasia. Typically, aphasia resulting from severe
trauma occurs suddenly and may be transient or permanent, depending on the extent of brain damage. Anomic aphasia may begin insidiously and then progress; associated signs include behavioral changes, memory loss, poor judgment, restlessness, myoclonus, and muscle rigidity. Alzheimer’s disease, a degenerative dementia, may also cause aphasia. Drug abuse, particularly heroin overdose, can cause any type of aphasia.

Depending on its severity, aphasia may impede communication slightly or may make it impossible. Anomic aphasia eventually resolves in more than 50 percent of patients, but global aphasia is irreversible.

In the pediatric population, aphasia is sometimes mistakenly attributed to children who fail to develop normal language skills but who are not considered mentally retarded or developmentally delayed. Aphasia refers solely to loss of previously developed communication skills, however, and should not be used in this context. Brain damage associated with aphasia in children most commonly follows anoxia (oxygen deprivation), the result of near-drowning or airway obstruction.

Treatment and Therapy

If a person suddenly develops aphasia, a physician should be notified immediately. The patient is assessed quickly for signs of increased intracranial pressure, such as papillary changes, decreased level of consciousness, vomiting, seizures, bradycardia (slow heart rate), widening pulse pressure, and irregular respirations. If signs are detected related to increased intracranial pressure, appropriate medications are administered to decrease cerebral edema. Emergency resuscitation equipment may be used to support respiratory and cardiac function, if necessary. Emergency surgery may be indicated.

If the patient does not display signs of increased intracranial pressure, or if the aphasia has developed gradually, then a thorough neurologic
assessment is performed, starting with the patient history. Information may be obtained from the patient’s family or companion because of the patient’s impairment. The staff member assigned to the patient’s care will ask about a history of headaches, hypertension, or seizure disorders, as well as about any drug use. The patient’s ability to communicate and to perform routine activities before the aphasia began is assessed. The patient is checked for obvious signs of neurologic deficit, such as ptosis or fluid leakage from the nose and ears. The patient’s vital signs are taken and level of consciousness assessed. Assessing the level of consciousness is often difficult, however, because the patient’s verbal responses may be unreliable. In addition, dysarthria or speech apraxia (the inability to control voluntarily the muscles of speech) may accompany aphasia. The patient should be allowed ample time to
respond and should be spoken to slowly. Assessment of pupil response, eye movements, and motor function, especially mouth and tongue movement and swallowing, is conducted. To best assess motor function, the care provider will first demonstrate and then have the patient imitate responses, rather than merely providing verbal directions.

Immediately after aphasia develops, the patient may become confused or disoriented. The care provider can help restore a sense of reality by frequently telling the patient what has happened, where he or she is and why, and the date. The patient needs careful explanation of diagnostic tests, such as computed tomography (CT) scans, angiography, and Electroencephalography (EEG). Later, periods of depression are expected as the patient recognizes the handicap. The patient can be aided in attempts at communication through a relaxed, accepting environment with a minimum of distracting stimuli. When speaking to the patient, the staff assigned to care cannot assume that he or she understands. The patient may simply be interpreting subtle clues to meaning, such as social context, facial expressions, and gestures. To help avoid misunderstanding, care providers should speak in simple phrases and use demonstration to clarify verbal directions. Because aphasia is a language disorder, not an emotional or auditory one, a normal tone of voice should be used when speaking to the patient. Necessary aids, such as eyeglasses or dentures, should be provided to facilitate communication. Referrals to speech
pathologists early in the development of the problem will help the patient cope with aphasia.

Aminoff, Michael J., David A. Greenberg, and Roger P. Simon. Clinical Neurology. 7th ed. New York: McGraw-Hill Medical, 2009.

Rowland, Lewis P., ed. Merritt’s Textbook of Neurology. 12th ed. Philadelphia: Lippincott Williams & Wilkins, 2010.

Samuels, Martin A., ed. Manual of Neurologic Therapeutics. 7th ed. New York: Lippincott Williams & Wilkins, 2004.

Victor, Maurice, and Allan H. Ropper. Adams and Victor’s Principles of Neurology. 9th ed. New York: McGraw-Hill, 2009.