Specific Types of Dysfunction

Many functions of the brain are performed by several areas of the brain working together (networks), not by a single area in the brain. Damage to these networks can cause aphasia, apraxia, agnosia, or amnesia.

Aphasia

Aphasia is a partial or complete loss of the ability to express or understand spoken or written language because of damage to the language areas of the brain.

In most people, part of the left temporal lobe called Wernicke's area and part of the frontal lobe called Broca's area control language function. Damage to any part of these small areas by a stroke, a tumor, a head injury, or an infection interferes with at least some aspect of language function.

Aphasia is loss of the ability to express or understand language, but it takes many forms and may be partial or complete. The variety reflects the complex nature of language function. Aphasia may involve loss of only the ability to comprehend written words (alexia) or the ability to recall or say the names of objects (anomia). Some people with anomia cannot remember the right word at all; others have a word in mind but cannot say it. People with conduction aphasia understand spoken and written words and can speak fluently but cannot repeat words, phrases, or sentences.

People with Wernicke's aphasia, which can result from damage to Wernicke's area, speak fluently, but the sentences come out as garbled, confused strings of words (sometimes referred to as word salad).

People with Broca's aphasia (expressive aphasia), which can result from damage to Broca's area, largely understand the meaning of words and know how they want to respond. However, they have trouble saying the words. Their words are forced out slowly and with great effort, sometimes interrupted by expletives. Usually, writing is affected the same way as speech.

Damage to the left temporal and frontal lobes may cause complete (global) aphasia, making a person almost entirely mute. The person may be able to utter expletives because the right side of the brain, which is more involved in emotions, is not damaged. During recovery, the person has impaired speech (dysphasia), writing (dysgraphia), and understanding of language (receptive aphasia).

Speech therapists can help people who develop aphasia after brain damage due to such disorders as a stroke or head injury (see Section 1, Chapter 7). Treatment is usually started as soon as the person is able to participate.

See the sidebar Testing a Person With Aphasia.

Dysarthria

Dysarthria is loss of the ability to articulate words normally.

Although dysarthria seems to be a language problem, it is really a muscular (motor) problem. It may be caused by damage to the brain stem or to the nerve fibers that connect the cerebral cortex to the brain stem. These parts of the brain control the muscles used to make sounds or to coordinate movements of the lips, tongue, palate, and vocal cords, which are used to produce speech.

People who have dysarthria produce sounds that approximate what they mean and that are in the correct order. Speech may be jerky, staccato, breathy, irregular, imprecise, or monotonous, depending on where the damage is. Because the ability to understand and use language is not usually affected, most people with dysarthria can read and write normally. Speech therapy helps some people with dysarthria (see Section 1, Chapter 7).

Apraxia

Apraxia is loss of the ability to perform tasks that require remembering patterns or sequences of movements.

Apraxia, an uncommon disability, is usually caused by damage to the parietal or frontal lobes. In apraxia, the memory of the sequence of movements needed to complete simple skilled or complex tasks is impaired. For example, buttoning a button, which consists of a series of steps, may be impossible, even though the hands are physically capable of performing the task. People with praxia cannot produce the basic sound units of speech because they cannot initiate, coordinate, or sequence the muscle movements needed to talk.

Some forms of apraxia affect only particular tasks. For example, a person may lose the ability to do any one of the following: draw a picture, write a note, button a jacket, tie a shoelace, pick up a telephone receiver, or play a musical instrument.

Occupational therapy may help some people with apraxia learn to compensate for their losses (see Section 1, Chapter 7).

Agnosia

Agnosia is loss of the ability to associate objects with their usual role or function.

Agnosia is relatively rare. Agnosia is caused by dysfunction in the parietal, temporal, or occipital lobes of the brain, where memories of the uses and importance of familiar objects, sights, and sounds are stored. Agnosia often develops suddenly after a head injury or stroke. When one parietal lobe is damaged (usually the result of a stroke), people have difficulty identifying a familiar object, such as a key or safety pin, that is placed in the hand on the side of the body opposite the damage. However, when they look at the object, they immediately recognize and can identify it. When the occipital lobe is damaged, people have visual agnosia. They cannot recognize familiar faces or common objects, such as a spoon or a pencil, even though they can see these things. When the temporal lobe is damaged, people have auditory agnosia. They cannot recognize sounds even though they can hear sounds. Some people with agnosia improve or recover spontaneously; others must learn to cope with their strange disability. No specific treatment exists.

Amnesia

Amnesia is total or partial loss of the ability to recall experiences or events that happened in the preceding few seconds (immediate memory), in the preceding few seconds to few days (intermediate memory), or further back in time (remote or long-term memory).

The causes of amnesia are only partly understood. Damage to the brain can produce memory loss of events that occurred just before (retrograde amnesia) or just after (posttraumatic amnesia) the damage occurred. Depending on the severity of the damage, most amnesias last for only minutes or hours and disappear without treatment. However, with severe brain damage, amnesia can be permanent.

Learning requires memory. The brain's mechanisms for storing information and recalling it from memory are located primarily in the temporal and frontal lobes. Emotions originating from the brain's limbic system can influence both the storing of memories and their retrieval. The limbic system is also closely connected to areas responsible for alertness and awareness. Because memory involves many interwoven brain functions, virtually any type of brain damage can result in memory loss.

Transient global amnesia is a sudden temporary loss of the ability to store new memories, resulting in forgetfulness and confusion about time, place, and sometimes the identity of other people. This type of amnesia may be caused by temporary blockage of the arteries that supply blood to the temporal lobe in people with atherosclerosis, especially older people. It may also be caused by a seizure originating in the temporal lobe. Often, the cause is unknown. In young adults, migraine headaches, which temporarily reduce blood flow to the brain, may cause transient global amnesia.

Most people with transient global amnesia have only one episode in a lifetime; about 10% have repeated episodes. Episodes can last from 30 minutes to about 12 hours. The amnesia may totally disorient a person and block recall of events that happened during the previous few years. After an episode, the confusion usually clears quickly, and total recovery is the rule.

The Wernicke-Korsakoff syndrome, an unusual form of amnesia, may develop in alcoholics and other malnourished people. The syndrome is a combination of two disorders: an acute confusional state (Wernicke's encephalopathy) and an amnesia (Korsakoff's syndrome). Korsakoff's syndrome accompanies Wernicke's encephalopathy in about 80% of people.

Both Wernicke's encephalopathy and Korsakoff's syndrome can be caused by a deficiency of thiamin (vitamin B₁), which is necessary for the body to process carbohydrates. Drinking large amounts of alcohol without eating foods that contain thiamin decreases the brain's supply of this vitamin. In malnourished people (who do not consume enough thiamin), Wernicke's encephalopathy can be suddenly triggered by eating a large carbohydrate-rich meal (such as spaghetti), drinking highly sweetened liquids, or receiving a large amount of glucose (a sugar) intravenously to treat dehydration.

The Wernicke-Korsakoff syndrome may also result from damage to the temporal lobe by an injury, a stroke, a tumor, or a brain infection (encephalitis).

In addition to confusion, symptoms of Wernicke's encephalopathy include loss of balance, drowsiness, a tendency to stagger, and eye movement problems, such as paralysis of eye movements, double vision, and a rapid movement of the eyes in one direction followed by a slower drift back to the original position (nystagmus). Memory loss is often severe initially.

Korsakoff's syndrome may be permanent if it follows severe or repeated episodes of encephalopathy or of severe symptoms after alcohol withdrawal (delirium tremens). Severe memory loss is often accompanied by agitation and delirium. In Korsakoff's syndrome, immediate memory is retained, but intermediate memory and memory for relatively remote events (of previous weeks or months) are lost. However, more remote memory sometimes survives. People with chronic Korsakoff's syndrome may be able to interact socially and converse coherently even though they cannot remember anything that happened in the preceding few days, months, or years or even in the preceding few minutes. Bewildered by the lack of memory, they tend to make things up (confabulate) rather than admit that they cannot remember. Then they cannot distinguish real memories from the ones they have made up. People with Korsakoff's syndrome are highly suggestible; for example, they can be led to say they see things that are not there. They can read the same magazine over and over as if for the first time.

For alcoholics, thiamin is given intravenously as soon as possible after symptoms begin. Such treatment can correct Wernicke's encephalopathy. Untreated, Wernicke's encephalopathy can be fatal. For this reason, alcoholics who go to the hospital for any reason are promptly given thiamin. Prompt treatment with thiamin also prevents Korsakoff's syndrome, which develops if treatment is delayed. Thiamin does not correct Korsakoff's syndrome but is necessary because Korsakoff's syndrome can be fatal unless treated promptly. Sometimes Wernicke-Korsakoff syndrome gradually resolves if alcohol is avoided and a healthy diet is consumed. However, when Wernicke-Korsakoff syndrome is due to temporal lobe damage, recovery is gradual and may be incomplete.