| Aphasia | |
|---|---|
| Classification and external resources | |
| ICD-10 | F80.0-F80.2, R47.0 |
| ICD-9 | 315.31, 784.3, 438.11 |
| DiseasesDB | 4024 |
| MedlinePlus | 003204 |
| eMedicine | neuro/437 |
| MeSH | D001037 |
| Dysphasia | |
|---|---|
| Classification and external resources | |
| ICD-10 | F80.1, F80.2, R47.0 |
| ICD-9 | 438.12, 784.5 |
Aphasia ( /əˈfeɪʒə/ or /əˈfeɪziə/, from Greek ἀφασία, "speechlessness"[1]) is an impairment of language ability. This class of language disorder ranges from having difficulty remembering words to being completely unable to speak, read, or write.
Aphasia disorders usually develop quickly as a result of head injury or stroke, but can develop slowly from a brain tumor, infection, or dementia, or can be a learning disability such as dysnomia.[2]
The area and extent of brain damage determine the type of aphasia and its symptoms. Aphasia types include Broca's aphasia, non-fluent aphasia, motor aphasia, expressive aphasia, receptive aphasia, global aphasia and many others (see Category:Aphasias).
Medical evaluations for the disorder range from clinical screenings by a neurologist to extensive tests by a language pathologist. [2]
Most aphasia patients can recover some or most skills by working with a speech and language therapist. This rehabilitation can take two or more years and is most effective when begun quickly. Only a small minority will recover without therapy, such as those suffering a mini-stroke. Patients with a learning-disorder aphasia such as dysnomia can learn coping skills, but cannot recover abilities that are congenitally limited.[3]
Improvement varies widely, depending on the aphasia's cause, type, and severity. Recovery also depends on the patient's age, health, motivation, handedness, and educational level. [2]
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Classifying the different subtypes of aphasia is difficult and has led to disagreements among experts. The localizationist model is the original model, but modern anatomical techniques and analyses have shown that precise connections between brain regions and symptom classification don't exist. The neural organization of language is complicated; language is a comprehensive and complex behavior and it makes sense that it isn't the product of some small, circumscribed region of the brain.
No classification of patients in subtypes and groups of subtypes is adequate. Only about 60% of patients will fit in a classification scheme such as fluent/nonfluent/pure aphasias. There is a huge variation among patients with the same diagnosis, and aphasias can be highly selective. For instance, patients with naming deficits (anomic aphasia) might show an inability only for naming buildings, or people, or colors.[4]
The localizationist model attempts to classify the aphasia by major characteristics and then link these to areas of the brain in which the damage has been caused. The initial two categories here were devised by early neurologists working in the field, namely Paul Broca and Carl Wernicke. Other researchers have added to the model, resulting in it often being referred to as the "Boston-Neoclassical Model". The most prominent writers on this topic have been Harold Goodglass and Edith Kaplan.
Aphasia can also be classified as
Receptive aphasias can be subdivided into
A - pure word deafness (patient can hear but not understand words)
B - alexia (patient can read but not understand words)
C - visual asymbolia (written words are disorganized and can not be recognized).
Intermediate - also called nominal amnestic aphasia.
Expressive aphasia also known as Broca's aphasia or cortical motor aphasia (patient has difficulty in putting his thoughts into words)
The different types of aphasia can be divided into three categories: fluent, non-fluent and "pure" aphasias.[6]
Aphasia can be divided into primary and secondary aphasia.
Isolation aphasia is a type of disturbance in language skill that causes the inability to comprehend what is being said to you or the difficulty in creating speech with meaning without affecting the ability to recite what has been said and to acquire newly presented words. This type of aphasia is caused by brain damage that isolates the parts of the brain from other parts of the brain that are in charge of speech. [7]
The cognitive neuropsychological model builds on cognitive neuropsychology. It assumes that language processing can be broken down into a number of modules, each of which has a specific function. [8] Hence there is a module which recognises phonemes as they are spoken and a module which stores formulated phonemes before they are spoken. Use of this model clinically involves conducting a battery of assessments (usually from the PALPA, the "psycholinguistic assessment of language processing in adult acquired aphasia ... that can be tailored to the investigation of an individual patient's impaired and intact abilities" http://www.psypress.com/palpa-9780863771668, last visited 1/21/2011), each of which tests one or a number of these modules. Once a diagnosis is reached as to where the impairment lies, therapy can proceed to treat the individual module.
Acquired childhood aphasia (ACA) is a language impairment resulting from some kind of brain damage. This brain damage can have different causes, such as head trauma, tumors, cerebrovascular accidents, or seizure disorders. Most, but not all authors state that ACA is preceded by a period of normal language development.[9] Age of onset is usually defined as from infancy until but not including adolescence.
ACA should be distinguished from developmental aphasia or developmental dysphasia, which is a primary delay or failure in language acquisition.[10] An important difference between ACA and developmental childhood aphasia is that in the latter there is no apparent neurological basis for the language deficit.[11]
ACA is one of the more rare language problems in children and is notable because of its contribution to theories on language and the brain.[10] Because there are so few children with ACA, not much is known about what types of linguistic problems these children have. However, many authors report a marked decrease in the use of all expressive language. Children can just stop talking for a period of weeks or even years, and when they start to talk again, they need a lot of encouragement. Problems with language comprehension are less common in ACA, and don't last as long.[12]
People with aphasia may experience any of the following behaviors due to an acquired brain injury, although some of these symptoms may be due to related or concomitant problems such as dysarthria or apraxia and not primarily due to aphasia.
The following table summarizes some major characteristics of different types of aphasia:
| Type of aphasia | Repetition | Naming | Auditory comprehension | Fluency | Presentation |
|---|---|---|---|---|---|
| Wernicke's aphasia | mild–mod | mild–severe | defective | fluent paraphasic | Individuals with Wernicke's aphasia may speak in long sentences that have no meaning, add unnecessary words, and even create new "words" (neologisms). For example, someone with Wernicke's aphasia may say, "You know that smoodle pinkered and that I want to get him round and take care of him like you want before", meaning "The dog needs to go out so I will take him for a walk". They have poor auditory and reading comprehension, and fluent, but nonsensical, oral and written expression. Individuals with Wernicke's aphasia usually have great difficulty understanding the speech of both themselves and others and are therefore often unaware of their mistakes. |
| Transcortical sensory aphasia | good | mod–severe | poor | fluent | Similar deficits as in Wernicke's aphasia, but repetition ability remains intact. |
| Conduction aphasia | poor | poor | relatively good | fluent | Conduction aphasia is caused by deficits in the connections between the speech-comprehension and speech-production areas. This might be caused by damage to the arcuate fasciculus, the structure that transmits information between Wernicke's area and Broca's area. Similar symptoms, however, can be present after damage to the insula or to the auditory cortex. Auditory comprehension is near normal, and oral expression is fluent with occasional paraphasic errors. Repetition ability is poor. |
| Nominal or Anomic aphasia | mild | mod–severe | mild | fluent | Anomic aphasia is essentially a difficulty with naming. The patient may have difficulties naming certain words, linked by their grammatical type (e.g. difficulty naming verbs and not nouns) or by their semantic category (e.g. difficulty naming words relating to photography but nothing else) or a more general naming difficulty. Patients tend to produce grammatic, yet empty, speech. Auditory comprehension tends to be preserved. |
| Broca's aphasia | mod–severe | mod–severe | mild difficulty | non-fluent, effortful, slow | Individuals with Broca's aphasia frequently speak short, meaningful phrases that are produced with great effort. Broca's aphasia is thus characterized as a nonfluent aphasia. Affected people often omit small words such as "is", "and", and "the". For example, a person with Broca's aphasia may say, "Walk dog" which could mean "I will take the dog for a walk", "You take the dog for a walk" or even "The dog walked out of the yard". Individuals with Broca's aphasia are able to understand the speech of others to varying degrees. Because of this, they are often aware of their difficulties and can become easily frustrated by their speaking problems. It is associated with right hemiparesis, meaning that there can be paralysis of the patient's right face and arm. |
| Transcortical motor aphasia | good | mild–severe | mild | non-fluent | Similar deficits as Broca's aphasia, except repetition ability remains intact. Auditory comprehension is generally fine for simple conversations, but declines rapidly for more complex conversations. It is associated with right hemiparesis, meaning that there can be paralysis of the patient's right face and arm. |
| Global aphasia | poor | poor | poor | non-fluent | Individuals with global aphasia have severe communication difficulties and will be extremely limited in their ability to speak or comprehend language. They may be totally nonverbal, and/or only use facial expressions and gestures to communicate. It is associated with right hemiparesis, meaning that there can be paralysis of the patient's right face and arm. |
| Mixed transcortical aphasia | moderate | poor | poor | non-fluent | Similar deficits as in global aphasia, but repetition ability remains intact. |
| Subcortical aphasias | Characteristics and symptoms depend upon the site and size of subcortical lesion. Possible sites of lesions include the thalamus, internal capsule, and basal ganglia. |
Jargon aphasia is a fluent or receptive aphasia in which the patient's speech is incomprehensible, but appears to make sense to them. Speech is fluent and effortless with intact syntax and grammar, but the patient has problems with the selection of nouns. They will either replace the desired word with another that sounds or looks like the original one, or has some other connection, or they will replace it with sounds. Accordingly, patients with jargon aphasia often use neologisms, and may perseverate if they try to replace the words they can't find with sounds.
Commonly, substitutions involve picking another (actual) word starting with the same sound (e.g. clocktower - colander), picking another semantically related to the first (e.g. letter - scroll), or picking one phonetically similar to the intended one (e.g. lane - late).
Research on understanding the nature, causes and treatment of aphasia is typically categorized into different components of language including phonological processing, lexical-semantic processing, syntactic processing, orthographic processing. There are two associations dedicated to the study of aphasia, the Academy of Aphasia and Clinical Aphasiology.
Aphasia usually results from lesions to the language-relevant areas of the frontal, temporal and parietal lobes of the brain, such as Broca's area, Wernicke's area, and the neural pathways between them. These areas are almost always located in the left hemisphere, and in most people this is where the ability to produce and comprehend language is found. However, in a very small number of people, language ability is found in the right hemisphere. In either case, damage to these language areas can be caused by a stroke, traumatic brain injury, or other brain injury. Aphasia may also develop slowly, as in the case of a brain tumor or progressive neurological disease, e.g., Alzheimer's or Parkinson's disease. It may also be caused by a sudden hemorrhagic event within the brain. Certain chronic neurological disorders, such as epilepsy or migraine, can also include transient aphasia as a prodromal or episodic symptom. Aphasia is also listed as a rare side effect of the fentanyl patch, an opioid used to control chronic pain.[13]
There is no one treatment proven to be effective for all types of aphasias. The reason that there is no universal treatment for aphasia is because of the nature of the disorder and the various ways it is presented, as explained in the above sections. Aphasia is rarely exhibited identically, implying that treatment needs to be catered specifically to the individual. Studies have shown that although there isn't consistency on treatment methodology in literature, there is a strong indication that treatment in general has positive outcomes[14].
A multi-disciplinary team, including doctors (often a physician is involved, but more likely a clinical neuropsychologist will head the treatment team), physiotherapist, occupational therapist, speech-language pathologist, and social worker, works together in treating aphasia. For the most part, treatment relies heavily on repetition and aims to address language performance by working on task-specific skills. The primary goal is to help the individual and those closest to them adjust to changes and limitations in communication[14].
Treatment techniques mostly fall under two approaches:
Several treatment techniques include the following:
More recently, computer technology has been incorporated into treatment options. A key indication for good prognosis is treatment intensity. A minimum of 2-3 hours per week has been specified to produce positive results[15]. The main advantage of using computers is that it can greatly increase intensity of therapy. These programs consist of a large variety of exercises and can be done at home in addition to face-to-face treatment with a therapist. However, since aphasia presents differently among individuals, these programs must be dynamic and flexible in order to adapt to the variability in impairments. Another barrier is the capability of computer programs to imitate normal speech and keep up with the speed of regular conversation. Therefore, computer technology seems to be limited in a communicative setting, however is effective in producing improvements in communication training[15].
Several examples of programs used are StepByStep, Linguagraphica, Computer-Based Visual Communication (C-VIC), TouchSpeak (TS), and Sentence Shaper[15].
Melodic intonation therapy is often used to treat non-fluent aphasia and has proved to be very effective in some cases[16].
Zolpidem, a drug with the trade name of Ambien, may provide short-lasting but effective improvement in symptoms of aphasia present in some survivors of stroke. The mechanism for improvement in these cases remains unexplained and is the focus of current research by several groups, to explain how a drug which acts as a hypnotic-sedative in people with normal brain function, can paradoxically increase speech ability in people recovering from severe brain injury. Use of zolpidem for this application remains experimental at this time, and is not officially approved by any pharmaceutical manufacturers of zolpidem or medical regulatory agencies worldwide.
The first recorded case of aphasia is from an Egyptian papyrus, the Edwin Smith Papyrus, which details speech problems in a person with a traumatic brain injury to the temporal lobe.[17]
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