Aphasia

Aphasia
Classification and external resources
ICD-10 F80.0-F80.2, R47.0
ICD-9 315.31, 784.3
DiseasesDB 4024
MedlinePlus 003204
eMedicine neuro/437 
MeSH D001037

Aphasia (from Greek, aphatos : 'speechless'), also known as rhymnasia, is a loss of the ability to produce and/or comprehend language, due to injury to brain areas specialized for these functions, Broca's area, which governs language production, or Wernicke's area, which governs the interpretation of language. It is not a result of deficits in sensory, intellectual, or psychiatric functioning,[1] nor due to muscle weakness or a cognitive disorder.

Depending on the area and extent of the damage, someone suffering from aphasia may be able to speak but not write, or vice versa, or display any of a wide variety of other deficiencies in language comprehension and production, such as being able to sing but not speak. Aphasia may co-occur with speech disorders such as dysarthria or apraxia of speech, which also result from brain damage.

Aphasia can be assessed in a variety of ways, from quick clinical screening at the bedside to several-hour-long batteries of tasks that examine the key components of language and communication. The prognosis of those with aphasia varies widely, and is dependent upon age of the patient, site and size of lesion, and type of aphasia.

Contents

Causes

Usually, aphasias are a result of damage (lesions) to the language centres of the brain (like Broca's area). 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.

Symptoms

Any of the following may be considered symptoms of aphasia:

Types

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. They are also often unaware of their surroundings, and may present a risk to themselves and others around them.
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 Caused by damage to the arcuate fasciculus, the structure that transmits information between Wernicke's area and Broca's area. Auditory comprehension is near normal, and oral expression is fluent with occasional paraphasic errors. Repetition ability is poor.
Nominal 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" meaning, "I will take the dog for a walk". The same sentence could also mean "You take the dog for a walk", or "The dog walked out of the yard", depending on the circumstances. 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 will be paralysis of the patient's right arm, leg, and face.
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 will be paralysis of the patient's right arm, leg, and face.
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 will be paralysis of the patient's right arm, leg, and face.
Transcortical mixed 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.

Acquired childhood aphasia

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.[2] 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.[3] An important difference between ACA and developmental childhood aphasia is that in the latter there is no apparent neurological basis for the language deficit.[4]
ACA is one of the more rare language problems in children but it is interesting because of its contribution to theories on language and the brain.[3] 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.[5]

Classification

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. [6]

Localizationist model

Cortex

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.

  1. Pure word deafness
  2. Conduction aphasia
  3. Apraxia of speech, which is now considered a separate disorder in itself.
  4. Transcortical motor aphasia
  5. Transcortical sensory aphasia

Fluent, non-fluent and "pure" aphasias

The different types of aphasia can be divided into three categories: fluent, non-fluent and "pure" aphasias.[7]

Cognitive neuropsychological model

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. 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), 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.

A few less common subtypes include:

A combination of subtypes is possible.

Primary and secondary aphasia

Aphasia can be divided into primary and secondary aphasia.[8]

History

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.[9]

Famous sufferers

See also

Sources

Academic references

Personal experiences of aphasia

References

  1. ↑ Brookshire, 1992; Goodglass 1993
  2. ↑ B.E. Murdoch: Acquired Neurological Speech/Language Disorders in Childhood: Language Disorders in Childhood (1990)
  3. ↑ 3.0 3.1 B.T. Woods: Acquired Childhood Aphasia, in: H.S. Kirshner: Handbook of neurological speech and language disorders (1994).
  4. ↑ P.F. Paquier & H.R. van Dongen: Is Acquired Childhood Aphasia Atypical? In: P. Coppens et al.: Aphasia in Atypical Populations (1998)
  5. ↑ D.P: Cantwell: Developmental Speech and Language Disorders (1987)
  6. ↑ Kolb & Whishaw: Fundamentals of Human Neuropsychology (2003), page 502, 505, 511.
  7. ↑ Kolb & Whishaw: Fundamentals of Human Neuropsychology (2003), pages 502-504. The whole paragraph "fluent, non-fluent and pure aphasias" is written with help of this reference.
  8. ↑ http://christofflab.psych.ubc.ca/psych260/docs/L12-Language.pdf
  9. ↑ Paul R. McCrory and Samuel F. Berkovic (2001). Concussion: The history of clinical and pathophysiological concepts and misconceptions. Neurology, 57(12): 2283-2289. PMID 11756611.
  10. ↑ Richardson, Robert D. Jr. Emerson: The Mind on Fire. Berkeley, California: University of California Press, 1995: 569. ISBN 0-520-08808-5.

External links

Symptoms and signs: Speech and voice (R47-R49, 784)
Aphasia/Dysphasia
Expressive aphasia - Receptive aphasia - Conduction aphasia
Other speech disturbances
Dysarthria - Schizophasia
Symbolic dysfunctions
Dyslexia - Alexia - Agnosia (Prosopagnosia, Astereognosis) - Apraxia (Ideomotor apraxia) - Acalculia - Agraphia
Voice disturbances
Dysphonia - Aphonia