User:Dolfrog/Acquired and Progressive
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Tables
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| Vision | ||
| Perceptual Analysis | ||
| Letter Sound Converter | Visual Word Store | Semantic Processor |
| Phonological Processor | ||
| Speech | ||
| Example | Example | Example |
| Examples | ←↑↓→ … | ↔ — ♦♥♣♠‘’‘’ |
REF
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Alexia dual route
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| Perceptual Analysis | → | ↓ | ||
| ↓ | ↓ | |||
| Semantic Processor | ← | Visual Word Memory | Symbol to Sound Processor | |
| ↓ | ↓ | ↓ | ||
| → | → | Phonological Processor | ← | ← |
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| Speech Oral Reading |
Aphasia
[edit]| Acute | Progressive | Primary | Secondary |
|---|---|---|---|
| Transcortal motor (dynamic aphasia) | Dynamic aphasia | plan of message | dysexectuive subcotical syndromes |
| Amonia | Progressive Amonia | word retrieval | visual perceptual impairment |
| episodic memory impairment | |||
| Transcortical sensory | Semantic Dementia | verbal stores | |
| Receptive | Logopenic | sensory and motor mapping of stored words | |
| Conduction | Jargon? | repetition / monitoring of own speech | auditory perceptual impairment |
| Expressive | PNFA | grammar | |
| phonology | |||
| Apraxia of Speech | Progressive Apraxia of Speech | phonetics | |
| Dysarthria | Progressive Dysarthria | articulation | subcortical and peripheral dysarthrias |
Expressive → Broca's
Receptive → Wernicke's
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[edit]Research paper Collections
[edit]PubMed
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Ataxia
[edit]Wikipedia articles
- Ataxia
- Ataxia telangiectasia
- Cerebellar ataxia
- Episodic ataxia
- Friedreich's ataxia
- Spinocerebellar ataxia
- Trinucleotide repeat disorders
- Vestibulocerebellar syndrome
Information
- Genetic code the RNA codon table
- Anatomy of the cerebellum
- Subramony, SH; Ashizawa, T;. "Spinocerebellar Ataxia Type 1". GeneReviews. PMID 20301363.
{{cite book}}: Unknown parameter|editors=ignored (|editor=suggested) (help)CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)
Aphasia Article Extracts
[edit]work area 0 old aphasia
[edit]
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".
- Individuals with Expressive aphasia (also called Broca's aphasia) were once thought to have ventral temporal damage, though more recent work by Dr. Nina Dronkers using imaging and 'lesion analysis' has revealed that patients with Expressive aphasia have lesions to the medial insular cortex. Broca missed these lesions because his studies did not dissect the brains of diseased patients, so only the more temporal damage was visible. Dronkers and Dr. Odile Plaisant scanned Broca's original patients' brains using a non-invasive MRI scanner to take a closer look. [1] Damage to a region of the motor association cortex in the left frontal lobe (Broca's area) disrupts the ability to speak.[2] Individuals with Expressive aphasia often have right-sided weakness or paralysis of the arm and leg, because the frontal lobe is also important for body movement. Video clips showing patients with Expressive-type aphasia can be found here.
- In contrast to Expressive aphasia, damage to the temporal lobe may result in a fluent aphasia that is called Receptive aphasia (also known as Sensory aphasia and Wernicke's aphasia). These individuals usually have no body weakness, because their brain injury is not near the parts of the brain that control movement. A video clip with a patient exhibiting Receptive aphasia can be found here
- Working from Wernicke's model of aphasia, Ludwig Lichtheim proposed five other types of aphasia, but these were not tested against real patients until modern imaging made more in-depth studies available. The other five types of aphasia in the localizationist model are:
- Anomic aphasia, also known as Anomia, is another type of aphasia proposed under what is commonly known as the Boston-Neoclassical model, which is essentially a difficulty with naming.
- Global aphasia, results from damage to extensive portions of the perisylvian region of the brain. An individual with global aphasia will have difficulty understanding both spoken and written language and will also have difficulty speaking. This is a severe type of aphasia which makes it quite difficult when communicating with the individual.[3]
- Isolation Aphasia, also known as Mixed Transcortical 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.[4] The brain damages are caused to left temporal/parietal cortex that spares the Wernicke's area. Isolation aphasia patients can repeat what other people say, thus they do recognize words but they can't comprehend the meaning of what they hear and repeat themselves. However, they can not produce meaningful speech of their own. [5]
Primary progressive aphasia (PPA)
[edit]Primary progressive aphasia (PPA) is associated with progressive illnesses or dementia, such as frontotemporal dementia / Pick Complex Motor neuron disease, Progressive supranuclear palsy, and Alzheimer's disease; which is the gradual process of losing the ability to think. It is characterized by the gradual loss of the ability to name objects. People suffering from PPA may have difficulties comprehending what others are saying. They can also have difficulty trying to find the right words to make a sentence.[6][7][8]
There are three classifications of Primary Progressive Aphasia:[9]
Progressive nonfluent aphasia (PNFA),
Semantic Dementia (SD),
Logopenic progressive aphasia (LPA)
Progressive 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).
Sub categorisations of aphasia
[edit]Fluent, non-fluent and "pure" aphasias
[edit]The different types of aphasia can be divided into three categories: fluent, non-fluent and "pure" aphasias.[10]
- Receptive aphasias, also called Fluent aphasias, are impairments related mostly to the input or reception of language, with difficulties either in auditory verbal comprehension or in the repetition of words, phrases, or sentences spoken by others. Speech is easy and fluent, but there are difficulties related to the output of language as well, such as paraphasia. Examples of fluent aphasias are: Receptive aphasia, Transcortical sensory aphasia, Conduction aphasia, Anomic aphasia[10]
- Expressive aphasias, also called Nonfluent aphasias, are difficulties in articulating, but in most cases there is relatively good auditory verbal comprehension. Examples of nonfluent aphasias are: Expressive aphasia, Transcortical motor aphasia, Global aphasia[10]
- Acute Expressive (nonfluent) aphasias: Expressive aphasia, Transcortical motor aphasia,
- "Pure" aphasias are selective impairments in reading, writing, or the recognition of words. These disorders may be quite selective. For example, a person is able to read but not write, or is able to write but not read. Examples of pure aphasias are: Pure alexia, Agraphia, Auditory verbal agnosia[10]
Primary and secondary cognitive processes
[edit]Aphasias can be divided into primary and secondary cognitive processes.
- Primary aphasia is due to problems with cognitive language-processing mechanisms, which can include: Transcortical sensory aphasia, Semantic Dementia, Apraxia of speech, Progressive nonfluent aphasia, and Expressive aphasia
- Secondary aphasia is the result of other problems, like memory impairments, attention disorders, or perceptual problems, which can include: Transcortical motor aphasia, Dynamic aphasia, Anomic aphasia, Receptive aphasia, Progressive jargon aphasia, Conduction aphasia, and Dysarthria.[11]
Cognitive neuropsychological model
[edit]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.[12] 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" [13]), 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.
- 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.
- Apraxia of speech (now considered a separate disorder in itself)
Aphasia 1 (classification)
[edit]work area 1
[edit]| Form of aphasia | Acute / Progessive | Cognitive Process | Auditory comprehension | Fluency |
|---|---|---|---|---|
| Receptive aphasia | Acute | Secondary | defective | fluent paraphasic |
| Transcortical sensory aphasia | Acute | Primary | poor | fluent |
| Conduction aphasia | Secondary | relatively good | fluent | |
| Anomic aphasia | mild | fluent | ||
| Expressive aphasia | Acute | Primary | mild difficulty | non-fluent, effortful, slow |
| Transcortical motor aphasia | Acute | Secondary | mild | non-fluent |
| Global aphasia | poor | non-fluent | ||
| Mixed transcortical aphasia | Acute | poor | non-fluent | |
| Progressive nonfluent aphasia(PNFA) | Progessive | Primary | ||
| Semantic Dementia(SD) | Progessive | Primary | ||
| Logopenic progressive aphasia(LPA) | Progessive | Primary | ||
Classification
[edit]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.[14]
Classifying the different subtypes of aphasia is difficult and has led to disagreements among experts. 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.[15]
Acute Aphasias
[edit]- Expressive aphasia, also called Broca's aphasia, damage to a region of the motor association cortex in the left frontal lobe (Broca's area) disrupts the ability to speak.[16] Individuals with Expressive aphasia often have right-sided weakness or paralysis of the arm and leg, because the frontal lobe is also important for body movement. Video clips showing patients with Expressive-type aphasia can be found here.
- Transcortical motor aphasia Similar deficits as Expressive 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.
- Receptive aphasia also called Sensory aphasia and Wernicke's aphasia, damage to the temporal lobe may result in a fluent aphasia that is called . These individuals usually have no body weakness, because their brain injury is not near the parts of the brain that control movement. A video clip with a patient exhibiting Receptive aphasia can be found here
- Transcortical sensory aphasia Similar deficits as in Receptive aphasia, but repetition ability remains intact.
- Conduction aphasia, also called Central 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.
- 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.
- Global aphasia, results from damage to extensive portions of the perisylvian region of the brain. An individual with global aphasia will have difficulty understanding both spoken and written language and will also have difficulty speaking. This is a severe type of aphasia which makes it quite difficult when communicating with the individual.[17]
- Mixed transcortical aphasia, also called 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.[18] The brain damages are caused to left temporal/parietal cortex that spares the Wernicke's area. Isolation aphasia patients can repeat what other people say, thus they do recognize words but they can't comprehend the meaning of what they hear and repeat themselves. However, they can not produce meaningful speech of their own. [19] Similar deficits as in global aphasia, but repetition ability remains intact.
Progressive aphasias
[edit]Primary progressive aphasia (PPA)
Primary progressive aphasia (PPA) is associated with progressive illnesses or dementia, such as frontotemporal dementia / Pick Complex Motor neuron disease, Progressive supranuclear palsy, and Alzheimer's disease; which is the gradual process of losing the ability to think. It is characterized by the gradual loss of the inability to name objects. People suffering from PPA may have difficulties comprehending what others are saying. They can also have difficulty trying to find the right words to make a sentence.[20][21][22]
There are three classifications of Primary Progressive Aphasia : Progressive nonfluent aphasia (PNFA), Semantic Dementia (SD), and Logopenic progressive aphasia (LPA)[23]
Progressive 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.
Aphasia sub classification
[edit]- Fluent/Nonfluent classification
The different types of aphasia can be divided into three categories: fluent, non-fluent, and pure aphasias
- Receptive aphasias, also called Fluent aphasias, are impairments related mostly to the input or reception of language, with difficulties either in auditory verbal comprehension or in the repetition of words, phrases, or sentences spoken by others. Speech is easy and fluent, but there are difficulties related to the output of language as well, such as paraphasia.
- Expressive aphasias, also called Nonfluent aphasias, are difficulties in articulating, but in most cases there is relatively good auditory verbal comprehension.
- Primary and Secondary cognitive processes
Aphasias can be divided into primary and secondary cognitive processes.
- Primary aphasia is due to problems with cognitive language-processing mechanisms,
- Secondary aphasia is the result of other problems, like memory impairments, attention disorders, or perceptual problems,
Table
[edit]| Form of aphasia | Acute / Progessive | Cognitive Process | Auditory comprehension | Fluency |
|---|---|---|---|---|
| Receptive aphasia | Acute | Secondary | defective | fluent paraphasic |
| Transcortical sensory aphasia | Acute | Primary | poor | fluent |
| Conduction aphasia | Secondary | relatively good | fluent | |
| Anomic aphasia | mild | fluent | ||
| Expressive aphasia | Acute | Primary | mild difficulty | non-fluent, effortful, slow |
| Transcortical motor aphasia | Acute | Secondary | mild | non-fluent |
| Global aphasia | poor | non-fluent | ||
| Mixed transcortical aphasia | Acute | poor | non-fluent | |
| Progressive nonfluent aphasia(PNFA) | Progessive | Primary | ||
| Semantic Dementia(SD) | Progessive | Primary | ||
| Logopenic progressive aphasia(LPA) | Progessive | Primary | ||
Aphasia 2 (characteristics)
[edit]working area 2
[edit]presentation / characteristics'
Acute Aphasias
[edit]- Individuals with Receptive aphasia may speak in long sentences that have no meaning, add unnecessary words, and even create new "words" (neologisms). For example, someone with Receptive 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 Receptive aphasia usually have great difficulty understanding the speech of both themselves and others and are therefore often unaware of their mistakes.
- Individuals with Transcortical sensory aphasia Similar deficits as in Receptive aphasia, but repetition ability remains intact.
- Individuals with 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.
- Individuals with 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.
- Individuals with Expressive aphasia frequently speak short, meaningful phrases that are produced with great effort. Expressive 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 Expressive 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 Expressive 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
- Individuals with Transcortical motor aphasia Similar deficits as Expressive 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.
- 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.
- Individuals with Mixed transcortical aphasia have similar deficits as in global aphasia, but repetition ability remains intact.
The following table summarizes some major characteristics of different acute of aphasia:
| Type of aphasia | Repetition | Naming | Auditory comprehension | Fluency |
|---|---|---|---|---|
| Receptive aphasia | mild–mod | mild–severe | defective | fluent paraphasic |
| Transcortical sensory aphasia | good | mod–severe | poor | fluent |
| Conduction aphasia | poor | poor | relatively good | fluent |
| Anomic aphasia | mild | mod–severe | mild | fluent |
| Expressive aphasia | mod–severe | mod–severe | mild difficulty | non-fluent, effortful, slow |
| Transcortical motor aphasia | good | mild–severe | mild | non-fluent |
| Global aphasia | poor | poor | poor | non-fluent |
| Mixed transcortical aphasia | moderate | poor | poor | non-fluent |
Progressive aphasias
[edit]Subcortical aphasias
[edit]- 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.
Aphasia 3 (history)
[edit]History
[edit]Localizationist model
[edit]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".
- Individuals with Expressive aphasia (also called Broca's aphasia) were once thought to have ventral temporal damage, though more recent work by Dr. Nina Dronkers using imaging and 'lesion analysis' has revealed that patients with Expressive aphasia have lesions to the medial insular cortex. Broca missed these lesions because his studies did not dissect the brains of diseased patients, so only the more temporal damage was visible. Dronkers and Dr. Odile Plaisant scanned Broca's original patients' brains using a non-invasive MRI scanner to take a closer look. [24] Damage to a region of the motor association cortex in the left frontal lobe (Broca's area) disrupts the ability to speak.[25] Individuals with Expressive aphasia often have right-sided weakness or paralysis of the arm and leg, because the frontal lobe is also important for body movement. Video clips showing patients with Expressive-type aphasia can be found here.
- In contrast to Expressive aphasia, damage to the temporal lobe may result in a fluent aphasia that is called Receptive aphasia (also known as Sensory aphasia and Wernicke's aphasia). These individuals usually have no body weakness, because their brain injury is not near the parts of the brain that control movement. A video clip with a patient exhibiting Receptive aphasia can be found here
- Working from Wernicke's model of aphasia, Ludwig Lichtheim proposed five other types of aphasia, but these were not tested against real patients until modern imaging made more in-depth studies available. The other five types of aphasia in the localizationist model are:
- Pure word deafness
- Conduction aphasia
- Apraxia of speech (now considered a separate disorder in itself)
- Transcortical motor aphasia
- Transcortical sensory aphasia
- Anomic aphasia, also known as Anomia, is another type of aphasia proposed under what is commonly known as the Boston-Neoclassical model, which is essentially a difficulty with naming.
- Global aphasia, results from damage to extensive portions of the perisylvian region of the brain. An individual with global aphasia will have difficulty understanding both spoken and written language and will also have difficulty speaking. This is a severe type of aphasia which makes it quite difficult when communicating with the individual.[26]
work area
[edit]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.[27]
Additions to this section
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.[27]
Localizationist model
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.
Individuals with Expressive aphasia (also called Broca's aphasia) were once thought to have ventral temporal damage, though more recent work by Dr. Nina Dronkers using imaging and 'lesion analysis' has revealed that patients with Expressive aphasia have lesions to the medial insular cortex. Broca missed these lesions because his studies did not dissect the brains of diseased patients, so only the more temporal damage was visible. Dronkers and Dr. Odile Plaisant scanned Broca's original patients' brains using a non-invasive MRI scanner to take a closer look. [2] Damage to a region of the motor association cortex in the left frontal lobe (Broca's area) disrupts the ability to speak.[3] Individuals with Expressive aphasia often have right-sided weakness or paralysis of the arm and leg, because the frontal lobe is also important for body movement. Video clips showing patients with Expressive-type aphasia can be found here. In contrast to Expressive aphasia, damage to the temporal lobe may result in a fluent aphasia that is called Receptive aphasia (also called Sensory aphasia and Wernicke's aphasia). These individuals usually have no body weakness, because their brain injury is not near the parts of the brain that control movement. A video clip with a patient exhibiting Receptive aphasia can be found here Working from Wernicke's model of aphasia, Ludwig Lichtheim proposed five other types of aphasia, but these were not tested against real patients until modern imaging made more in-depth studies available.
End of Page
[edit]ref
[edit]- ^ Dronkers NF, Plaisant O, Iba-Zizen MT, Cabanis EA (2007). "Paul Broca's historic cases: high resolution MR imaging of the brains of Leborgne and Lelong". Brain. 130 (Pt 5): 1432–41. doi:10.1093/brain/awm042. PMID 17405763.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) - ^ Masdeu, Joseph (June 2000). "Aphasia". Archives of Neurology. 57 (6).
{{cite journal}}:|access-date=requires|url=(help)CS1 maint: year (link) - ^ Taylor Sarno, M. (2007). Neurogenic disorders of speech and language. In: O’Sullivan, S.B. & Schmitz, T.J. (2007). Physical Rehabilitation (5th ed.). Philadelphia (PA): F.A. Davis Company.
- ^ Carlson, Neil (2007). Psychology the Science of Behaviour. Toronto: Pearson. p. 278. ISBN 978-0-205-64524-4.
- ^ Carlson, Neil (2007). Psychology the Science of Behaviour. Toronto: Pearson. p. 305. ISBN 978-0-205-64524-4.
- ^ Mesulam MM (2001). "Primary progressive aphasia". Ann. Neurol. 49 (4): 425–32. doi:10.1002/ana.91.abs. PMID 11310619.
{{cite journal}}: Unknown parameter|month=ignored (help) - ^ Wilson SM, Henry ML, Besbris M; et al. (2010). "Connected speech production in three variants of primary progressive aphasia". Brain. 133 (Pt 7): 2069–88. doi:10.1093/brain/awq129. PMC 2892940. PMID 20542982.
{{cite journal}}: Explicit use of et al. in:|author=(help); Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) - ^ Harciarek M, Kertesz A (2011). "Primary progressive aphasias and their contribution to the contemporary knowledge about the brain-language relationship". Neuropsychol Rev. 21 (3): 271–87. doi:10.1007/s11065-011-9175-9. PMC 3158975. PMID 21809067.
{{cite journal}}: Unknown parameter|month=ignored (help) - ^ Harciarek M, Kertesz A (2011). "Primary progressive aphasias and their contribution to the contemporary knowledge about the brain-language relationship". Neuropsychol Rev. 21 (3): 271–87. doi:10.1007/s11065-011-9175-9. PMC 3158975. PMID 21809067.
{{cite journal}}: Unknown parameter|month=ignored (help) - ^ a b c d Kolb, Bryan; Whishaw, Ian Q. (2003). Fundamentals of human neuropsychology. [New York]: Worth. pp. 502–504. ISBN 0-7167-5300-6. OCLC 464808209.
{{cite book}}: CS1 maint: multiple names: authors list (link) - ^ Rohrer JD, Knight WD, Warren JE, Fox NC, Rossor MN, Warren JD (2008). "Word-finding difficulty: a clinical analysis of the progressive aphasias". Brain. 131 (Pt 1): 8–38. doi:10.1093/brain/awm251. PMC 2373641. PMID 17947337.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) - ^ Luria's Areas of the Human Cortex Involved in Language Illustrated summary of Luria's book Traumatic Aphasia
- ^ Coltheart, Max; Kay, Janice; Lesser, Ruth (1992). PALPA psycholinguistic assessments of language processing in aphasia. Hillsdale, N.J: Lawrence Erlbaum Associates. ISBN 0-86377-166-1.
{{cite book}}: CS1 maint: multiple names: authors list (link) - ^ Kolb, Bryan; Whishaw, Ian Q. (2003). Fundamentals of human neuropsychology. [New York]: Worth. pp. 502, 505, 511. ISBN 0-7167-5300-6. OCLC 464808209.
{{cite book}}: CS1 maint: multiple names: authors list (link) - ^ Kolb, Bryan; Whishaw, Ian Q. (2003). Fundamentals of human neuropsychology. [New York]: Worth. pp. 502, 505, 511. ISBN 0-7167-5300-6. OCLC 464808209.
{{cite book}}: CS1 maint: multiple names: authors list (link) - ^ Masdeu, Joseph (June 2000). "Aphasia". Archives of Neurology. 57 (6).
{{cite journal}}:|access-date=requires|url=(help)CS1 maint: year (link) - ^ Taylor Sarno, M. (2007). Neurogenic disorders of speech and language. In: O’Sullivan, S.B. & Schmitz, T.J. (2007). Physical Rehabilitation (5th ed.). Philadelphia (PA): F.A. Davis Company.
- ^ Carlson, Neil (2007). Psychology the Science of Behaviour. Toronto: Pearson. p. 278. ISBN 978-0-205-64524-4.
- ^ Carlson, Neil (2007). Psychology the Science of Behaviour. Toronto: Pearson. p. 305. ISBN 978-0-205-64524-4.
- ^ Mesulam MM (2001). "Primary progressive aphasia". Ann. Neurol. 49 (4): 425–32. doi:10.1002/ana.91.abs. PMID 11310619.
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