172:(ICF) framework, the comprehensive assessment encompasses not only speech and language, but also impairments in body structure and function, co-morbid deficits, limitations in activity and participation, and contextual (environmental and personal) factors. The assessment can be static (current functioning) or dynamic (ongoing) and the assessment tools can be standardized or nonstandardized. Typically, the assessment for aphasia includes a gathering of a case history, a self-report from the patient, an oral-motor examination, assessment of expressive and receptive language in spoken and written forms, and identification of facilitators and barriers to patient success. From this assessment, the SLP will determine type of aphasia and the patient's communicative strengths and weaknesses and how their diagnosis may impact their overall quality of life.
184:. The SLP chooses specific therapy tasks and goals based on the speech and language abilities and needs of the individual. In general for individuals with TMoA, treatment should capitalize on their strong auditory comprehension and repetition skills and address the individual's reduced speech output and difficulty initiating and maintaining a conversation. New research in aphasia treatment is showing the benefit of the Life Participation Approach to Aphasia (LPAA) in which goals are written based on the skills needed by the individual patient to participate in specific real-life situations (i.e. communicating effectively with nurses or gaining employment). Based on the specific needs of the patient, SLPs can provide a variety of treatment activities.
45:(CVA). TMoA is generally characterized by reduced speech output, which is a result of dysfunction of the affected region of the brain. The left hemisphere is usually responsible for performing language functions, although left-handed individuals have been shown to perform language functions using either their left or right hemisphere depending on the individual. The anterior frontal lobes of the language-dominant hemisphere are essential for initiating and maintaining speech. Because of this, individuals with TMoA often present with difficulty in speech maintenance and initiation.
241:
transitioned to TMoA. All participants in the study regained full language abilities within 18 months following their stroke. This suggests a positive long-term prognosis for patients with TMoA. However, this might not be the case for all patients and more research is needed in order to solidify these findings. Another study found that prognosis of TMoA is affected by lesion size. Smaller lesions typically cause delays in speech initiation; whereas, larger lesions lead to more profound language abnormalities and difficulty with abstract language abilities.
101:, people with TMoA have deficits in initiation and maintenance of conversations, which results in reduced speech output. A person with TMoA may seldom produce utterances and typically remain silent. The utterances that they do produce are typically only one to two words long. However, in more structured and predictable interactions, individuals with TMoA tend to respond more fluently and promptly. In addition, these individuals are characterized by their attentiveness and cooperation and are often described as being task-oriented.
192:
based on the patient's experiences, opinions, or general knowledge and prompt the patient to answer with phrases or sentences. To work on more connected speech, the clinician may ask the patient to describe procedures such as making a sandwich or doing laundry. A study found that syntax training in which sentence constructions are elicited on a hierarchy of difficulty produced gains in grammatically complete utterances and utterances that successfully communicated novel and accurate information.
188:
missing and expects the patient to fill in the blank. Limited research suggests that nonsymbolic limb movement on the left side (i.e. tapping the left hand on the table) during sentence production can increase verbal initiations. The use of the left arm in left space stimulates initiation mechanisms in the right hemisphere of the brain which can also be used for language allowing individuals to produce more grammatical sentences with higher fluency and more verbal initiation.
228:
With regard to intensity and duration of treatment, studies reported maximum recovery occurred with intense weekly therapy (approximately 8 hours per week) was delivered over a 2â3 month period. Other research shows that distributed therapy may be more beneficial than high intensity therapy. More research is needed to determine which is best, but it may be found that the ideal duration and intensity of therapy is variable depending on the patient and their needs.
158:
assessment. A screening typically includes evaluation of oral motor functions, speech production skills, comprehension, use of written and verbal language, cognitive communication, swallowing, and hearing. Both the screening and assessment must be sensitive to the patient's linguistic and cultural differences. An individual will be recommended to receive a comprehensive assessment if their screening shows signs of aphasia. Under the
154:(SLP). The overall sign of TMoA is nonfluent, reduced, fragmentary echoic, and perseverative speech with frequent hesitations and pauses. Patients with TMoA also have difficulty initiating and maintaining speech. However, speech articulation and auditory comprehension remain typical. The hallmark sign of TMoA is intact repetition in the presence of these signs and symptoms.
237:
of recovery may look different depending on the type of stroke that caused the aphasia. With an ischemic stroke, recovery is greatest within the first two weeks and then diminishes overtime until the progress stabilizes. With a hemorrhagic stroke, the patient often shows little improvement in the first few weeks and then has relatively rapid recovery until they stabilize.
196:
guidelines so that the patient's responses go beyond the clinician's request and so the clinician does not do the majority of the talking. Research shows that conversation therapy can improve percent of complex utterances, the efficiency of the utterances for expressing ideas, and total time spent talking over more traditional stimulation therapy.
256:. Since the lesion that results in TMoA usually occurs in the watershed area and does not directly involve the areas of the brain responsible for general language abilities, prognosis for these patients is good overall. Other factors that determine a patient's prognosis include age, education prior to the stroke, gender, motivation, and support.
209:
Aphasia from the
Aphasia Institute. In this program, the focus is put on acknowledging the patient's competence and helping them to reveal that competence. Strategies include saying âI know you knowâ when appropriate, using gestures to supplement messages, limiting background noise, and given sufficient time for response.
220:, taken by mouth, has provided positive outcomes during intervention for non-fluent types of aphasia, such as TMoA or adynamic aphasia. Studies have found that bromocriptine increased neural networks which assist with the initiation of speech in individuals who possess non-fluent characteristics of speech.
77:
of aphasia may present with a contiguity disorder in which they have difficulty combining linguistic elements. For dynamic aphasia, this is most apparent when the patient is asked to sequence at the sentence level whereas for other aphasias contiguity disorder can be seen at the phoneme or word level.
236:
In relation to other types of aphasia, TMoA occurs less frequently, so there is less information on its prognosis. In general, for individuals with aphasia, most recovery is seen within 6 months of the stroke or injury although more recovery may continue in the following months or years. The timeline
157:
TMoA, or any other type of aphasia, is identified and diagnosed through the screening and assessment process. Screening can be conducted by an SLP or other professional when there is a suspected aphasia. The screening does not diagnose aphasia, rather it points to the need for a further comprehensive
76:
There are some other forms of aphasia that relate to TMoA. For instance, adynamic aphasia is a form of TMoA that is characterized by sparse speech. This occurs as a result of executive functioning in the frontal lobe. Another form of aphasia related to TMoA is dynamic aphasia. Patients with this form
64:
related to language use are often affected. Executive functions relevant to language include activating language responses, controlling syntax (grammar), and narrative discourse. Difficulties in these areas can lead to supplementary deficits involving difficulties forming complex sentences, choosing
208:
Additionally, they may train the patient's communication partners to support the conversational abilities of the patient by facilitating the use of preserved cognitive and social functions. Research supports the use of various partner training programs such as
Supported Conversation for Adults with
244:
Research has shown that treatment has a direct effect on aphasia outcomes. Intensity, duration and timing of treatment all need to be taken in to consideration when choosing a course of treatment and determining a prognosis. In general, greater intensity leads to greater improvement. For duration,
227:
for treatment of all types of aphasia, timing, intensity, duration, and repetition of treatment should be taken into consideration. Research has found that aphasia treatment initiated during the earlier acute post-injury phase is more effective compared to treatment initiated in the chronic phase.
199:
In order to improve the patient's abilities to functionally communicate in their natural settings, the SLP will provide strategies and techniques to enhance their success in communicative settings (i.e. supplementing speech with nonverbal communication). Research supports the use of reduced syntax
191:
To increase speech output, the clinician may provide a set of pictures and prompt the patient to describe or elaborate on the events pictured. The clinician can also provide spoken or written words and prompt the patient to use the words in a sentence. Additionally, the clinician can ask questions
204:
inhibits the patient's ability to form grammatically correct sentences, this type of treatment involves reducing these agrammatic deficits and teaching the patient to simplify linguistic structures while still conveying the message in order for language used to be more productive in conversation.
245:
longer-term treatment produces more permanent changes. As for timing, beginning treatment too early may be difficult for the system which has not recovered enough to do intensive therapy, but beginning too late may result missing the window of the opportunity in which the most change can occur.
195:
To improve conversational skills, SLPs may engage the patient in structured conversations in which supports are provided to help the patient take appropriate conversational turns, maintain the topic of conversation, and formulate appropriate sentences. Clinicians often need to provide pragmatic
187:
To improve word retrieval and initiation difficulties, clinicians may use confrontation naming in which the patient is asked to name various objects and pictures. Depending on the severity, they may also use sentence completion tasks in which the clinician says sentences with the final word(s)
240:
In a study involving eight patients with border zone lesions, all patients presented with transcortical mixed aphasia initially after the stroke. Three of these patients made a complete recovery within a few days post-stroke. For three other patients with more anterior lesions, their aphasia
249:, the brain's natural ability to reorganize itself following a traumatic event, occurs best when treatment connects simultaneous events, maintains attention, taps into positive emotion, utilizes repetition tasks, and is specific to the individual's needs.
117:
area of the left, or language-dominant, hemisphere. The anterior superior frontal lobe is known as the prefrontal cortex which is responsible for the initiation and ideation of verbal speech. The damage leaves the major language networks,
68:
The extent and location of the brain damage will impact the degree and variety of language functioning characteristics (i.e. damage deep to the frontal lobe and/or damage across multiple regions will greatly impair language). Right
849:
Kagan, Aura; Black, Sandra; Duchan, Judith; Simmons-Mackie, Nina; Square, Paula (June 2001). "Training
Volunteers as Conversation Partners Using "Supported Conversation for Adults with Aphasia" (SCA): A Controlled Trial".
1331:
97:(a wide category of speech errors that are caused by aphasia). Regardless of any relative communication strengths, individuals with TMoA are typically poor conversational partners. Due to damage in the anterior superior
1112:
Flamand-Roze C, Cauquil-Michon C, Roze E, Souillard-Scemama R, Maintigneux L, Ducreux D, Adams D, Denier C (December 2011). "Aphasia in border-zone infarcts has a specific initial pattern and good long-term prognosis".
168:
85:
TMoA is classified as a non-fluent aphasia that is characterized by a significantly reduced output of speech, but good auditory comprehension. Auditory comprehension skills remain intact because the
93:
are not impaired. Individuals with TMoA also exhibit good repetition skills and can repeat long, complex phrases effortlessly and without error. However, spontaneous speech often presents with
1324:
669:
Chapey, Roberta; Duchan, Judith; Elman, Roberta; Garcia, Linda; Kagan, Aura; Lyon, Jon; Simmons-Mackie, Nina. "Life-Participation
Approach to Aphasia: A Statement of Values for the Future".
960:
Berthier ML, Starkstein SE, Leiguarda R, Ruiz A, Mayberg HS, Wagner H, et al. (1991). "Transcortical aphasia: Importance of the nonspeech dominant hemisphere in language repetition".
1317:
159:
1207:
Raymer AM, Beeson P, Holland A, Kendall D, Maher LM, Martin N, et al. (February 2008). "Translational research in aphasia: from neuroscience to neurorehabilitation".
769:
Savage, Meghan; Donovan, Neila (January 2017). "Comparing linguistic complexity and efficiency in conversations from stimulation and conversation therapy in aphasia".
804:
Ruiter MB, Kolk HH, Rietveld TC (2010). "Speaking in ellipses: the effect of a compensatory style of speech on functional communication in chronic agrammatism".
684:
Raymer AM, Rowland L, Haley M, Crosson, B (2002). "Nonsymbolic movement training to improve sentence generation in transcortical motor aphasia: A case study".
349:
ZakariĂĄs, Lilla; Keresztes, Attila; Demeter, Gyula; LukĂĄcs, Ăgnes (2013-12-01). "A specific pattern of executive dysfunctions in transcortical motor aphasia".
479:
Ardila A (2017). "Some rare neuropsychological syndromes: Central achromatopsia, BĂĄlint's syndrome, pure word-deafness, supplementary motor area aphasia".
73:, or right-sided paralysis, may coincide with TMoA if the lesion in the anterior frontal lobe is large enough and extends into the posterior frontal lobe.
995:
Kleim JA, Jones TA (February 2008). "Principles of experience-dependent neural plasticity: implications for rehabilitation after brain damage".
671:
Section III: Psychosocial/Functional
Approaches to Intervention: Focus on Improving Ability to Perform Communication Activities of Daily Living
1570:
1609:
1309:
1376:
1366:
1247:
Bayles, Kathryn; Tomoeda, Cheryl (November 2010). "Neuroplasticity: Implications for
Treating Cognitive-Communication Disorders".
1762:
1371:
1600:
711:
Murray LL, Heather Ray A (2001). "A comparison of relaxation training and syntax stimulation for chronic nonfluent aphasia".
384:
Gold; et al. (1997). "Adynamic
Aphasia: A Transcortical Motor Aphasia with Defective Semantic Strategy Information".
265:
1638:
1619:
578:
1565:
1507:
1736:
1678:
1665:
1577:
1550:
181:
163:
151:
1605:
131:
60:; instead, the damage isolates these areas from the rest of the brain. If there is damage to the frontal lobe,
49:
42:
200:
therapy to help patients overcome the non-fluent speech and agrammatism that often occurs with TMoA. Because
1643:
1615:
1429:
427:
PhD, Alfredo Ardila (2010-03-01). "A proposed reinterpretation and reclassification of aphasic syndromes".
1711:
1685:
1582:
1490:
139:
1073:"Intensive Versus Distributed Aphasia Therapy: A Nonrandomized, Parallel-Group, Dosage-Controlled Study"
1623:
1695:
180:
Treatment for all types of aphasia, including transcortical motor aphasia, is usually provided by a
1731:
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1409:
61:
57:
53:
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90:
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Dignam J, Copland D, McKinnon E, Burfein P, O'Brien K, Farrell A, Rodriguez AD (August 2015).
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114:
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1008:
863:
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1459:
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1126:
500:
217:
413:
886:
531:
98:
38:
516:"Modality-specific cognitive function of medial and lateral human Brodmann area 6"
1089:
1072:
609:
Freedman, M.; Alexander (1984). "Anatomic Basis of transcortical motor aphasia".
362:
1444:
201:
135:
70:
973:
747:
462:
928:
817:
697:
440:
110:
94:
1134:
448:
370:
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1016:
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790:
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549:
397:
1174:
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65:
which words to use appropriately, and initiating speech in conversation.
1381:
492:
17:
826:
1480:
1394:
253:
41:
of the language-dominant hemisphere. This damage is typically due to
130:, unaffected. Brain injury can result from a stroke caused by left
109:
Neurological imaging has shown that TMoA is typically caused by an
1348:
169:
252:
Other factors affecting prognosis includes location and site of
1313:
771:
International
Journal of Language & Communication Disorders
212:
From a neuroscience perspective, research has found that a
52:
does not directly harm the areas of the brain involved in
1601:
Upper dorsal pontine syndrome/RaymondâCĂ©stan syndrome
887:"Communication Tools: Communicative Access & SCA"
1724:
1704:
1652:
1593:
1558:
1549:
1506:
1470:
1359:
1032:"Intensity of aphasia therapy, impact on recovery"
333:Introduction to Neurogenic Communication Disorders
852:Journal of Speech, Language, and Hearing Research
150:TMoA is diagnosed by the referring physician and
1030:Bhogal SK, Teasell R, Speechley M (April 2003).
37:, results from damage in the anterior superior
644:American Speech Language Hearing Association.
142:(TBI), or progressive neurological disorders.
1325:
113:of the anterior superior frontal lobe in the
8:
583:American-Speech-Language-Hearing Association
514:Tanaka S, Honda M, Sadato N (January 2005).
160:American Speech-Language-Hearing Association
1555:
1332:
1318:
1310:
1287:
1183:
1173:
1088:
1047:
936:
913:"Aphasia therapy on a neuroscience basis"
825:
539:
1264:"Neuroplasticity: evidence from aphasia"
748:"Rehabilitation of poststroke cognition"
746:Shigaki CL, Frey SH, Barrett AM (2014).
276:
1566:Lateral medullary syndrome/Wallenberg
1242:
1240:
1238:
1158:"Therapy efficacy in chronic aphasia"
326:
324:
322:
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318:
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7:
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474:
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344:
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288:
286:
284:
282:
280:
1578:Medial medullary syndrome/Dejerine
1049:10.1161/01.STR.0000062343.64383.D0
911:PulvemĂŒller F, Bethier ML (2008).
14:
806:Neuropsychological Rehabilitation
1127:10.1111/j.1468-1331.2011.03422.x
1347:associated with lesions of the
532:10.1523/JNEUROSCI.4324-04.2005
1:
1280:10.1016/S0021-9924(00)00031-9
725:10.1016/s0021-9924(00)00043-5
481:Psychology & Neuroscience
463:"Transcortical motor aphasia"
266:Transcortical sensory aphasia
1639:Internuclear ophthalmoplegia
1090:10.1161/STROKEAHA.115.009522
363:10.1080/02687038.2013.835783
1221:10.1044/1092-4388(2008/020)
1009:10.1044/1092-4388(2008/018)
864:10.1044/1092-4388(2001/051)
182:speech-language pathologist
152:speech-language pathologist
23:Transcortical motor aphasia
1779:
331:Brookshire, R. H. (2007).
223:In order to capitalize on
15:
1737:Upper motor neuron lesion
1209:J. Speech Lang. Hear. Res
1156:Basso A, Macis M (2011).
997:J. Speech Lang. Hear. Res
929:10.1080/02687030701612213
818:10.1080/09602010903399287
698:10.1080/02687030244000239
441:10.1080/02687030802553704
166:(WHO) guidelines and the
164:World Health Organization
1606:Lateral pontine syndrome
974:10.1093/brain/114.3.1409
132:anterior cerebral artery
43:cerebrovascular accident
1763:Complications of stroke
1644:One and a half syndrome
1620:MillardâGubler syndrome
1616:Medial pontine syndrome
783:10.1111/1460-6984.12252
335:. St. Louis, MO: Mosby.
1712:Alternating hemiplegia
617:(4). Naeser: 409â417.
398:10.1006/brln.1997.1750
140:traumatic brain injury
35:white matter dysphasia
579:"Aphasia: Assessment"
31:commissural dysphasia
1262:Thompson CK (2000).
623:10.1212/wnl.34.4.409
1732:Pseudobulbar affect
1686:Parinaud's syndrome
1677:ventral tegmentum,
1491:Parkinson's disease
1410:Hemispatial neglect
1175:10.1155/2011/313480
885:Aphasia Institute.
673:. pp. 279â289.
62:executive functions
54:language production
1664:ventral peduncle,
1634:Locked-in syndrome
1624:Foville's syndrome
1524:Dysdiadochokinesia
1435:Cortical blindness
1415:Gerstmann syndrome
1390:Expressive aphasia
1341:Signs and symptoms
493:10.1037/pne0000093
386:Brain and Language
87:arcuate fasciculus
81:Symptoms and signs
1745:
1744:
1720:
1719:
1696:Claude's syndrome
1673:Benedikt syndrome
1539:Cerebellar ataxia
1498:Thalamic syndrome
1455:Cortical deafness
1430:BĂĄlint's syndrome
1405:Receptive aphasia
357:(12): 1426â1439.
134:(ACA) occlusion,
128:arcuate fasiculus
29:), also known as
1770:
1660:Weber's syndrome
1556:
1529:Intention tremor
1334:
1327:
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1244:
1233:
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1204:
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1153:
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1121:(12): 1397â401.
1109:
1103:
1102:
1092:
1068:
1062:
1061:
1051:
1027:
1021:
1020:
992:
986:
985:
968:(3): 1409â1427.
957:
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901:
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829:
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692:(4â6): 493â506.
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214:dopamine agonist
50:watershed region
1778:
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1748:
1747:
1746:
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1700:
1648:
1589:
1545:
1502:
1466:
1426:Occipital lobe
1360:Cerebral cortex
1355:
1338:
1307:
1305:
1268:J Commun Disord
1261:
1260:
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1249:ASHA Convention
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719:(1â2): 87â113.
713:J Commun Disord
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392:(57): 374â393.
383:
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348:
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278:
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247:Neuroplasticity
234:
225:neuroplasticity
178:
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107:
91:Wernicke's area
83:
20:
12:
11:
5:
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1477:Basal ganglia
1474:
1472:
1468:
1467:
1465:
1464:
1463:
1462:
1457:
1451:Temporal lobe
1449:
1448:
1447:
1442:
1440:Anton syndrome
1437:
1432:
1424:
1423:
1422:
1417:
1412:
1407:
1401:Parietal lobe
1399:
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1397:
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1384:
1379:
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1356:
1339:
1337:
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1329:
1322:
1314:
1304:
1303:
1254:
1234:
1215:(1): S259â75.
1199:
1148:
1115:Eur. J. Neurol
1104:
1083:(8): 2206â11.
1063:
1022:
1003:(1): S225â39.
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1377:PCA syndrome
1372:MCA syndrome
1367:ACA syndrome
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1162:Behav Neurol
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99:frontal lobe
84:
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39:frontal lobe
34:
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26:
22:
21:
1612:) (lateral)
1445:Pure alexia
917:Aphasiology
896:14 November
686:Aphasiology
589:October 22,
520:J. Neurosci
429:Aphasiology
351:Aphasiology
202:agrammatism
162:(ASHA) and
115:perisylvian
95:paraphasias
71:hemiparesis
1752:Categories
1508:Cerebellum
891:aphasia.ca
827:2066/72791
655:2017-11-13
272:References
124:Wernickeâs
1551:Brainstem
1519:Dysmetria
1471:Subcortex
1353:brainstem
1345:syndromes
1135:1468-1331
646:"Aphasia"
611:Neurology
501:148765359
449:0268-7038
371:0268-7038
232:Prognosis
176:Treatment
146:Diagnosis
1758:Aphasias
1653:Midbrain
1515:Lateral
1486:Dystonia
1298:11001162
1229:18230850
1194:22063820
1143:21554494
1099:26106114
1058:12649521
1017:18230848
947:18923644
872:11407567
836:20155573
791:27296243
752:Medscape
733:11322572
650:asha.org
550:15647494
414:24469031
260:See also
1628:basilar
1559:Medulla
1535:Medial
1382:Aphasia
1289:3086401
1185:5377972
982:2065258
938:2557073
631:6538298
541:6725497
406:9126422
120:Broca's
111:infarct
18:Aphasia
1481:Chorea
1395:Abulia
1343:, and
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1077:Stroke
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585:. 2017
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254:lesion
105:Causes
1725:Other
1705:Other
1349:brain
962:Brain
497:S2CID
410:S2CID
1610:AICA
1594:Pons
1571:PICA
1351:and
1294:PMID
1225:PMID
1190:PMID
1139:PMID
1131:ISSN
1095:PMID
1054:PMID
1013:PMID
978:PMID
943:PMID
898:2017
868:PMID
832:PMID
787:PMID
729:PMID
627:PMID
591:2018
546:PMID
445:ISSN
402:PMID
367:ISSN
122:and
89:and
27:TMoA
1679:PCA
1666:PCA
1583:ASA
1284:PMC
1276:doi
1217:doi
1180:PMC
1170:doi
1123:doi
1085:doi
1044:doi
1005:doi
970:doi
966:114
933:PMC
925:doi
860:doi
822:hdl
814:doi
779:doi
721:doi
694:doi
619:doi
536:PMC
528:doi
489:doi
437:doi
394:doi
359:doi
56:or
33:or
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