Conduction aphasia
| Conduction aphasia | |
 | |
|---|---|
| Broca's area and Wernicke's area | |
| MeSH | D018886 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmad Muneeb, MBBS[2] Synonyms and keywords: Dysphasia, Conduction; Associative Aphasia; Aphasia, Associative; Associative Aphasias; Dysphasias, Conduction; Aphasias, Associative; Conduction Aphasia; Conduction Dysphasias; Associative Dysphasias; Associative Dysphasia; Conduction Dysphasia; Dysphasias, Associative; Dysphasia, Associative; Aphasias, Conduction; Conduction Aphasias
Overview
Conduction aphasia, also called associative aphasia, is a relatively rare form of aphasia, thought to be caused by a disruption in the fiber pathways connecting Wernicke's and Broca's areas. The arcuate fasciculus is the most commonly involved pathway although evidence of other pathway involvement has also been found. Conduction aphasia is characterized by impaired repetition. Usually, writing, comprehension, and fluency remain intact. Neuroimaging can identify the underlying etiology. Speech therapy can improve recovery in patients suffering from conduction aphasia.
Historical Perspective
- Conduction aphasia was first described by Carl Wernicke in the year 1874. At first, Wernicke hypothesized that conduction aphasia was caused by damage to a pathway running through the insula and connecting Broca's area and auditory association area but later the evidence proved that arcuate fasciculus was the main pathway involved in conduction aphasia. In 1885, Lichtheim described this disorder further.[1][2]
Classification
- Conduction aphasia may be classified into 2 subtypes.[3]
Pathophysiology
- The pathogenesis of conduction aphasia involves damage to arcuate fasciculus. Arcuate fasciculus is a white matter tract connecting Broca's and Wernicke's areas, the areas responsible for motor and sensory components of speech. Thus, when arcuate fasciculus is damaged the connection between Broca's and Wernicke's areas is lost. As a consequence, the transmission of information between the 2 speech centers is halted, leading to impairment of repetition.[4] Recent studies have indicated that conduction aphasia can result from brain damage to areas other than arcuate fasciculus, though the underlying mechanism involves disruption of connections between language centers. [5]
Causes
The most common cause of conduction aphasia is damage to arcuate fasciculus lying deep to left supra marginal gyrus. Other common causes of conduction aphasia include damage to other brain areas including leftsuperior temporal gyrus, left primary auditory cortices, insula and left inferior parietal lobe. Damage can be caused by multiple insults including stroke, tumors, infections. [6][7][4]
Differentiating conduction aphasia from other Diseases
- Conduction aphasia must be differentiated from other diseases that cause speech/language problems such as:[4]
Epidemiology and Demographics
- Prevalenece of aphasia in United States is approximately 1 million.[8]
- The annual incidence of aphasia in United States is estimated to be 180,000 cases. [8] Separate epidemiological data for conduction aphasia is not availabe.
Age
Gender
- Conduction aphasia affects men and women equally.
Race
- There is no racial predilection for conduction aphasia.
Risk Factors
- Common risk factors in the development of conduction aphasia are stroke, CNS infections, tumor. [4]
Natural History, Complications and Prognosis
- Prognosis depends upon the underlying etiology. If the conduction aphasia occurs as a result of stroke, then there is a probability of making a good recovery but persistent speech deficits may still remain. [4]
Diagnosis
Diagnostic Criteria
There is no established diagnostic criteria for the diagnosis of conduction aphasia.
History and Symptoms
- Symptoms of conduction aphasia may include the following:[4][10]
- impaired repetition
- paraphasic errors e.g fireball → firewall
- "conduit d’approache" (Often the responses are close to the target words, and the patient does repeated effort to correct the errors)
- abnormal confrontational naming
- Difficulty reading in loud voice
- Speech fluency, reading, writing and comprehension may remain intact.
In some cases, symptoms of conduction aphasia may only last for few hours or few days.
Physical Examination
- Physical examination is usually normal but may be remarkable for different findings depending upon the part of brain damaged. These may include:[10]
Laboratory Findings
- There are no specific laboratory findings associated with conduction aphasia.
Electrocardiogram
There are no ECG findings associated with conduction aphasia.
X-ray
There are no x-ray findings associated with conduction aphasia.
Echocardiography or Ultrasound
There are no echocardiography/ultrasound findings associated with conduction aphasia.
CT scan
Brain CT scan may be helpful in the diagnosis of underlying etiology of conduction aphasia. As conduction aphasia is caused by damage in dominant hemisphere so ct scan can show stroke, tumor, infection or other pathologies of dominant hemisphere. [4]
MRI
Brain MRI may also be helpful in the diagnosis of the underlying etiology of conduction aphasia, as it can identify the pathologies of dominant hemisphere including stroke, infection, tumor etc. [4]
Other Imaging Findings
There are no other imaging findings associated with conduction aphasia.
Other Diagnostic Studies
Other diagnostic tests for conduction aphasia include Western Aphasia Battery-Revised and Boston Diagnostic Aphasia Examination. These tests assess attributes like comprehension, articulation, writing, problem-solving, and other features that can be affected by aphasia. [11] [12]
Treatment
Medical Therapy
- There is no medical treatment for [conduction aphasia]; the mainstay of therapy is speech and language therapy. Most patients make a considerable recovery with speech and language therapy. [4]
Surgery
- There is no surgical treatment directed for improvement of aphasia. However, surgery can be performed to eradicate certain causes leading to aphasia like tumors or infections. [4]
Prevention
- There are no primary preventive measures available for conduction aphasia.
References
- ↑ Hickok G (September 2009). "The functional neuroanatomy of language". Physics of Life Reviews. 6 (3): 121–43. doi:10.1016/j.plrev.2009.06.001. PMC 2747108. PMID 20161054.
- ↑ Benson, D. Frank (1973). "Conduction Aphasia". Archives of Neurology. 28 (5): 339. doi:10.1001/archneur.1973.00490230075011. ISSN 0003-9942.
- ↑ Dronkers, N.F.; Baldo, J.V. (2009). "Language: Aphasia": 343–348. doi:10.1016/B978-008045046-9.01876-3.
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 4.8 4.9 Acharya AB, Maani CV. "Conduction Aphasia - StatPearls - NCBI Bookshelf". statpearls publishing.
- ↑ Benson DF, Sheremata WA, Bouchard R, Segarra JM, Price D, Geschwind N (May 1973). "Conduction aphasia. A clinicopathological study". Archives of Neurology. 28 (5): 339–46. doi:10.1001/archneur.1973.00490230075011. PMID 4696016.
- ↑ Jiménez de la Peña MM, Gómez Vicente L, García Cobos R, Martínez de Vega V (2018). "Neuroradiologic correlation with aphasias. Cortico-subcortical map of language". Radiologia. 60 (3): 250–261. doi:10.1016/j.rx.2017.12.008. PMID 29439808.
- ↑ Damasio H, Damasio AR (June 1980). "The anatomical basis of conduction aphasia". Brain : a Journal of Neurology. 103 (2): 337–50. doi:10.1093/brain/103.2.337. PMID 7397481.
- ↑ 8.0 8.1 "Aphasia: Incidence & Prevalence".
- ↑ Ellis C, Urban S (December 2016). "Age and aphasia: a review of presence, type, recovery and clinical outcomes". Topics in Stroke Rehabilitation. 23 (6): 430–439. doi:10.1080/10749357.2016.1150412. PMID 26916396.
- ↑ 10.0 10.1 Swanberg, Margaret M.; Nasreddine, Ziad S.; Mendez, Mario F.; Cummings, Jeffrey L. (2007). "Speech and Language": 79–98. doi:10.1016/B978-141603618-0.10006-2.
- ↑ Roth, Carole (2011). "Boston Diagnostic Aphasia Examination": 428–430. doi:10.1007/978-0-387-79948-3_868.
- ↑ "WAB-R Western Aphasia Battery-Revised".