J Clin Neurol.  2006 Sep;2(3):149-162. 10.3988/jcn.2006.2.3.149.

Aphasia and the Diagram Makers Revisited: an Update of Information Processing Models

Affiliations
  • 1The James E. Rooks Jr. Distinguished Professor, Department of Neurology, University of Florida College of Medicine, and VAMC, Gainesville, Florida, USA. heilman@neurology.ufl.edu

Abstract

Aphasic syndromes from diseases such as stroke and degenerative disorders are still common and disabling neurobehavioral disorders. Diagnosis, management and treatment of these communication disorders are often dependent upon understanding the neuropsychological mechanisms that underlie these disorders. Since the work of Broca it has been recognized that the human brain is organized in a modular fashion. Wernicke realized that the types of signs and symptoms displayed by aphasic patients reflect the degradation or disconnection of the modules that comprise this speech-language network. Thus, he was the first to propose a diagrammatic or information processing model of this modular language-speech network. Since he first published this model many new aphasic syndromes have been discovered and this has led to modifications of this model. This paper reviews some of the early (nineteenth century) models and then attempts to develop a more up-to-date and complete model.

Keyword

Aphasia; Module; Information processing model; Speech; Language

MeSH Terms

Aphasia*
Automatic Data Processing*
Brain
Communication Disorders
Diagnosis
Humans
Stroke

Figure

  • Figure 1 Wernicke's schema. In this model disruption of Wernicke's area (B) induces Wernicke's aphasia (fluent jargon, impaired comprehension, repetition and naming), C; conduction aphasia (fluent with phonemic paraphasic errors, impaired repetition, naming, intact comprehension of major lexical items), D; Broca's aphasia (non-fluent, impaired naming and repetition, intact comprehension of major lexical items).

  • Figure 2 Wernicke-Lichtheim's schema. In this model interruption of pathway E or degradation of F (the semantic-conceptual field) would produce transcortical sensory aphasia with fluent speech, impaired comprehension, but normal repetition. Interuption of pathway G would induce transcortical motor aphasia with a loss of spontaneous speech, but with intact repetition and comprehension.

  • Figure 3 Wernicke-Kussmaul's Schema. In this model interruption of pathway G would induce an anomic aphasia (fluent with circumlocution, impaired naming with intact repetition and comprehension). Degradation of the semantic conceptual representations or interruption of pathways E and G would induce a transcortical sensory aphasia. The difference between the latter and former forms of transcortical aphasia is that unlike degradation of the conceptual representations, disruption of the pathways would be associated with the preservation of semantic conceptual representations as assessed by associative or categorical picture tests.

  • Figure 4 Modified Wernicke-Kussmaul schema. The former model could not account to the two forms of transcortical aphasia and this model can explain speech akinesia (pathway P-O), adynamic aphasia (pathway P-J) or a combination. In addition, interruption of pathway C would induce "deep aphasia" and injury to the output lexicon (D) or it connection the Broca's area would induce conduction aphasia.

  • Figure 5 Modified Wernicke-Kussmaul-Lichtheim schema. In this modification there is a direct pathway (Q) from the semantic conceptual field (I) to Broca's area. Patients with anomic aphasia (disruption of pathway M) and conduction aphasia (interruption of E or injury to the phonological output lexicon (D) can often circumlocute and make semantic paraphasic errors and it is possible that this speech is mediated by pathway I-Q-F.

  • Figure 6 Modified Wernicke-Kussmaul-Lictheim-Freund schema. This final schema allows us to explain both optic aphasia (interruption or impairment of pathway L-N-D-E-F) and non-optic aphasia (impairment of the network represented by pathway L, K, I). This final combination model also helps explain almost all the known forms of aphasia. In this model interruption of the following areas or pathways induce the following forms of aphasia. A; pure word deafness, B; Wernicke's aphasia, C; deep dysphasia, D and E; conduction aphasia, F; Broca's aphasia, H; transcortical aphasia with intact naming and concepts, I; transcortical sensory aphasia with impaired concepts. G; aphemia, M; anomic aphasia, J; adynamic aphasia, O; speech akinesia.


Reference

1. Head H. Aphasia and Kindred Disorders of Speech. 1926. Volume 1. Cambridge: Cambridge University Press;54–60. Chapter 4.
2. Broca P. Remarques sur le siege de la faculte du language articule, suivies d' une observation d' aphemie. Bull Soc Anat. 1861. 2:330–357.
3. Trousseau A. De l' aphasie, maladie decrite recemment souls le nom improper d' aphemie. Gaz Hop. 1864. 37.
4. Mohr JP, Pessin MS, Finkelstein S, Funkenstein HH, Duncan GW, Davis KR. Broca aphasia: pathologic and clinical. Neurology. 1978. 28:311–324.
Article
5. Whitaker HA, Etlinger SC. Theodor Meynert's contribution to classical 19th century aphasia studies. Brain Lang. 1993. 45:560–571.
Article
6. Wernicke C. Das Aphasiche Symptomenkomplex. 1874. Breslau: Cohn and Weigart.
7. Bastian HC. Aphasia and Other Speech Defects. 1898. London: H. K. Lewis.
8. Kussmaul A. Die Storungen der Sprache. 1877. Leipsig: Vogel.
9. Lichtheim L. On Aphasia. Brain. 1885. 7:433–484.
Article
10. Feinberg TE, Gonzalez-Rothi LJ, Heilman KM. Inner speech' in conduction aphasia. Arch Neurol. 1981. 43:591–593.
Article
11. Heilman KM, Tucker DM, Valenstein E. A Case of Mixed Transcortical Aphasia with Intact Naming. Brain. 1976. 99:415–525.
Article
12. Heilman KM, Gonzalez-Rothi LJ, McFarling D, Rottman A. Transcortical Sensory Aphasia with Relatively Spared Spontaneous Speech in Naming. Arch Neurol. 1981. 38:236–239.
Article
13. Benson DF. Ardila Aphasia. 1996. New York: Oxford University Press.
14. Michel F, Andreewsky E. Deep dysphasia: an analog of deep dyslexia in the auditory modality. Brain Lang. 1983. 18:212–223.
Article
15. Katz RB, Goodglass H. Deep dysphasia: analysis of a rare form of repetition disorder. Brain Lang. 1990. 39:153–185.
Article
16. Roth HL, Nadeau SE, Hollingsworth AL, Marie Cimino-Knight A, Heilman KM. Naming concepts: evidence of two routes. Neurocase. 2006. 12:61–70.
Article
17. Freund CS. Uber optische Aophasie und Seelenblindheit. Arch. F. Psychiat. 1889. 20.
18. Feinberg T, Gonzalez-Rothi LJ, Heilman KM. Multimodal agnosia from a unilateral left hemisphere lesion. Neurology. 1986. 36:864–867.
Article
19. Shuren J, Geldmacher D, Heilman KM. Non-optic aphasia. Neurology. 1993. 43:1900–1907.
20. Nadeau SE. Phonology: a review and proposals from a connectionist perspective. Brain Lang. 2001. 79:511–579.
Article
21. Heilman KM, Voeller K, Alexander A. Developmental dyslexia: a motor articulatory feedback hypothesis. Annals of Neurology. 1996. 39:407–412.
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