Brain and Language 71, 258–260 (2000)doi:10.1006/brln.1999.2264, available online at http://www.idealibrary.com on

‘‘Exceptional’’ Case: What Does It Mean?

Atsushi Yamadori

Tohoku University Graduate School of Medicine, Sendai, Japan

Mechanisms of the production of neuropsychological symptoms in a braindamaged patient and mechanisms of normal cognitive processes should notbe confused. Cognitive pathologies vary depending on patients, but cognitiveprocesses should (or may) not. The clinical practice is a continuation of en-counters with exceptional cases reflecting the unavoidable variability of thesesymptoms. For instance, the symptomatic concept of fluency and nonfluencyin describing an aphasic speech proposed by Geschwind many years agoremains to be a very useful and important criteria for the bedside diagnosis indifferentiating posterior and anterior cerebral damage in aphasia (Goodglass,1993). Yet there exists exceptions. Sometimes anterior aphasics do producea fluent speech (Yamadori et al., 1984), suggesting that the anterior speecharea may not only serve as a mediator of verbal expression but also sharea similar role that is carried out by the posterior speech area whatever it maybe.

Based on enormous clinical facts collected over the past 150 years andsupported by well established anatomo-physiological knowledge of the brainfunction, we regard Broca’s and Wernicke’s aphasia as two of the most im-portant core syndromes among aphasic syndromes. Broca’s aphasia is inter-changeably called as anterior, motor, or nonfluent aphasia. Wernicke’s apha-sia likewise as posterior, sensory, or fluent aphasia. These names betray ourbelief that even language, the most human mental achievement, can be under-stood as a combined work of input and output processors. When output pro-cessors are disturbed, language would be impaired in its output function re-sulting in Broca’s aphasia. When input processors are damaged, it woulddestroy its input function resulting in Wernicke’s aphasia. Recent cognitivetheories of language processing is also built upon this implicit common un-

Address correspondence and reprint requests to Atsushi Yamadori, Section of Neuropsy-chology, Division of Disability Science, Tohoku University Graduate School of Medicine,2-1, Seiryomachi, Aobaku, Sendai, 980-8575, Japan. E-mail: yamadori@mail.cc.tohoku.ac.jp.

2580093-934X/00 $35.00Copyright 2000 by Academic PressAll rights of reproduction in any form reserved.

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derstanding. Take for example, a representative processing model of words(Rapp & Caramazza, 1998). A word is fed into the modality specific inputlexicon, that is, if it is written, into the orthographic input lexicon or if it’sspoken, into the phonological one, then into the semantic lexicon, then againto the orthographic or phonological output lexicon, and finally into the mo-dality specific output buffer. In this model, only the semantics is thought tobe free from input–output dichotomy.

This is a very reasonable model. But does it truly reflect our way of cogni-tive processing? Recently, I have encountered a puzzling patient. He showedevery sign of severe Wernicke’s aphasia. Auditory comprehension was se-verely impaired. Repetition was also impaired when a stimulus included twoor more syllables. Auditory sensory function was normal. Confrontationnaming was badly contaminated with paraphasias at syllabic level resultingin neologisms. Spontaneous speech was fluent, but composed of neologisticjargons. Oral reading was also chaotic with neologistic paraphasias. How-ever, at least at the word level, he showed a remarkably well-preserved nam-ing capacity, which was mostly written in kana characters (syllabographs).Interestingly, he was often able to correct his own writing errors of kanaspontaneously by reading them aloud character by character, indicating hepreserved ‘‘phonological lexicon’’ for referral. Comprehension of writtenwords which was tested both in kanji (ideographs or more accurately logo-graphs) and kana were also preserved.

How can we explain this exceptional Wernicke’s aphasia? Impairment ofthe selective phonological ‘‘input’’ lexicon cannot explain the picture. Inthat case, the phonological ‘‘output’’ lexicon and semantic lexicon are ex-pected to remain normal, which would result in mostly normal speech output.Impairment of both the phonological input lexicon and semantic lexicon isinconceivable because the latter must have been normal as evidenced bypreserved comprehension of written words. A rather ad hoc way to explainthe case may be to hypothesize that both the input and output phonologicallexicon were impaired, leaving the semantic lexicon in between intact. How-ever, it still cannot explain why he often succeeded in correcting his kanaerrors by reading aloud. With the impaired phonological output lexicon, itmust have been impossible. An unconventional, but plausible way to explainthis particular syndrome would be to hypothesize the existence of a phono-logical processor system undivided by input–output attribute. This amodalor in Jacksonian phraseology sensory-motor phonological processor must bethe one that was selectively damaged in this case. This system works as agate to the phonological lexicon which is also amodal and functions at a bithigher level. The semantic system must also have been preserved. Impair-ment of this hypothetical phonological processor would cause errors in deci-phering auditory verbal information resulting in comprehension difficultyand at the same time cause encoding difficulty resulting in paraphasic speech.This hypothesis may be applied to some of the published cases of Wernicke’s

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aphasia with incongruously well preserved written naming against distinctlydisturbed oral naming (Hier & Mohr, 1977). As many PET studies haveshown, ‘‘concurrent’’ cortical activities around the left Sylvian fissure is anorm rather than an exception with many linguistic tasks (Posner & Raichle,1994). Clinical studies also indicated the difficulty of separating sensory andarticulatory component in aphasic speech even with typical anterior or poste-rior aphasia cases (Blumstein, 1998).

As pointed out at the beginning, although classical symptomatology is ahelpful tool for clinical diagnosis and understanding of gross pathology ofthe brain, it may not necessarily lead to a correct insight into the essentialnature of normal brain functions of language. Exceptional cases keep posinga formidable challenge to students of clinical neuropsychology.

REFERENCES

Blumstein, S. A. 1998. Questions posed on anterior/posterior anatomical distinction andexpressive/receptive functional distinction: Phonological aspects of aphasia. In M. T.Sarno (Ed.), Acquired aphasia (third ed., pp. 157–185). San Diego: Academic Press.

Goodglass, H. 1993. Understanding aphasia. San Diego: Academic Press.

Hier, D. B., & Mohr, J. P. 1977. Incongruous oral and written naming. Brain and Language,4, 115–126.

Posner, M. I., & Raichle, M. E. 1994. Images of mind. New York: Scientific American Library.

Rapp, B. C., & Caramazza, A. 1998. Lexical deficits. In M. T. Sarno (Ed.), Acquired aphasia(third ed., pp. 187–227). San Diego: Academic Press.

Yamadori, A., Ohira, T., Seriu, M., & Ogura, J. 1984. Transcortical sensory aphasia producedby lesions of the anterior basal ganglia area. Brain and Nerve (Tokyo), 36, 261–266.