Imura called Gogi aphasia “semantic form of aphasia” [14] or “semantic-form aphasia” [17] contrasting it with “phonetic form of aphasia” such as Broca’s and Wernicke’s aphasia.
As for the fourth feature of Gogi aphasia, Imura’s stance was rather vague. Although he included it as one of the core features of Gogi aphasia, he was prudent to regard the difficulty as an integral part of the syndrome. Thus, in the original paper [1], he admitted that no complete correspondence between symptoms of speech and written language could be confirmed, since every case he had encountered did not necessarily show this pattern of difficulty in written language. But in the subsequent papers, he seemed to have gained confidence to claim that this particular pattern of kanji-kana dissociation is an essential part of the syndrome [14, 16, 17]. Imura also argued that the selective difficulty in kanji handling in Gogi aphasia is caused by its logographic nature, in which a single kanji character stands for multiple sounds and concepts simultaneously [16]. This complexity necessarily burdens a reader with the decision making to choose a correct pronunciation from possible candidates every time he has to read a sentence aloud.
Later studies either included the fourth feature of Imura’s Gogi aphasia as one of the core symptoms [5, 9] or excluded it as coincidental [18, 19].
Responsible Lesions
Imura speculated that responsible lesions for Gogi aphasia are rather diffuse, involving the second and third temporal gyri and adjacent parietal lobe on the left side [16].
One of his cases (the above quoted case E) had been slowly deteriorating, leading Imura to presume a possibility of presenile dementia for its etiology [6]. The autopsy finding described by Pick of the case with “surdite verbale representative” (case F) which had also been slowly progressive showed the presence of diffuse cerebral atrophy, mainly affecting the left temporal lobe [15].
In 1991, Kurachi and Matsubara reported their experience on 11 cases of clinically diagnosed Pick’s disease, of them three had been autopsy confirmed [20]. Of the three, one had been reported as a typical case of Gogi aphasia 7 years earlier [21]. The case showed prominent bilateral atrophy of the middle and inferior temporal gyrus and the fusiform gyrus, but the extent of atrophy was much stronger on the left side.
In the following year, Tanabe et al. [7] reported their experience on 7 cases of Gogi aphasia, of which 6 were diagnosed as suffering from Pick’s disease of temporal lobe type. All the diagnosis was based on the findings of CT or MRI studies, which showed bilateral atrophy of the anterior and middle temporal lobes, the left being more affected. The present author also encountered 2 cases of typical Gogi aphasia caused by temporal lobe degeneration [9, 22].
But it has to be emphasized that Pick’s disease is not the only cause of Gogi aphasia. Imura’s 2 other cases suffered from non-progressive brain pathology, that is, hemorrhage and infarction. The patient of Sasanuma and Monoi [5] suffered from a head trauma. A surgical operation confirmed the presence of brain contusion as well as hematoma in the left second and third temporal gyri and the parietal lobe. Tanabe’s experience includes a case of herpes simplex encephalitis [7]. Such non-progressive etiology continues to be reported. For instance, Matsuda et al. [10] described 2 cases of stroke and one case of head trauma with MRI confirmation. Funayama described a case of cerebral infarction caused by sinus thrombosis [23].
Thus, it seems there are 2 types of Gogi aphasia. One is progressive, and wider mental deterioration eventually ensues. This type is closely associated with Pick’s disease of temporal lobe type [20]. The lesion involves bilateral temporal lobes even though the atrophy of the left side is much more prominent. The other is caused by various etiologies such as stroke, trauma, and encephalitis involving the lower temporal lobe. Symptoms of this type either remain stable or improve. The herpes simplex case and traumatic cases almost certainly must have suffered from bilateral damage of the temporal lobes. Even with stroke cases, bilateral lesions were demonstrated by MRI studies [10]. Thus, bilateral lesions of the temporal lobes seem to be a necessary condition for the emergence of Gogi aphasia. But the possibility of a left unilateral lesion causing this unique loss of lexical meaning cannot be easily discarded [23].
Gogi Aphasia and Semantic Dementia
In 1989, Snowden et al. [24] reported three cases of “semantic dementia,” characterized by progressive breakdown in language and visual perception. All three showed loss of symbolic meaning affecting both verbal and non-verbal domains. All suffered from progressive lobar degeneration limited to bilateral anterior temporal lobes (temporal lobe type of Pick’s disease in older terminology). The linguistic part of the syndrome is characterized by impaired comprehension and naming, but with well articulated speech with normal syntax and preserved repetition [24]. Based on experiences of 5 cases, Hodges et al. [25] further elaborated the nature of this “semantic dementia” as characterized by fluent dysphasia with severe anomia, reduced vocabulary, and prominent impairment of single-word comprehension. Of course, the concept of “semantic dementia” implies combined deterioration of linguistic meaning such as words and non-linguistic meaning such as faces, the linguistic part of the clinical picture corresponds with Gogi aphasia [26, 27].
Preferred occurrence of single-word meaning loss by damage of the left temporal lobe at a certain stage of progressive lobar degeneration suggests that a yet to be identified region or regions in the lobe occupies a pivotal part of a distributed neural network responsible for such a complex cognitive experience as “meaning” of a word.
References
1Imura
