We have four cases of conduction aphasia to report. From a detailed neuropsychological analysis, we have subclassified conduction aphasia into three types. Case I : a 64 year old, right-handed man. He had showed the feature of aphasia similar to that of motor aphasia at the onset. He had severe difficulty in conversational speech. He had serious problems in naming and was prone to repetition. The difficulty in naming was greater than the difficulty of repetition. Conversational speech, naming and repetition contained abundant literal paraphasias. Case II : a 59 year old, right-handed man. He was chracterized by the following clinical picture : great impairment of spontaneous speech in contrast to good auditory comprehension, disturbance of repetition, abundant literal paraphasias in spontaneous speech and repetition, literal paralexia, and a large amount of literal paragraphias. Naming was invariably poor, with defects identical to those in repetition. Case III : a 65 year old, right-handed man. Case IV : a 68 year old, right-handed housewife. They had all exhibited the feature of aphasia similar to that of sensory aphasia at the onset and had a poor comprehension of spoken language. The problem of repetition was greater than the naming disability. Although the auditory comprehension improved soon, there was little improvement of the disturbance of repetition. As the auditory comprehension improved, the patients recovered to an anomic stage in which abundant literal paraphasias in spontaneous speech, naming and repetition was reduced. Ideomotor apraxia and constructive apraxia was present mildly. We have subclassified conduction aphasia as follows, 1. Broca (anterior) type: Case I 2. typical type: Case II 3. Wernicke (Posterior) type: Case III, IV We consider that the basic syndromes of conduction aphasia are literal paraphasia in spontaneous speech, naming and repetition. We also feel that conduction aphasia preserves word concepts, but in uttering the demanded word, there is a disorder in adequate selection and arrangement of phonemes in sequence, a disturbance at the level of phonemic programming.
Eighty-six stroke patients which was comprised of 63 cases of cerebral infarction and 23 cases of cerebral hemorrhage with speech disturbance and sign of dominant hemispheric lesion in chronic stage were investigated using the Standard Language Test for Aphasia, EEG including photic stimulation and cranial computed tomography (CCT). The purpose of this study was to demonstrate the differences between cerebral infarction and cerebral hemorrhage as seen in aphasic symptoms, EEG and CCT findings and also investigate the possible causes of those differences. In cerebral infarction, aphasic symptoms were variable in each case according to its type and severity. Although in cerebral hemorrhage, mild aphasia such as amnestic aphasia and mild Broca's aphasia were more commonly observed. In the cases of cerebral infarction, EEG findings were also variable and tended to show mild to moderate abnormality and low voltage in nature. Many of the cerebral hemorrhagics indicated severely abnormal EEG which consisted of high voltage slow wave and defective photic driving on both sides. In cerebral infarction, CCT revealed that distribution of low density area was again variable and was located mainly in the cortex. Although in the cases of cerearal hemorrhage, the low density area had a tendency to be confined to the basal ganglia and /or to the internal capsule. Some cases of cerebral infarction with wide spread low density area including more than three cerebral lobes showed normal to slightly abnormal EEG. In contrast with this, severely abnormal EEGs were rather common among the cases of cerebral hemorrhage with low density area which tended to be strictly confined to the basal ganglia and / or the internal capsule. From these results, the common site of the lesion was considered to be a major factor in the difference between cerebral infarction and cerebral hemorrhage as seen in aphasic symptoms, EEG and CCT findings. Namely, many cases of cerebral infarction have lesions in the cerebral cortex which produce aphasic symptoms of various kinds and affected voltage generator which is manifested by a low voltage pattern of EEG. In the cases of cerebral hemorrhage, common lesions were found in the deep structure involving the thalamocortical projection, which bring deafferentiation effect on EEG which is characterized by a high voltage slow wave.
As expressed using words such as “break down crying” or “roll with laughter” , crying or laughing is an expression of not only the face but also the feeling with the whole body. In 4 cases of forced laugher accompanied with astasia due to brain stem lesion and 5 cases of “Locked-in” syndrome, forced crying and forced laughter were clinicopathologically examined from the brain stem level. In an autopsy case of forced laughter, there was a lesion in the pars triangularis of Guillain-Mollaret, containing an element of clonus in the laughter. In a chronic case of “Locked-in” syndrome, tetraplegia was unchanged but head control, rotation to the gaze direction, anteflexion and retroflexion became possible. In addition, winking, swallowing and yauning were observed and a movement of mimic muscle then appeared, leading to forced crying. These events may be mediated by tectospinal tract. Three factors consisted of confrontation and antagonism existing between pyramidal tract and tectospinal tract in addition to myoclonus due to a lesion in the pars triangularis of Guillain-Mollaret may control the expressions of feeling, consequently giving such expressions as crying, laughing, break down crying, and roll with laughter.
A 20-year-old patient suffered from subarachnoidal hemorrhage, resulting from A-V malformation, and was admitted to our hospital three months after onset. At the time of admission, he exhibited amnestic aphasia, right homonimous hemianopia, and hyperreflexia in the right upper and lower extremities and also in the left upper extremity. He had marked difficulty in confrontation naming, and writing and oral reading of kanji, while his performance in other language tasks was relatively intact. We assumed that these three tasks required in some part the common neurolinguistic processes, which might be impaired in this patient. In confrontation naming, visual information undergoes semantic and phonological processing before being realized as speech sounds. Writing and oral reading of kanji also requires both semantic and phonological processing, since a kanji represents certain semantic information as well as phonological information. It follows from the above assumption, that training of one of the three tasks may restore the common impaired processes, thus improving the patient's performance in the other two tasks. A naming-training and an oral-reading-training of kanji were conducted successively. Use of language modalities was strictly controlled during the training so that the other two tasks would not be trained at the same time. Examination of the three tasks before and after each training revealed parallel improvement in confrontation naming and oral reading of kanji for the drilled words, but no improvement in writing. A similar error pattern was observed in confrontation naming and oral reading of kanji. Thus the result supported a part of our assumption that confrontation naming and oral reading of kanji shared the same processes, which were impaired in this patient. Error analysis based upon Fromkin's speech production model, together with other such findings as absence of neither visual agnosia nor articulatory disorders, and relatively intact repetition and kana manipulation suggested the impairment of semantic processing and /or the connexion between semantic and phonological processing. Writing ability of kanji did not improve in either training, which suggested involvement of other processes than those mentioned above.