ABSTRACT
OBJECTIVE: To investigate the neuroanatomical correlation of conduction aphasia by analyzing neuroimage data of patients who were diagnosed as conduction aphasia after stroke. METHOD: Nine patients with conduction aphasia after stroke were retrospectively reviewed with their medical records. Language functions of patients were assessed by Korean-version Western Aphasia Battery (K-WAB). Stroke lesions were assessed by brain computed tomography or magnetic resonance images taken within 1 month after onset of stroke. RESULTS: The stroke subtypes were cerebral infarction in 5 patients and intracranial hemorrhage in 4 patients. The lesions were located in left hemisphere in 8 subjects and right hemisphere in 1 subject. The left hemispheric lesion were located in the insula and superior temporal lobe in 3, the inferior parietal lobe in 2, the corona radiate in 1, the basal ganglia in 1 patient and both corona radiata and basal ganglia in 1. The right hemispheric lesion was located in the inferior parietal and superior temporal lobe. CONCLUSION: 6 of 9 patients with conduction aphasia had brain lesions in the path of arcuate fasciculus in the left hemisphere, however, 3 of 9 patients showed other brain lesions. These findings suggested that conduction aphasia could be caused by heterogeneous brain lesions. The characteristic features of conduction aphasia according to diverse brain lesions may need further investigation.
ABSTRACT
We present a 79-year-old male with aphasic status that was confirmed by a 99m-Tc ethyl cysteinate diethylester (ECD) single photon emission computed tomography (SPECT). He was admitted to our hospital due to a sudden onset of aphasia. In a Korean-version Western Aphasia Battery (K-WAB) test, the patient was diagnosed with Wernicke's aphasia (aphasia quotient (AQ)=54.50). In a brain magnetic resonance image (MRI) revealed the lesion of an old intracranial hemorrhage in the left posterior temporal area. An electroencephalography (EEG) showed continuous slowing in the left temporal area. SPECT demonstrated focal hyperperfusion in the left temporal cortex anterior to the lesion. After the administration of phenytoin, the aphasia was much improved (follow-up K-WAB : AQ=70.00). In follow-up studies two months later, EEG showed no interval changes and SPECT revealed no focal hyperperfusion in the left temporal area. Simple partial seizure is not easy to diagnose especially when manifesting with nonmotor symptoms such as aphasia. In this case, Wernicke's apha-sia was the only manifestation of epileptic seizure, the EEG did not show any definite epileptiform discharges. SPECT showed focal hyperperfusion in the left temporal area which was supposed to be a seizure focus. We conclude that SPECT might be useful in diagnosing a simple partial seizure manifesting as aphasia without EEG change.