Abstract
Thalamic hemorrhage of the dominant hemisphere has been known to lead to abnormalities of language. However, the role of thalamus in language function and the pathophysiology of language disorders following a damage of the thalamus in the dominant hemisphere remain controversial. Recently, main clinical pictures of language disturbances following left thalamic hemorrhage has been recognized to be similar to the “transcortical” aphasia.
In this report, two patients with left thalamic hemorrhage who showed clinical pictures of the transcortical sensory aphasia were presented. A 62-year-old and a 66-year-old male were admitted to the National Cardiovascular Center with complaints of slightly disturbed consciousness, motor weakness of right extremities and no verbal output. Computed tomographic examinations revealed left thalamic hemorrhage with rupture into the ventricles in both patients. Language disturbances in the acute stage were characterized by paucity of spontaneous speech with diminished voice volume, marked disturbances of verbal comprehension and intact repetition with echolalia.
The Standard Language Tests for Aphasia (SLTA) that were performed two months after the insults revealed pronounced disturbances of verbal comprehension with paraphasia and perseveration. Agraphia and acalculia were apparent. Although almost all modalities of language function were impaired, ability of repetition was characteristically preserved. They were able to repeat a sentence with several words completely and fluently. Results of the SLTA suggested that language disturbances in these two patients were consistent with those of the transcortical sensory aphasia.
Measurements of regional cerebral blood flow by 133Xe inhalation technique revealed pronounced ischemia in the left parieto-temporo-occipital region in the first case and diffuse ischenia in the left cerebral hemisphere in the second. Topographical mapping of the electroencephalography showed depletion of alpha and beta components and predominance of diffuse theta and delta components especially in the left cerebral hemisphere.
The pathophysiologic mechanisms of the transcortical aphasia following the left thalamic lesion were discussed.
