Overt naming fMRI pre- and post-TMS: Two nonfluent aphasia patients, with and without improved naming post-TMS

Two chronic, nonfluent aphasia patients participated in overt naming fMRI scans, pre- and post-a series of repetitive transcranial magnetic stimulation (rTMS) treatments as part of a TMS study to improve naming. Each patient received 10, 1-Hz rTMS treatments to suppress a part of R pars triangularis. P1 was a ‘good responder’ with improved naming and phrase length; P2 was a ‘poor responder’ without improved naming.Pre-TMS (10 years poststroke), P1 had significant activation in R and L sensorimotor cortex, R IFG, and in both L and R SMA during overt naming fMRI (28% pictures named). At 3 mo. post-TMS (42% named), P1 showed continued activation in R and L sensorimotor cortex, R IFG, and in R and L SMA. At 16 mo. post-TMS (58% named), he also showed significant activation in R and L sensorimotor cortex mouth and R IFG. He now showed a significant increase in activation in the L SMA compared to pre-TMS and at 3 mo. post-TMS (p < .02; p < .05, respectively). At 16 mo. there was also greater activation in L than R SMA (p < .08). At 46 mo. post-TMS (42% named), this new LH pattern of activation continued. He improved on the Boston Naming Test from 11 pictures named pre-TMS, to scores ranging from 14 to 18 pictures, post-TMS (2–43 mo. post-TMS). His longest phrase length (Cookie Theft picture) improved from three words pre-TMS, to 5–6 words post-TMS.Pre-TMS (1.5 years poststroke), P2 had significant activation in R IFG (3% pictures named). At 3 and 6 mo. post-TMS, there was no longer significant activation in R IFG, but significant activation was present in R sensorimotor cortex. On all three fMRI scans, P2 had significant activation in both the L and R SMA. There was no new, lasting perilesional LH activation across sessions for this patient. Over time, there was little or no change in his activation. His naming remained only at 1–2 pictures during all three fMRI scans. His BNT score and longest phrase length remained at one word, post-TMS.Lesion site may play a role in each patient’s fMRI activation pattern and response to TMS treatment. P2, the poor responder, had an atypical frontal lesion in the L motor and premotor cortex that extended high, near brain vertex, with deep white matter lesion near L SMA. P2 also had frontal lesion in the posterior middle frontal gyrus, an area important for naming (Duffau et al., 2003); P1 did not. Additionally, P2 had lesion inferior and posterior to Wernicke’s area, in parts of BA 21 and 37, whereas P1 did not.The fMRI data of our patient who had good response following TMS support the notion that restoration of the LH language network is linked in part, to better recovery of naming and phrase length in nonfluent aphasia.     

Dissociations of writing and praxis: Two cases in point

For normal writing it is essential that both motoric and linguistic competence be present; disruption of one or the other of these faculties may result in qualitatively different types of agraphia. Two right-handed patients became agraphic after left hemisphere lesions; pure apraxic agraphia in the absence of limb apraxia developed in one patient and pure linguistic agraphia in association with severe ideomotor limb apraxia in the other. The performance of these patients not only serves to illustrate the dissociation between the motoric and linguistic faculties that underlie writing but also confirms that ideomotor limb apraxia and apraxic agraphia are distinct and dissociable entities.     

Category-Specific Naming Deficit for Medical Terms after Dominant Thalamic/Capsular Hemorrhage

Postmortem, retrograde degeneration, and electrical stimulation studies have implicated the anterior pulvinar in language processing. We examined a patient who, after a hemorrhage affecting the dominant pulvinar and internal capsule, exhibited a circumscribed anomia for medical items and conditions. No other language disturbance was noted. Five category-specific word lists, matched for word frequency, were administered in a naming-to-definition format. Results indicated that the patient exhibited a significant category-specific naming deficit for medical items and conditions compared to matched control subjects. Although medical item lists were found to differ from nonmedical item lists in imageability and abstractness, B.C.'s category-specific deficit did not seem to be caused by word frequency, concept familiarity, imageability, or abstractness. Nor could the patient's performance be explained on the basis of deficits in broader semantic classifications (i.e., animate vs inanimate or man-made vs natural). The patient was unable to retrieve medical items even when given phonemic cues for those he could not name. Findings indicate that subtotal damage in the dominant pulvinar may create category-specific deficits.     

Apraxia in a patient with atypical cerebral dominance

Liepmann postulated that the left hemisphere of right-handed persons contains the "movement formulas" that control purposeful skilled movements of the limbs on both sides of the body. Accordingly, in right-handers apraxia should follow damage to the left hemisphere, whereas right hemisphere damage should not lead to apraxia. Although this is generally true, we recently examined a right-handed man who after a right hemispheric stroke became aphasic and apraxic with his nonparalyzed right hand. Our observations suggest that the right hemisphere of this right-handed man made a critical contribution to the planning and execution of skilled movements. This case provides evidence that right-handers should not be considered a homogeneous group in terms of cerebral motor dominance and that contrary to Liepmann's postulate, hemispheric dominance for the control of skilled movements does not entirely determine handedness.