Improved language in a chronic nonfluent aphasia patient after treatment with CPAP and TMS.

OBJECTIVE: To present pretreatment and post-treatment language data for a nonfluent aphasia patient who received 2 treatment modalities: (1) continuous positive airway pressure (CPAP) for his sleep apnea, starting 1-year poststroke; and (2) repetitive transcranial magnetic brain stimulation (TMS), starting 2 years poststroke. BACKGROUND: Language data were acquired beyond the spontaneous recovery period of 3 to 6 months poststroke onset. CPAP restores adequate oxygen flow throughout all stages of sleep, and may improve cognition. A series of slow, 1 Hz repetitive TMS treatments to suppress a posterior portion of right pars triangularis has been shown to improve phrase length and naming in chronic nonfluent aphasia. METHOD: The Boston Diagnostic Aphasia Examination and Boston Naming Test were administered pre-CPAP, and after 2 to 5 months of CPAP. These same tests were administered pre-TMS, and at 3 and 6 months post-TMS, and again 2.4 years later. RESULTS: Post-CPAP testing showed increased Phrase Length, Auditory Comprehension, and naming Animals and Tools/Implements (Boston Diagnostic Aphasia Examination). Testing at 3 and 6 months post-TMS showed significant increase in Phrase Length, Auditory Comprehension, and Boston Naming Test compared with pre-TMS. These gains were retained at 2.4 years post-TMS. CPAP use continued throughout. CONCLUSIONS: Physiologic treatment interventions may promote language recovery in chronic aphasia.

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.