Motion information can reach V5/MT through two parallel routes: one conveying information at early latencies through a direct subcortical route and the other reaching V5 later via recurrent projections through V1. Here, we tested the hypothesis that input via the faster direct pathway depends on motion characteristics. To this end, we presented motion stimuli to healthy human observers at different velocities (4.4°/sec vs. 23°/sec) with static stimuli as controls while applying transcranial magnetic stimulation (TMS) pulses over V5 or V1. We probed for TMS interference with objective (two-alternative forced choice [2AFC]) and subjective (awareness) measures of motion processing at six TMS delays from stimulus onset (poststimulus window covered: ∼27–160 msec). Our results for V5–TMS showed earlier interference with objective performance for fast motion (53.3 msec) than slow motion (80 msec) stimuli. Importantly, TMS-induced decreases in objective measures of motion processing did correlate with decreases in subjective measures for slow but not fast motion stimuli. Moreover, V1–TMS induced a temporally unspecific interference with visual processing as it impaired the processing of both motion and static stimuli at the same delays. These results are in accordance with fast moving stimuli reaching V5 through a different route than slow moving stimuli. The differential latencies and coupling to awareness suggest distinct involvement of a direct (i.e., colliculo-extrastriate) connection bypassing V1 depending on stimulus velocity (fast vs. slow). Implication of a direct pathway in the early processing of fast motion may have evolved through its behavioral relevance.

Changes in brain activity characterizing impaired speech production after brain damage have usually been investigated by comparing aphasic speakers with healthy subjects because prestroke data are normally not available. However, when interpreting the results of studies of stroke patients versus healthy controls, there is an inherent difficulty in disentangling the contribution of neuropathology from other sources of between-subject variability. In the present work, we had an unusual opportunity to study an aphasic patient with severe anomia who had incidentally performed a picture naming task in an ERP study as a control subject one year before suffering a left hemisphere stroke. The fortuitous recording of this patient's brain activity before his stroke allows direct comparison of his pre- and poststroke brain activity in the same language production task. The subject did not differ from other healthy subjects before his stroke, but presented major electrophysiological differences after stroke, both in comparison to himself before stroke and to the control group. ERP changes consistently appeared after stroke in a specific time window starting about 250 msec after picture onset, characterized by a single divergent but stable topographic configuration of the scalp electric field associated with a cortical generator abnormally limited to left temporal posterior perilesional areas. The patient's pattern of anomia revealed a severe lexical–phonological impairment and his ERP responses diverged from those of healthy controls in the time window that has previously been associated with lexical–phonological processes during picture naming. Given that his prestroke ERPs were indistinguishable from those of healthy controls, it seems highly likely that the change in his poststroke ERPs is due to changes in language production processes as a consequence of stroke. The patient's neurolinguistic deficits, combined with the ERPs results, provide unique evidence for the role of left temporal cortex in lexical–phonological processing from about 250 to 450 msec during word production.

Impaired word production after brain damage can be due to impairment at lexical–semantic or at lexical–phonological levels of word encoding. These processes are thought to involve different brain regions and to have different time courses. The present study investigated the time course of electrophysiological correlates of anomia in 16 aphasic speakers, divided in two subgroups according to their anomic pattern (8 with lexical–semantic impairment and 8 with lexical–phonological impairment), in comparison to 16 healthy control subjects performing the same picture naming task. Differences in amplitudes and in topographic maps between groups were differently distributed when the whole heterogeneous group of aphasic patients was compared to the control group and when the two more homogeneous subgroups of anomic patients were analyzed. The entire aphasic group expressed different waveforms and topographic patterns than the control group starting about 100 msec after picture presentation. When two subgroups of aphasic patients are considered according to the underlying cognitive impairment, early event-related potential (ERP) abnormalities (100–250 msec) appeared only in the lexical–semantic subgroup, whereas later ERP abnormalities (300–450 msec) occurred only in the lexical–phonological subgroup. These results indicate that the time windows of ERP abnormalities vary depending on the underlying anomic impairment. Moreover, the findings give support to current hypotheses on the time course of processes involved in word production during picture naming.