The present study used the altered auditory feedback (AAF) paradigm to investigate how post-stroke damages to the left hemisphere may impair sensorimotor processing of auditory feedback during speech motor control in patients with aphasia. We utilized the combination of neuroimaging-based lesion-symptom-mapping analysis, behavioral testing, and electrophysiological recordings to examine the pervasiveness of speech sensorimotor deficit and its relationship to the brain regions implicated. We recruited 20 patients with aphasia and 20 age-matched control subjects to complete a speech motor control task under AAF. The task involved producing a steady vowel sound while listening to the real-time pitch-shifted feedback of their speech. The implementation of this task allowed us to develop an objective biomarker of speech sensorimotor impairment by measuring the degree to which each subject behaviorally responded to AAF stimuli to compensate for errors in their speech auditory feedback signal. Results indicated that compensatory speech responses to AAF were significantly diminished in patients with aphasia compared with the control group, and this effect was accompanied by the attenuation of ERP components in response to AAF stimuli in the aphasic group. The correlation analysis revealed a strong and direct relationship between AAF responses and speech repetition ability, as indexed by the Western Aphasia Battery (WAB) scores. A region-of-interest lesion-symptom-mapping analysis revealed that the early phase (50-150 ms) of diminished AAF responses in aphasia was best predicted by damages to the cortical auditory regions within the superior and middle temporal gyri, whereas the middle (150-250 ms) and late (250-350 ms) phases of diminished AAF responses were correlated with damages to the inferior frontal gyrus (IFG) and supramarginal gyrus areas, respectively. These findings suggest that damage to the auditory, motor and auditory-motor integration networks are associated with impaired sensorimotor function for speech error processing in patients with aphasia. Our data suggest that specific aspects of language impairment (i.e. speech repetition deficit) are accounted for by dysfunctions of the speech sensorimotor integration network as revealed by diminished responses to AAF. These findings provide new insights into the relationship between pathologically-diminished integrative function underlying speech auditory feedback processing and the implicated brain lesions associated with language deficits in patients with post-stroke aphasia.