Spinal cord injury (SCI) pain is a debilitating chronic condition that is severe and unrelenting. Despite decades of extensive research, the neuropathological mechanisms responsible for the development of this devastating condition remain largely unknown, hindering our ability to develop effective treatments. Because several lines of evidence implicate abnormalities of the thalamus and cortex in the etiology of SCI pain, we hypothesized that SCI pain results from abnormal functional connectivity of brain areas heavily implicated in pain processing. We performed a longitudinal study in a rat model of SCI (SCI group, n = 8; sham-operated group, n = 6) and acquired resting-state functional magnetic resonance imaging scans before spinal surgery and 3, 7, 14, and 21 (SCI only) days after surgery in the same animals. Functional connectivity was decreased between the ventroposterior lateral thalamus (VPL) and primary somatosensory cortex (S1) 7 d after SCI. This reduction preceded an increase in connectivity between S1 and other cortical areas involved in nociceptive processing. In addition, VPL had increased connectivity to contralateral thalamus at 7 and 14 d after injury. The temporal pattern of the increase in functional connectivity within the thalamus and between cortical areas (particularly S1 and retrosplenial cortex) had a striking resemblance to the temporal pattern for the development of a "below-level" mechanical hypersensitivity in the same animals. Our findings suggest that below-level hypersensitivity is associated with functional disconnection (asynchrony) between the thalamus and cortical areas involved in nociceptive processing.