Central pain syndrome originates from damage to the spinothalamic tract, the primary neural pathway that carries pain and temperature signals from the body to the thalamus for processing. When stroke, trauma, or disease disrupts this pathway, the thalamus and surrounding cortical areas lose their normal regulatory input. Studies estimate that 8-14% of stroke survivors develop central post-stroke pain, typically within the first year following the cerebrovascular event.
This loss of normal signaling triggers a process called central sensitization, in which surviving neurons become hyperexcitable and begin firing spontaneously or in response to normally innocuous stimuli. The thalamus, deprived of its balanced input, amplifies pain signals rather than filtering them, producing the constant burning, aching, or lancinating sensations characteristic of CPS.
The brain's descending pain-modulation system, which normally suppresses excessive pain signals through serotonergic and noradrenergic pathways, also becomes impaired after CNS damage. This dual failure of both ascending sensory processing and descending inhibition creates a self-sustaining pain state that conventional analgesics often cannot adequately control.
