CP is pain due to a CNS lesion along the spinothalamoparietal path. Thus, an appropriate lesion must be demonstrated in such a location. At the same time, the presence of PNP, which may mimic CP (e.g., diabetic polyneuropathy in stroke patients), but also nociceptive musculoskeletal pains, must be excluded. A common source of diagnostic uncertainty is that symptoms of CPSP regularly occur after a significant passage of time from the precipitating event, calling for careful interviewing.

CP is a somatosensory symptom. Nonsensory symptoms and signs do occur in many patients with CP, because they are a direct consequence of the lesions, which are seldom restricted to somatosensory structures, but these may be lacking completely.

CP is independent of nonsensory abnormalities, namely in muscle function, coordination, vision, hearing, vestibular functions and higher cortical functions, and these may be present at the moment of examination or have subsided. In addition, the degree of pain and sensory abnormalities may not be necessarily correlated with the severity of other neurologic disabilities (Riddoch 1938; Garcin 1968; Tasker 2001). The distribution of these abnormalities will overlap or contain the perceived location of the pain.

Mental status is usually normal and CP patients are no more depressed or anxious than other chronic pain patients; psychiatric consultation is unnecessary.