The sensation is seen in almost 100 % of surgical patients during the first month. The strongest sensation is associated with amputations above the elbow and weakest in amputations below the knee. It is seen in 85 % of amputations in the first 3 weeks of amputation. Most sensations resolve on their own within 2–3 years without any therapy, but some may extend onto and become phantom limb pain.

The phantom pain is seen in 55–65 % of amputations. The pain can occur as early as 1 week and may eventually fade away, but 60 % of patients continue to have pain. Although pain can occur at any time after the amputation, only 10 % of patients develop pain after 1 year of amputation. The pain may be associated with pain in other parts of the body, sore throat, abdominal pain and back pain.

The risk factors for phantom pain include phantom sensations, stump pain, prosthesis use, bilateral amputation and lower-limb amputation and previous severe pain before amputation.

Sunderland’s classification (based on pain):

Cortical imprinting of the body image once established does not change even with amputation, leading to phantom sensation. Phantom pain is a mix of peripheral, central and psychological mechanisms. Neuromas form in the stump in almost all the patients. Abnormal evoked activity is seen in nerve end neuromas due to up-regulation of sodium channels. Increased sympathetic discharge associated with stress activates neurons and may aggravate the pain. Increased stimuli from peripheral neurons and dorsal neurons cause long-term changes in projection neurons (spontaneous nerve activity, increase in spinal cord metabolism and increase in the diameter of reception fields). After the amputation, Aβ mechanoreceptors sprout and form connections with second-order neurons in lamina II due to degeneration of afferent C-fibre terminals. This causes pain on simple touch.