Phantom limb pain: are cutaneous nociceptors and spinothalamic neurons involved in the signaling and maintenance of spontaneous and touch-evoked pain? A case report

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Abstract
A patient suffered multiple fractures of the right leg and a left brain-stem infarction involving the anterolateral fasciculus of the central nociceptive system following multiple trauma. Later, the right leg was amputated, resulting in spontaneous and touch-evoked phantom pain and mechanical stump allodynia. However, quantitative sensory testing revealed considerable impairment of sensations normally mediated by cutaneous nociceptors and central spinothalamic systems on the right body side, including the stump but nearly intact touch and vibration senses. Quantitative assessment of peripheral nociceptive C-fiber function (axon reflex vasodilatation and flare) showed no abnormalities on both sides. Sympathetic blocks did not change spontaneous and evoked pain. Epidural and spinal anesthesia abolished evoked pain but had no effect on spontaneous phantom pain. Extirpation of a neuroma of the sciatic nerve did not alter spontaneous and evoked pain. TENS resulted in an increase in pain. We concluded the following. (i) Painful somatosensory memories that are responsible for phantom limb pain are located in the brain, most probably in the thalamus or cortex. (ii) Touch-evoked phantom pain and stump allodynia are not mediated by cutaneous nociceptive C and A delta fibers and spinal nociceptive pathways (spinothalamic tract). Activity in the lemniscal system (low-threshold mechanoreceptive A beta afferents, dorsal columns and medial lemnicus system) may be transferred to central pain signaling neurons in the thalamus or cortex resulting in touch-evoked pain sensations. (iii) Ongoing activity in cutaneous nociceptive C fibers and spinal nociceptive systems is not necessary to maintain central processes that account for spontaneous and touch-evoked pain sensations. Activity in nociceptors of deep somatic tissues might be more important.