In the syndrome of post-herpetic neuralgia (PHN), the nature of the sensory disturbance and its relationship both to the severity and cause of the pain is controversial. To address these issues, sensory mapping and quantitative thermal sensory testing was carried out four times in separate sessions on 35 subjects with established PHN. All subjects had pain affecting the torso or extremities and brush-evoked allodynia. Each session included rating of ongoing pain, mapping of the area of any sensory disturbance and the area of greatest pain, grading of allodynia severity within the area of greatest ongoing pain, and quantitative testing of thermal sensation in both the painful and the contralateral unaffected mirror-image skin. The severity of allodynia was positively correlated with reported ongoing pain severity. As a group, subjects had a sensory deficit to thermal stimuli in PHN skin compared with unaffected mirror-image skin. However, the magnitude of the heat pain sensory deficit was inversely correlated with both pain intensity and severity of allodynia. In fact, 12 subjects had heat hyperalgesia in their region of maximum pain. Compared with the 23 subjects with heat hypoalgesia, the group of 12 heat hyperalgesic subjects had significantly higher pain ratings and allodynia severity. Sensory loss was less strongly, but still inversely related to pain severity for the thermal modalities of innocuous warming, cooling and cold pain. This implies that there is no simple relationship between loss of peripheral nerve function and spontaneous or evoked pain. Rather, the preservation of several sensory modalities in their area of maximal pain suggests that in some PHN patients, activity in primary afferent nociceptors that remain connected to both their peripheral and central targets contributes significantly to ongoing pain. Although other mechanisms are likely to contribute to the pain, the demonstrated responsivity of PHN to topical agents including local anaesthetics, capsaicin, and non-steroidal anti-inflammatory drugs, supports this proposed mechanism of pain generation.