Background and aims Following spinal cord injury (SCI), a majority of individuals may develop neuropathic pain, which further reduces quality of life. Pain is difficult to treat by medication; in fact, medication overuse may aggravate neuropathic pain in SCI by causing central sensitization (CS): a mechanism of hyper-reactivity of the dorsal horn neurons in the spinal cord with amplified cerebral pain response. The purpose of this study was to examine the presence of neuropathic pain and CS above the spinal lesion in SCI, and to investigate whether injury characteristics or medication influenced pain response. Methods Twenty-four SCI patients with various injury characteristics (eight subacute, traumatic injuries, eight chronic, traumatic injuries, eight non-traumatic injuries) and 12 able-bodied controls underwent sensory testing:pressure algometry, Von Frey filaments (sensitivity), and repetitive pinprick stimulation (pain windup). SCI participants also fulfilled a modified version of the McGill Pain Questionnaire. Data were analyzed regarding (i) SCI patients compared with controlgroup and (ii) SCI subgroup comparison (grouped by a) injury characteristics and (b) intake of analgesics, where low-medicated subgroup were prescribed only non-opioids and high-medicated potent opioids). Results Neuropathic pain was present in 21 of 24 SCI patients. Chronic and non-traumatic SCI patients reported considerably higher present pain intensity than sub-acute traumatic SCI patients on a five-point scale (3.13±0.99, 1.75±1.75 and 0.13±0.35, respectively, p<0.005). Reduced pressure pain detection thresholds (PPDT) were found in SCI patients at several supra-lesional anatomical points compared to controls. Contrarily, tactile detection thresholds were higher in SCI. SCI subgroup analyses showed that i) the low-medicated SCI subgroup displayed significantly lower PPDT compared to the high-medicated subgroup, ii) pain-windup was present in all subgroups although the sub-acute and non-traumatic subgroups displayed lesser pain windup than controls, and the chronic SCI subgroup mainly displayed higher pain windup. Conclusions The reduced PPDT found above lesion suggests the presence of CS in SCI. However, findings regarding SCI subgroup comparison did not support our hypothesis that more medication leads to increased CS. Implications The development of CS may complicate diagnosis and pain treatment following SCI. Prospective studies of SCI with a healthy control group are needed.