Abstract-We aimed to investigate for the first time the blood pressure (BP)-lowering effect of renal sympathetic denervation (RDN) versus clinically adjusted drug treatment in true treatment-resistant hypertension (TRH) after excluding patients with confounding poor drug adherence. Patients with apparent TRH (n=65) were referred for RDN, and those with secondary and spurious hypertension (n=26) were excluded. TRH was defined as office systolic BP (SBP) >140 mm Hg, despite maximally tolerated doses of ≥3 antihypertensive drugs including a diuretic. In addition, ambulatory daytime SBP >135 mm Hg after witnessed intake of antihypertensive drugs was required, after which 20 patients had normalized BP and were excluded. Patients with true TRH were randomized and underwent RDN (n=9) performed with Symplicity Catheter System versus clinically adjusted drug treatment (n=10

The prevalence and classification of pain were investigated in 46 patients admitted consecutively with traumatic spinal cord injury to a rehabilitation hospital. All were studied within 2 years of trauma_ Forty-six percent experienced pain of moderate-to-severe intensity_ The patients with pain were classified into five categories: diffuse pain, segmental pain, root pain, visceral pain and non-neurogenic pain, Most patients experienced more than one type of pain, Pain appeared more intense in the evening than in the morning or at noon. Older age (median 40 years vs 24 years) was related to increased prevalence of pain. Significantly more patients with pain (70%) than without pain (24%) had a case-score on the 20-item version of the General Health Questionnaire, indicating psychological distress and reduced quality of life. The present study indicates that pain causes emotional distress in addition to the distress associated with the spinal cord injury itself.

The role of central N-methyl-D-aspartate (NMDA) receptors in the pathogenesis of central pain was examined in nine patients with central dysesthesia pain after spinal cord injury. The central pain syndrome included spontaneous continuous and intermittent pain as well as evoked pain. Pain was evoked by non-noxious stimulation of the skin (allodynia) and by repeated pricking of the skin (wind-up-like pain). The severity of continuous and evoked pain was examined before and after the intravenous infusion of either the NMDA receptor antagonist ketamine (6 micrograms/kg/min after a bolus dose of 60 micrograms/kg), the mu-opioid receptor agonist alfentanil (0.6 microgram/kg/min after after a bolus dose of 7 micrograms/kg), or placebo (0.9% NaCl). A randomized, double-blind, crossover study design was used. It was found that both continuous and evoked pain were markedly reduced by the blockade of NMDA receptors by ketamine as well as by the activation of mu-opioid receptors by alfentanil. Neither ketamine nor alfentanil significantly changed thresholds for the sensation of heat pain. The reduction of pain was not associated with severe side effects; the most severe side effect of ketamine was bothersome dizziness in one patient, and only modest side effects were caused by alfentanil. The present data provide clinical evidence that the development of central dysesthesia pain after traumatic spinal cord injury is dependent on the activation of central NMDA receptors. The results further indicate that mu-opioid receptors are involved in the control of this type of pain.

Objective-To determine whether central pain in patients with spinal cord injury is only dependent on the lesioning of spinothalamic pathways. Methods-In sixteen patients with spinal cord injury and central dysaesthesia pain, somatosensory abnormalities in painful denervated skin areas were compared with somatosensory findings in normal skin areas as well as in non-painful denervated skin areas. Results-The threshold values for detection of thermal (heat, cold, heat pain, or cold pain) and tactile stimulation were significantly changed in denervated skin areas although there were no significant differences in the threshold values between painful and non-painful denervated skin areas. The reductions of sensations of touch, vibration, joint position, and two point discrimination in painful and non-painful denervated skin areas were not significantly different. Allodynia (pain caused by non-noxious stimulation) and wind up-like pain (pain caused by repeatedly pricking the skin) were significantly more common in painful than nonpainful denervated skin areas. Conclusions-Because pain and thermal sensory perception are primarily mediated to the brain via spinothalamic pathways, whereas the sensations of touch, vibration and joint position are primarily mediated by dorsal column-medial lemniscal pathways, the results indicate that central pain is not only dependent on the lesioning of either dorsal column-medial lemniscal pathways or spinothalamic pathways. The findings of abnormal evoked pain (allodynia and wind up-like pain) may be consistent with the experimental findings of hyperexcitability in nociceptive spinothalamic tract neurons, that may be involved in the pathogenesis of central pain. Severe and disabling chronic pain is a major sequel after spinal cord injury, with an estimated prevalence ranging from 18 to 63%.1 Pain in patients with spinal cord injury includes musculoskeletal pain, radicular pain, visceral pain, central dysaesthesia pain, psychogenic pain, lesional pain, reflex sympathetic dystrophy, and limb pain secondary to compressive mononeuropathies.2 Central dysaesthesia pain is characterised by spontaneous continuous and intermittent pain as well as by pain evoked by non-noxious stimulation (allodynia).2 It is difficult to treat this type of pain as central pain is not effectively relieved by traditional analgesics or neurosurgical procedures.34 Increased knowledge of the pathogenesis of central dysaesthesia pain after spinal cord injury is desired.An important hypothesis is that the development of central pain is dependent on the lesioning of spinothalamocortical pathways.35 The hypothesis is partly based on the finding that sensory perception mediated to the brain via spinothalamocortical pathways is more often affected than sensory perception mediated by dorsal column-medial lemniscal pathways in this group of patients.3 6In the present study, somatosensory testing of patients with spinal cord injury and central dysaesthesia pain was undertaken to further examine whether central pain is ...