Search

Introduction: There are over 40,000 people living in Ireland with inflammatory arthritis (IA), a condition that is potentially destructive in nature and can have personal, social and economic consequences. Although we have witnessed dramatic changes in the treatment of IA in the last two decades, methotrexate (MTX) remains the first‐line treatment for patients with a diagnosis of IA. Despite the fact that MTX is so commonly prescribed, there is a lack of educational materials both for healthcare professionals (HCPs) and patients. The aim of the present study was to develop a suite of MTX material for patients. Methods: A comprehensive literature review of MTX (evidence, educational materials and practice guidelines) in the treatment of IA was undertaken. The content of the documents was developed, and the format and structure of the documents were agreed. A tailored patient educational guide, information/monitoring booklet and alert card were designed to address the lack of educational materials for this condition. A national pilot study of the documents was conducted (a postal questionnaire for patients and electronic survey for clinical nurse specialists). Results and recommendations were incorporated into the final documents. These documents were also incorporated into the National Clinical Care Programme–rheumatology–methotrexate pathway. Results: A 26‐page evidence‐based educational guide was produced to support the HCP in educating patients taking MTX, in conjunction with a patient information/monitoring booklet and alert card to support the patient. Conclusions: These documents are now widely available and used in clinical practice in Ireland, providing patients with standardized, evidence‐based information about MTX. [ABSTRACT FROM AUTHOR]

Renal denervation (RDN) has emerged as a potential device-based treatment for resistant hypertension. The authors present their experience of the use of catheter-based RDN as part of routine clinical care in two specialist hypertension clinics. Thirty-four patients with uncontrolled hypertension underwent RDN. All patients had ambulatory blood pressure (BP) monitoring and directly observed medication administration prior to the procedure to exclude white-coat hypertension and nonadherence, respectively. Overall, there was a significant change in clinic systolic BP of -15.1 mm Hg (95% confidence interval, -23.4 to -6.8; P=.001) and clinic diastolic BP of -6.2 mm Hg (95% confidence interval, -11.5 to -0.9; P=.02) 6 months postprocedure, and a nonsignificant change in daytime ambulatory BP of -5.4/-2.9 mm Hg. Eighteen patients (51.4%) showed a significant reduction in their clinic systolic BP (≥10 mm Hg) and 16 (47%) had a significant reduction in their daytime ambulatory systolic BP (≥5 mm Hg) at 6 months. [ABSTRACT FROM AUTHOR]

Reduced perception of somatosensory stimulation in patients with essential hypertension may be due to deficits in the ascending somatosensory pathway. Function in the ascending somatosensory pathway was assessed by measuring N9, N13, and N20 somatosensory-evoked potentials in 14 unmedicated essential hypertensives and 22 normotensives. N9 amplitudes were smaller and N13 amplitudes marginally smaller in hypertensives than normotensives. N9 amplitudes were inversely associated with blood pressure. N20 amplitudes and N9, N13, and N20 latencies did not differ between groups. In addition, plexus-to-cord, cord-to-cortex, and plexus-to-cortex conduction times were not different between groups. These data suggest that hypertension affects the peripheral nervous system by reducing the number of active sensory nerve fibers without affecting myelination. However, hypertension does not seem to affect the afferent somatosensory pathway within the brain. [ABSTRACT FROM AUTHOR]

Sensorimotor deficits in patients with essential hypertension may be due to impaired nerve function. Cutaneous sensory thresholds, median nerve sensory and motor conduction velocities, and median nerve sensory action potential amplitudes were assessed in 30 patients with unmedicated essential hypertension and 29 normotensives. Cutaneous sensory thresholds were higher and sensory action potential amplitudes smaller in hypertensives than normotensives whereas sensory and motor nerve conduction velocities did not differ between groups. These data suggest that hypertension may reduce the number of active sensory nerve fibers without affecting myelination. Sensory action potential amplitudes were inversely related to cutaneous sensory thresholds, suggesting that subclinical axonal neuropathy of sensory afferents may help account for perceptual deficits that characterize hypertension. [ABSTRACT FROM AUTHOR]

Hypertension is characterized by cognitive deficits. As evidence for impaired psychomotor speed, including slower reaction times, is mixed, we aimed to provide a detailed investigation of simple reaction time in hypertension. Pre-motor and motor reaction times were measured across the cardiac cycle in 30 hypertensives and 29 normotensives to determine the effects of phasic and tonic blood pressure on performance. Auditory, visual, and tactile simple reaction time tasks were completed with stimuli presented 0, 300, and 600 ms after the R-wave of the electrocardiogram. Reaction times did not differ between hypertensives and normotensives. Although pre-motor reaction times were faster during the late phase than the early phase of the cardiac cycle whereas motor reaction times were unchanged, this effect was similar for hypertensives and normotensives. No sensory-motor deficits were evident in these hypertensives regardless of baroreceptor activity. [ABSTRACT FROM AUTHOR]

Abstract The arterial baroreflex may mediate hypertensive hypoalgesia. Carotid baroreceptors can be artificially stimulated by neck suction and inhibited by compression. Effects of brief neck suction and compression on nociceptive responding and pain were studied in 25 normotensive adults. The sural nerve was electrocutaneously stimulated at threshold intensity during systole or diastole combined with neck suction, neck compression, or no pressure. Nociceptive responding was indexed by electromyographic activity elicited in the biceps femoris. Participants rated the intensity of sural stimulation. Although artificial baroreceptor stimulation (suction) did not affect nociceptive responding, baroreceptor inhibition (compression) reduced pain ratings. In contrast, natural baroreceptor stimulation during systole reduced nociceptive responding compared to diastole, but did not affect pain ratings. The data provide partial support for baroreflex modulation of pain. [ABSTRACT FROM AUTHOR]

A baroreflex mechanism may explain hypertensive hypoalgesia. At rest, arterial baroreceptors are stimulated during the systolic upstroke of the pressure pulse wave. This study examined the effects of naturally occurring variations in baroreceptor activity during the cardiac cycle on an objective measure of pain, the nociceptive flexion reflex (NFR). Two interleaved up-down staircase procedures determined separate NFR thresholds during systole and diastole in 36 healthy, normotensive young adults. On odd-numbered trials, the sural nerve was stimulated electrocutaneously at R + 300 ms whereas on even-numbered trials, stimulation was delivered at R + 600 ms. The NFR threshold was higher at R + 300 ms than R + 600 ms. In contrast, stimulus intensity ratings did not differ between R + 300 ms and R + 600 ms. Stimulation of baroreceptors by natural increases in blood pressure during the systolic phase of the cardiac cycle was associated with dampened nociception. [ABSTRACT FROM AUTHOR]