Extraforaminal Lumbar Disk Herniations Lead To Neuroplastic Changes: a Study Using Quantitative Sensory Testing.

INTRODUCTION: Extraforaminal lumbar disk herniations are characterized by distinct clinical features in comparison to paramedian lumbar disk herniations. METHODS: We applied the quantitative sensory testing (QST) protocol of the German Research Network on Neuropathic Pain in 63 patients with a single lumbar disk herniation. They were categorized in 2 groups: (I) an intraspinal (group I; n = 47, 75%) and an extraforaminal (group E; n = 16, 25%). RESULTS: The wind-up ratio for assessing endogenous pain-modulating pathways was higher in group E (2.9 ± 2) than in group I (1.4 ± 1; P = 0.021). After a subsequent series of pinprick stimuli, an increase in pain assessed by the numeric rating scale could be shown in group E (2.1 ± 2 vs 1.1 ± 1; P = 0.032). DISCUSSION: Extraforaminal compression is associated with chronic as well as neuropathic pain, presumably caused by direct compression of the dorsal root ganglion, which may preferentially promote specific chronic pain mechanisms. Muscle Nerve 58: 676-680, 2018.

Vasopressin and methylprednisolone and hemodynamics after in-hospital cardiac arrest - A post hoc analysis of the VAM-IHCA trial.

INTRODUCTION: The Vasopressin and Methylprednisolone for In-Hospital Cardiac Arrest (VAM-IHCA) trial demonstrated a significant improvement in return of spontaneous circulation (ROSC) with no clear effect on long-term outcomes. The objective of the current manuscript was to evaluate the hemodynamic effects of intra-cardiac arrest vasopressin and methylprednisolone during the first 24 hours after ROSC. METHODS: The VAM-IHCA trial randomized patients with in-hospital cardiac arrest to a combination of vasopressin and methylprednisolone or placebo during the cardiac arrest. This study is a post hoc analysis focused on the hemodynamic effects of the intervention after ROSC. Post-ROSC data on the administration of glucocorticoids, mean arterial blood pressure, heart rate, blood gases, vasopressor and inotropic therapy, and sedation were collected. Total vasopressor dose between the two groups was calculated based on noradrenaline-equivalent doses for adrenaline, phenylephrine, terlipressin, and vasopressin. RESULTS: The present study included all 186 patients who achieved ROSC in the VAM IHCA-trial of which 100 patients received vasopressin and methylprednisolone and 86 received placebo. The number of patients receiving glucocorticoids during the first 24 hours was 22/86 (26%) in the placebo group and 14/100 (14%) in the methylprednisolone group with no difference in the cumulative hydrocortisone-equivalent dose. There was no significant difference between the groups in the mean cumulative noradrenaline-equivalent dose (vasopressin and methylprednisolone: 603 ug/kg [95CI% 227; 979] vs. placebo: 651 ug/kg [95CI% 296; 1007], mean difference -48 ug/kg [95CI% -140; 42.9], p = 0.30), mean arterial blood pressure, or lactate levels. There was no difference between groups in arterial blood gas values and vital signs. CONCLUSION: Treatment with vasopressin and methylprednisolone during cardiac arrest caused no difference in mean arterial blood pressure, vasopressor use, or arterial blood gases within the first 24 hours after ROSC when compared to placebo.