Dorsal column stimulation (DCS) is used clinically to provide pain relief from peripheral vascular disease and has the benefit of increasing cutaneous blood flow to the affected lower extremities. The purpose of this study was to examine the role of dorsal roots, calcitonin gene-related peptide (CGRP), and substance P in the cutaneous vasodilation induced by DCS. Male rats were anesthetized with pentobarbital sodium (60 mg/kg ip). A unipolar ball electrode was placed unilaterally on the spinal cord at the L1-L2 spinal segment. Blood flow was recorded in each hindpaw foot pad with laser Doppler flowmeters. Blood flow responses were assessed during 1 min of DCS (either 0.2 mA subdural or 0.6 mA epidural at 50 Hz, 0.2-ms pulse duration). Dorsal rhizotomy of L3-L5 (n = 5) abolished the cutaneous vasodilation to subdural DCS, whereas removal of T10-T12 (n = 5) and T13-L2 dorsal roots (n = 5) did not attenuate the DCS-induced vasodilation. The CGRP antagonist, CGRP-(8-37) (2.6 mg/kg iv, n = 7), eliminated the epidural DCS-induced vasodilation, whereas the substance P receptor antagonist, CP-96345 (1 mg/kg iv, n = 6), had no effect. In summary, L3-L5 dorsal roots and CGRP are essential for the DCS-induced vasodilation. We propose that DCS antidromically activates afferent fibers in the dorsal roots, thus causing peripheral release of CGRP, which produces cutaneous vasodilation.

Our results demonstrated that nitric oxide played a significant role in producing the DCS-induced increase in rat cutaneous hindpaw blood flow. The involvement of nitric oxide does not require the presence of autonomic efferent function; however, ganglionic blockade may unmask a mechanism for vasodilation during DCS that is independent of nitric oxide release.

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By applying automatic data-driven feature extraction and classification to short EEG records, it is possible to construct subject-independent computational models that can detect subtle post clamp changes possibly caused by small perturbations in cerebral blood flow. These subtle changes are missed by visual inspection of the EEG and by other quantitative EEG techniques such as r-sBSI and r-tBSI. Within our subject group, the intricate post-clamp EEG signatures were predominantly anterior, bilateral, and had a strong delta rhythm presence.

BackgroundA ketogenic diet (KD) may have a role in treating patients in super-refractory status epilepticus (SRSE). Sodium-glucose cotransporter 2 (SGLT2) inhibitors have a risk of ketoacidosis that could facilitate induction of KD.Case summaryA 42-year-old with a history of drug resistant epilepsy developed SRSE requiring several pharmacological interventions during her hospital course including the initiation of KD that failed. SGLT2 inhibitor therapy was initiated in a successful attempt to augment ketone production.ConclusionSGLT2 inhibitors may have a therapeutic value in SRSE patients who cannot achieve ketosis with KD alone.