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BackgroundRepetitive somatosensory electrical stimulation (SES) of forelimb peripheral nerves is a promising therapy; studies have shown that SES can improve motor function in stroke subjects with chronic deficits. However, little is known about how SES can directly modulate neural dynamics. Past studies using SES have primarily used noninvasive methods in human subjects. Here we used electrophysiological recordings from the rodent primary motor cortex (M1) to assess how SES affects neural dynamics at the level of single neurons as well as at the level of mesoscale dynamics.MethodsWe performed acute extracellular recordings in 7 intact adult Long Evans rats under ketamine-xylazine anesthesia while they received transcutaneous SES. We recorded single unit spiking and local field potentials (LFP) in the M1 contralateral to the stimulated arm. We then compared neural firing rate, spike-field coherence (SFC), and power spectral density (PSD) before and after stimulation.ResultsFollowing SES, the firing rate of a majority of neurons changed significantly from their respective baseline values. There was, however, a diversity of responses; some neurons increased while others decreased their firing rates. Interestingly, SFC, a measure of how a neuron's firing is coupled to mesoscale oscillatory dynamics, increased specifically in the δ-band, also known as the low frequency band (0.3- 4 Hz). This increase appeared to be driven by a change in the phase-locking of broad-spiking, putative pyramidal neurons. These changes in the low frequency range occurred without a significant change in the overall PSD.ConclusionsRepetitive SES significantly and persistently altered the local cortical dynamics of M1 neurons, changing both firing rates as well as the SFC magnitude in the δ-band. Thus, SES altered the neural firing and coupling to ongoing mesoscale dynamics. Our study provides evidence that SES can directly modulate cortical dynamics.

Objective: To identify the most common locations of cluster headache pain from an international, non–clinic‐based survey of participants with cluster headache, and to compare these locations to other cluster headache features as well as to somatotopic maps of peripheral, brainstem, thalamic, and cortical areas. Background: Official criteria for cluster headache state pain in the orbital, supraorbital, and/or temporal areas, yet studies have noted pain extending beyond these locations, and the occipital nerve appears relevant, given the effectiveness of suboccipital corticosteroid injections and occipital nerve stimulation. Furthermore, cranial autonomic features vary between patients, and it is not clear if the trigeminovascular reflex is dermatome specific (e.g., do patients with maxillary or V2 division pain have more rhinorrhea?). Finally, functional imaging studies show early activation of the posterior hypothalamus in a cluster headache attack. However, the first somatosensory area to be sensitized is unclear; the first area can be hypothesized based on the complete map of pain locations. Methods: The International Cluster Headache Questionnaire was an internet‐based cross‐sectional survey that included a clickable pain map of the face. These data were compared to several other datasets: (1) a meta‐analysis of 22 previous publications of pain location in cluster headache (consisting of 6074 patients); (2) four cephalic dermatome maps; (3) participants' survey responses for demographics, autonomic features, and effective medications; and (4) previously published somatotopic maps of the brainstem, thalamus, primary somatosensory cortex, and higher order somatosensory cortex. Results: One thousand five hundred eighty‐nine participants completed the pain map portion of the survey, and the primary locations of pain across all respondents was the orbital, periorbital, and temporal areas with a secondary location in the lower occiput; these primary and secondary locations were consistent with our meta‐analysis of 22 previous publications. Of the four cephalic dermatomes (V1, V2, V3, and a combination of C2‐3), our study found that most respondents had pain in two or more dermatomes (range 85.7% to 88.7%, or 1361–1410 of 1589 respondents, across the four dermatome maps). Dermatomes did not correlate with their respective autonomic features or with medication effectiveness. The first area to be sensitized in the canonical somatosensory pathway is either a subcortical (brainstem or thalamus) or higher order somatosensory area (parietal ventral or secondary somatosensory cortices) because the primary somatosensory cortex (area 3b) and somatosensory area 1 have discontinuous face and occipital regions. Conclusions: The primary pain locations in cluster headache are the orbital, supraorbital, and temporal areas, consistent with the official International Classification of Headache Disorders criteria. However, activation of the occiput in many participants suggests a role for the occipital nerve, and the pain locations suggest that somatosensory sensitization does not start in the primary somatosensory cortex. Plain Language Summary: Cluster headache (CH) pain is often thought to be located in or around the eye; however, multiple studies have documented pain elsewhere, and procedures that target nerves in the back of the head can help CH. In this large survey (1604 respondents) with a clickable pain map of the face, we found that (1) most respondents had pain extending beyond the area of the eye, and (2) the pain location did not correlate with autonomic symptoms, medication effectiveness, or other CH features. Cluster headache pain beyond the eye is common, and based on the pattern of areas activated, we hypothesized which parts of the brain's somatosensory system may be activated first in cluster attacks. [ABSTRACT FROM AUTHOR]

Recent pilot clinical studies have demonstrated that subjects with severe disorders of movement and communication can exert direct neural control over assistive devices using invasive Brain-Machine Interface (BMI) technology, also referred to as 'cortical neuroprosthetics'. These important proof-of-principle studies have generated great interest among those with disability and clinicians who provide general medical, neurological and/or rehabilitative care. Taking into account the perspective of providers who may be unfamiliar with the field, we first review the clinical goals and fundamentals of invasive BMI technology, and then briefly summarize the vast body of basic science research demonstrating its feasibility. We emphasize recent translational progress in the target clinical populations and discuss translational challenges and future directions.

BACKGROUND: Acquired hemophilia A (AHA) is a rare coagulopathy linked to a variety of etiologies including autoimmune diseases, neoplasms, diabetes, respiratory diseases, and the post-partum state. While bleeding in AHA is often seen in mucocutaneous or intramuscular locations, intracranial and intraspinal bleeds are exceedingly rare. CASE PRESENTATION: We report an unusual case of spontaneous multifocal subdural hematomas in a 25 year old Asian woman with lupus who presented with headache and backache, and was found to have an elevated partial thromboplastin time (PTT) level and new diagnosis of AHA. CONCLUSIONS: Subdural hematomas as the initial sign of AHA are all but unknown in the medical literature. We bring this entity to the attention of the neurology community because lumbar puncture and/or conventional angiogram are often indicated in the work-up of idiopathic multifocal subdural hematomas, but may be dangerous in patients with AHA.

Linked article: https://doi.org/10.1111/head.14670 [ABSTRACT FROM AUTHOR]

Infusion of glucose into the hepatic artery blocks the stimulatory effect of the 'portal signal' on net hepatic glucose uptake (NHGU) during portal glucose delivery. We hypothesized that hepatic artery ligation (HAL) would result in enhanced NHGU during peripheral glucose infusion because the arterial glucose concentration would be perceived as lower than that in the portal vein. Fourteen dogs underwent HAL ~16 days before study. Conscious 42-h-fasted dogs received somatostatin, intraportal insulin, and glucagon infusions at fourfold basal and at basal rates, respectively, and peripheral glucose infusion to create hyperglycemia. After 90 min (period 1), seven dogs ([HAL.sub.po]) received intraportal glucose (3.8 mg*[kg.sup.-1]*[min.sup.-1]) and seven ([HAL.sub.pe]) continued to receive only peripheral glucose for 90 min (period 2). These two groups were compared with nine non-HAL control dogs (control) treated as were [HAL.sub.pe.] During period 2, the arterial plasma insulin concentrations (24 [+ or -] 3, 20 [+ or -] 1, and 24 [+ or -] 2 [micro]U/ml) and hepatic glucose loads (39.1 [+ or -] 2.5, 43.8 [+ or -] 2.9, and 37.7 [+ or -] 3.7 mg*[kg.sup.- 1]*[min.sup.-1]) were not different in [HAL.sub.pe], [HAL.sub.po], and control, respectively. [HAL.sub.po] exhibited greater (P < 0.05) NHGU than [HAL.sub.pe] and control (3.1 [+ or -] 0.3, 2.0 [+ or -] 0.4, and 2.0 [+ or -] 0.1 mg*[kg.sup.-1]*[min.sup.-1], respectively). Net hepatic carbon retention was approximately twofold greater (P < 0.05) in [HAL.sub.po] than in [HAL.sub.pe ]and control. NHGU and net hepatic glycogen synthesis during peripheral glucose infusion were not enhanced by HAL. Even though there exists an intrahepatic arterial reference site for the portal vein glucose concentration, the failure of HAL to result in enhanced NHGU during peripheral glucose infusion suggests the existence of one or more comparison sites outside the liver. liver glucose uptake; portal vein

To determine the effects of an increase in lipolysis on the glycogenolytic effect of epinephrine (EPI), the catecholamine was infused portally into 18-h-fasted conscious dogs maintained on a pancreatic clamp in the presence [portal (Po)-EPI+FFA, n = 6] and absence (Po-EPI+SAL, n = 6) of peripheral Intralipid infusion. Control groups with high glucose (70% increase) and free fatty acid (FFA; 200% increase; HG+FFA, n = 6) and high glucose alone (HG+SAL, n = 6) were also included. Hepatic sinusoidal EPI levels were elevated ([DELTA]568 [+ or -] 77 and [DELTA]527 [+ or -] 37 pg/ml, respectively) in Po-EPI+SAL and EPI+FFA but remained basal in HG+FFA and HG+SAL. Arterial plasma FFA increased from 613 [+ or -] 73 to 1,633 [+ or -] 101 and 746 [+ or -] 112 to 1,898 [+ or -] 237 [micro]mol/l in Po-EPI+FFA and HG+FFA but did not change in EPI+SAL or HG+SAL. Net hepatic glycogenolysis increased from 1.5 [+ or -] 0.3 to 3.1 [+ or -] 0.4 mg * [kg.sup.-1] * [min.sup.-1] (P < 0.05) by 30 min in response to portal EPI but did not rise (1.8 [+ or -] 0.2 to 2.1 [+ or -] 0.3 mg * [kg.sup.-1] * [min.sup.-1]) in response to Po-EPI+FFA. Net hepatic glycogenolysis decreased from 1.7 [+ or -] 0.2 to 0.9 [+ or -] 0.2 and 1.6 [+ or -] 0.2 to 0.7 [+ or -] 0.2 mg * [kg.sup.-1] * [min.sup.-1] by 30 min in HG+FFA and HG+SAL. Hepatic gluconeogenic flux to glucose 6-phosphate increased from 0.6 [+ or -] 0.1 to 1.2 [+ or -] 0.1 mg * [kg.sup.-1] * [min.sup.-1] (P < 0.05; by 3 h) and 0.7 [+ or -] 0.1 to 1.6 [+ or -] 0.1 mg * [kg.sup.-1] * [min.sup.-1] (P < 0.05; at 90 min) in HG+FFA and Po-EPI+FFA. The gluconeogenic parameters remained unchanged in the Po-EPI+SAL and HG+SAL groups. In conclusion, increased FFA markedly changed the mechanism by which EPI stimulated hepatic glucose production, suggesting that its overall lipolytic effect may be important in determining its effect on the liver. gluconeogenesis; glycogenolysis