Anesthesia care in the interventional neuroradiology suite: an update.

Purpose Of Review: The scope of procedures conducted by neurointerventionalists is expanding quickly, with lacking consensus over the best anesthesia modality. Although the procedures involve all age groups, the interventions may be complex and lengthy and may be provided in hospitals currently not yet familiar with the field. Here we review current literature addressing elective outpatient neurointerventional procedures and aim to provide an update on the management of intervention-specific crises, address special patient populations, and provide key learning points for everyday use in the neurointerventional radiology suite.

Subarachnoid hemorrhage in C57BL/6J mice increases motor stereotypies and compulsive-like behaviors.

Objective: Long-term behavioral, mood, and cognitive deficits affect over 30% of patients with subarachnoid hemorrhage (SAH). The aim of the present study was to examine the neurobehavioral outcomes following endovascular perforation induced SAH in mice.

Methods: C57BL/6 J (B6) mice were exposed to endovascular perforation induced SAH or control surgery.

Neuroanesthesia Practice During the COVID-19 Pandemic: Recommendations From Society for Neuroscience in Anesthesiology and Critical Care (SNACC).

The pandemic of coronavirus disease 2019 (COVID-19) has several implications relevant to neuroanesthesiologists, including neurological manifestations of the disease, impact of anesthesia provision for specific neurosurgical procedures and electroconvulsive therapy, and health care provider wellness. The Society for Neuroscience in Anesthesiology and Critical Care appointed a task force to provide timely, consensus-based expert guidance for neuroanesthesiologists during the COVID-19 pandemic. The aim of this document is to provide a focused overview of COVID-19 disease relevant to neuroanesthesia practice.

Assessment of Anesthesia Practice Patterns for Endovascular Therapy for Acute Ischemic Stroke: A Society for Neuroscience in Anesthesiology and Critical Care (SNACC) Member Survey.

Background: The choice of general anesthesia (GA) or conscious sedation (CS) may impact neurological outcomes of patients undergoing endovascular therapy (EVT) for acute ischemic stroke (AIS). The aim of this survey was to describe the practice patterns of members of the Society for Neuroscience in Anesthesiology and Critical Care (SNACC) for anesthetic management of AIS.

Methods: Following institutional review board approval, a 16-question online survey assessing anesthetic management of patients with AIS undergoing EVT was circulated to members of SNACC.

Impairment of neurovascular coupling in Type 1 Diabetes Mellitus in rats is prevented by pancreatic islet transplantation and reversed by a semi-selective PKC inhibitor.

Streptozotocin (STZ)-induced chronic hyperglycemia has a detrimental effect on neurovascular coupling, linked to increased PKC-mediated phosphorylation and PKC isoform expression changes. Here, we sought to determine whether: 1) selective PKC-α/β/γ inhibitor, GF109203X, could reverse the effects of chronic hyperglycemia on cerebrovascular reactivity; 2) pancreatic islet transplantation could prevent the development of cerebrovascular impairment seen in a rat model of Type 1 Diabetes. We studied the effect of GF109203X in diabetic (DM), non-diabetic (ND), and transplanted (TR) Lewis rats during either sciatic nerve stimulation (SNS) or the topical applications of the large-conductance Ca-operated K(BK) channel opener, NS1619, or the K inward rectifier (Kir) channel agonist, KCl.

Intracerebroventricular application of S100B selectively impairs pial arteriolar dilating function in rats.

S100B is an astrocyte-derived protein that can act through the receptor for advanced glycation endproducts (RAGE) to mediate either "trophic" or "toxic" responses. Its levels increase in many neurological conditions with associated microvascular dysregulation, such as subarachnoid hemorrhage (SAH) and traumatic brain injury. The role of S100B in the pathogenesis of microvasculopathy has not been addressed.

VAP-1 blockade prevents subarachnoid hemorrhage-associated cerebrovascular dilating dysfunction via repression of a neutrophil recruitment-related mechanism.

Our previous findings indicated that in rats subjected to subarachnoid hemorrhage (SAH), suppression of post-SAH neuroinflammation via vascular adhesion protein-1 (VAP-1) blockade provides significant neuroprotection. We and others have reported that neuroinflammation contributes to cerebral microvascular impairment. Thus, in the present study, we tested the hypotheses that: (1) treatment with LJP-1586, a selective VAP-1 blocker, prevents SAH-associated pial arteriolar dilating dysfunction; and (2) the vasculoprotective effect of LJP-1586 arises from inhibiting SAH-elicited neutrophil recruitment.

Protective role of fingolimod (FTY720) in rats subjected to subarachnoid hemorrhage.

Background: Subarachnoid hemorrhage (SAH) is a neurological emergency with limited pharmacological treatment options. Inflammation is increasingly recognized as a key pathogenic contributor to brain injury in this condition. In the present study, we examined the neuroprotective effects of the immunomodulatory agent, fingolimod, in rats subjected to SAH.

Pharmacologic blockade of vascular adhesion protein-1 lessens neurologic dysfunction in rats subjected to subarachnoid hemorrhage.

Aneurysmal subarachnoid hemorrhage (SAH) is a potentially devastating clinical problem. Despite advances in the diagnosis and treatment of SAH, outcome remains unfavorable. An increased inflammatory state, one that is characterized by enhanced leukocyte trafficking has been reported to contribute to neuronal injury in association with multiple brain insults, including hemorrhagic and ischemic stroke.

Complex modulation of the expression of PKC isoforms in the rat brain during chronic type 1 diabetes mellitus.

We previously demonstrated that chronic hyperglycemia has a detrimental influence on neurovascular coupling in the brain-an effect linked to an alteration in the protein kinase C (PKC)-mediated phosphorylation pattern. Moreover, the activity of PKC was increased, in diabetic rat brain, in a tissue fraction composed primarily of the superficial glia limitans and pial vessels, but trended toward a decrease in cerebral cortical gray matter. However, that study did not examine the expression patterns of PKC isoforms in the rat brain.

Post-ischemic vascular adhesion protein-1 inhibition provides neuroprotection in a rat temporary middle cerebral artery occlusion model.

We examined the neuroprotective efficacy associated with post-ischemic vascular adhesion protein-1 (VAP-1) blockade in rats subjected to transient (1 h) middle cerebral artery occlusion (MCAo). We compared saline-treated control rats to rats treated with a highly selective VAP-1 inhibitor, LJP-1586 [Z-3-fluoro-2-(4-methoxybenzyl) allylamine hydrochloride]. Initial intraperitoneal LJP-1586 (or saline control) treatments were delayed until 6 h or 12 h reperfusion.

Signal persistence of bispectral index and state entropy during surgical procedure under sedation.

Introduction: Bispectral index (BIS) and state entropy (SE) are prone to artifacts, especially due to electrocautery (EC). We compared the incidence of artifacts in BIS and SE during surgery under local anesthesia and sedation.

Methods: 28 females undergoing breast surgery under local anesthesia and sedation were studied.

Impairment of neurovascular coupling in type 1 diabetes mellitus in rats is linked to PKC modulation of BK(Ca) and Kir channels.

We hypothesized that chronic hyperglycemia has a detrimental effect on neurovascular coupling in the brain and that this may be linked to protein kinase C (PKC)-mediated phosphorylation. Therefore, in a rat model of streptozotocin-induced chronic type 1 diabetes mellitus (T1DM), and in nondiabetic (ND) controls, we monitored pial arteriole diameter changes during sciatic nerve stimulation and topical applications of the large-conductance Ca(2+)-operated K(+) channel (BK(Ca)) opener, NS-1619, or the K(+) inward rectifier (Kir) channel agonist, K(+). In the T1DM vs.

ATP hydrolysis pathways and their contributions to pial arteriolar dilation in rats.

ATP is thought to be released to the extracellular compartment by neurons and astrocytes during neural activation. We examined whether ATP exerts its effect of promoting pial arteriolar dilation (PAD) directly or upon conversion (via ecto-nucleotidase action) to AMP and adenosine. Blockade of extracellular direct ATP to AMP conversion, with ARL-67156, significantly reduced sciatic nerve stimulation-evoked PADs by 68%.

Interactions between adenosine and K+ channel-related pathways in the coupling of somatosensory activation and pial arteriolar dilation.

Multiple, perhaps interactive, mechanisms participate in the linkage between increased neural activity and cerebral vasodilation. In the present study, we assessed whether neural activation-related pial arteriolar dilation (PAD) involved interactions among adenosine (Ado) A(2) receptors (A(2)Rs), large-conductance Ca(2+)-operated K(+) (BK(Ca)) channels, and inward rectifier K(+) (K(ir)) channels. In rats with closed cranial windows, we monitored sciatic nerve stimulation (SNS)-induced PAD in the absence or presence of pharmacological blockade of A(2)Rs (ZM-241385), ecto-5'-nucleotidase (α,β-methylene-adenosine diphosphate), BK(Ca) channels (paxilline), and K(ir) channels (BaCl(2)).

Aldose reductase inhibition ameliorates the detrimental effect of estrogen replacement therapy on neuropathology in diabetic rats subjected to transient forebrain ischemia.

Estrogen replacement therapy (ERT) elicits a deleterious, instead of protective, effect on neuropathology in diabetic ovariectomized (OVX) rats subjected to cerebral ischemia. This transformation may be linked to an estrogen-associated increase in function of the receptor for advanced glycation end-products (RAGE). Moreover, under diabetic conditions, advanced glycation end-products (AGEs) are excessively generated through the aldose reductase (AR)-polyol pathway.

Age effects on brain oxygenation during hypercapnia.

Previous studies showed that the cerebrovasodilation response to hypercapnia is attenuated with aging. The purpose of this study was to determine if normal aging attenuates increases in brain oxygenation during hypercapnia. Prefrontal cortex oxyhemoglobin (OHb) and deoxyhemoglobin (HHb) concentrations were measured in 13 healthy subjects ages 26 to 59 years using a frequency domain tissue oximeter.

Astrocytes are a key conduit for upstream signaling of vasodilation during cerebral cortical neuronal activation in vivo.

Astrocytes play an important role in the coupling between neuronal activity and brain blood flow via their capacity to "sense" neuronal activity and transmit that information to parenchymal arterioles. Here we show another role for astrocytes in neurovascular coupling: the ability to act as a signaling conduit for the vitally important process of upstream vasodilation (represented by pial arterioles) during both excessive (seizure) and physiological (sciatic nerve stimulation) increases in cerebral cortical neuronal activity. The predominance of an astrocytic rather than a vascular route was indicated by data showing that pial arteriolar-dilating responses to neuronal activation were completely blocked following selective disruption of the superficial glia limitans, whereas interference with interendothelial signaling was without effect.

Sevoflurane anesthesia decreases cardiac vagal activity and heart rate variability.

We evaluated cardiac vagal activity during sevoflurane anesthesia in neurosurgical patients. Heart rate variability was determined by power spectral analysis and entropy with the patient awake and during sevoflurane anesthesia. High frequency power (0.

Autonomic activity during desflurane anesthesia in patients with brain tumors.

Objective: Although intracranial tumors may affect autonomic function, there are few reports of autonomic changes during anesthesia. The purpose of this study was to evaluate autonomic effects of anesthesia in patients with brain tumors compared to neurosurgical controls.

Methods: Two groups were evaluated: group 1 = 10 neurosurgical patients undergoing spinal cord surgery, group 2 = 10 patients with intracranial tumors.

Increased brain oxygenation during intubation-related stress.

Background And Objectives: The purpose of this study was to determine whether brain oxyhaemoglobin-deoxyhaemoglobin coupling was altered by anaesthesia or intubation-induced stress.

Methods: This was a prospective observational study in the operating room. Thirteen patients (ASA I and II) undergoing spinal or peripheral nerve procedures were recruited.