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A rare manifestation during the post-anesthetic period may include the occurrence of functional neurological symptom disorder (FNSD). FNSD is described as neurological symptoms that are not consistently explained by neurological or medical conditions. We report a case series consisting of six patients who underwent a general anesthetic at a tertiary referral hospital and experienced FNSD in the immediate post-anesthetic period. Life-threatening causes were excluded based on benign physical exam findings and knowledge of past history. Five of six cases manifested with FNSD only in the immediate post-operative setting after exposure to anesthesia, and never otherwise experienced these symptoms during their normal daily lives. MEDLINE and Google Scholar were searched through October 2019 using a highly-sensitive search strategy and identified 38 published cases of post-anesthetic FNSD. Meta-analysis of pooled clinical data revealed that a significant proportion of patients were females (86%), reported a history of psychiatric illness (49%), reported a prior history of FNSD (53%), and underwent general anesthesia as the primary anesthetic (93%). The majority of patients were exposed to diagnostic studies (66% received radiographic tests and 52% received electroencephalogram) as well as pharmacologic therapy (57%). While no deaths occurred, many patients had unanticipated admission to the hospital (53%) or to the intensive care unit (25%). These data may help inform the anesthesia literature on presentation, risk factors, and treatment outcomes of FNSD in the context of anesthetic administration. We contemplate whether anesthetic agents may predispose a vulnerable brain to manifest with involuntary motor and sensory control seen in FNSD.

Maximal relaxation of airway smooth muscle (ASM) in response to atrial natriuretic peptide (ANP), which stimulates particulate guanylyl cyclase (pGC), is less than that produced by nitric oxide (NO) and other compounds that stimulate soluble guanylyl cyclase (sGC). We hypothesized that stimulation of pGC relaxes ASM only by decreasing intracellular Ca2+concentration ([Ca2+]i), whereas stimulation of sGC decreases both [Ca2+]iand the force developed for a given [Ca2+]i(i.e., the Ca2+sensitivity) during muscarinic stimulation. We measured the relationship between force and [Ca2+]i(using fura 2) under control conditions (using diltiazem to change [Ca2+]i) and during exposure to ANP, diethylamine-NO (DEA-NO), sodium nitroprusside (SNP), and the Sp diastereoisomer of β-phenyl-1, N2-etheno-8-bromoguanosine-3′,5′-cyclic monophosphorothionate ( Sp-8-Br-PET-cGMPS), a cell-permeant analog of cGMP. Addition of DEA-NO, SNP, or Sp-8-Br-PET-cGMPS decreased both [Ca2+]iand force, causing a significant rightward shift of the force-[Ca2+]irelationship. In contrast, with ANP exposure, the force-[Ca2+]irelationship was identical to control, such that ANP produced relaxation solely by decreasing [Ca2+]i. Thus, during muscarinic stimulation, stimulation of pGC relaxes ASM exclusively by decreasing [Ca2+]i, whereas stimulation of sGC decreases both [Ca2+]iand Ca2+sensitivity.

Objective: We describe BIS values for a patient undergoing breast surgery under self-hypnosis in order to access the value of global surface EEG measures occurring during this process. Methods: Following verbal consent, a BISTM monitor (Aspect Medical, Newton MA) was placed and values measured while the patient performed self-hypnosis for a simple mastectomy and sentinel node biopsy. Results: Thirty-nine minutes after incision the BIS value decreased transiently to 72 followed by several other transient decreases, the lowest of which was 59. Values remained at approximately 90 throughout most of the operative period. The BIS value returned to baseline after completion of the operation. Conclusions: Our findings support the hypothesis that hypnosis is a dynamic cerebral process incorporating many changes within brain activation centers and one distinct from dissociative patterns seen under anesthesia. Current algorithms employed by the BISTM monitor add little to the management of patients utilizing hypnosis for analgesia.

UNLABELLED: Octreotide may be a life-saving treatment in the case of an acute carcinoid crisis, but when given as an i.v. bolus in larger doses, it may cause significant effects on the cardiac conduction system. We describe cardiac conduction impairment observed during octreotide administration in a patient undergoing carcinoid tumor surgery. In this patient, i.v. boluses of 100 microg of octreotide resulted in symptomatic bradycardia, Mobitz type II atrioventricular block, and complete heart block. Perioperative physicians especially need to be aware of these potential effects because they may be more likely to occur during surgery because of the larger doses and boluses that are used to treat acute symptoms secondary to tumor manipulation. IMPLICATIONS: In some susceptible patients, i.v. bolus administration of octreotide may cause significant bradycardia and cardiac conduction defects. Therefore, when octreotide is administered as a bolus, it may be advisable to give it slowly while monitoring the electrocardiogram.