Apnea with ketamine sedation in a patient with severe anorexia nervosa: A case report.

BACKGROUND: There is a paucity of literature around sedation and anesthesia in patients with severe anorexia nervosa. Chronically malnourished patients are known to have myopathy, neuropathy, and altered neurotransmitter signaling. Ketamine is a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist that is an established general anesthetic and short-acting dissociative analgesic agent. It generally has a reassuring adverse event profile and rarely has been reported to result in apnea. We aim to raise awareness of this untoward adverse event in patients with severe anorexia nervosa among sedation providers and those referring patients for hospitalization or sedation. CASE PRESENTATION: We describe an episode of apnea, a rare adverse event of ketamine, which was given for procedural sedation to a severely malnourished 13-year-old female with anorexia nervosa, generalized anxiety disorder, and high-functioning autism spectrum disorder. She had no history of apnea nor of ketamine sedation. She was given a standard dose of ketamine and had no other central nervous system depressants within 24 h. Within 1 min after slow medication administration, she had a 9-min period of apnea without laryngospasm. She was supported with bag-valve-mask ventilation throughout this period and did not require intubation. She returned to baseline shortly after procedural sedation. CONCLUSIONS: This case describes apnea after ketamine sedation in a patient with severe anorexia nervosa. It supports the importance of a thorough pre-procedure review of a patient's underlying medical problems and the consideration of how sedatives may interact with these conditions. We aim to alert those who care for this complex population of the possible altered neurotransmitters, myopathy, and adverse response to sedation, anesthetics, and analgesics.

Effects of mavoglurant on visual attention and pupil reactivity while viewing photographs of faces in Fragile X Syndrome.

BACKGROUND: Numerous preclinical studies have supported the theory that enhanced activation of mGluR5 signaling, due to the absence or reduction of the FMR1 protein, contributes to cognitive and behavioral deficits in patients with fragile X syndrome (FXS). However multiple phase 2 controlled trials in patients with FXS have failed to demonstrate efficacy of compounds that negatively modulate mGluR5, including two phase 2b randomized controlled trials (RCT) of mavoglurant (AFQ056, Novartis Pharma AG), when the primary measures of interest were behavioral ratings. This has cast some doubt onto the translation of the mGluR5 theory from animal models to humans with the disorder. METHODS: We evaluated social gaze behavior-a key phenotypic feature of the disorder-and sympathetic nervous system influence on pupil size using a previously-validated eye tracking paradigm as a biobehavioral probe, in 57 adolescent or adult patients with FXS at baseline and following three months of blinded treatment with one of three doses of mavoglurant or placebo, within the context of the AFQ056 RCTs. RESULTS: Patients with FXS treated with mavoglurant demonstrated increased total absolute looking time and number of fixations to the eye region while viewing human faces relative to baseline, and compared to those treated with placebo. In addition, patients had greater pupil reactivity to faces relative to baseline following mavoglurant treatment compared to placebo. DISCUSSION: The study shows that negative modulation of mGluR5 activity improves eye gaze behavior and alters sympathetically-driven reactivity to faces in patients with FXS, providing preliminary evidence of this drug's impact on behavior in humans with the disorder.