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[This corrects the article DOI: 10.1371/journal.pone.0228725.].

Abstract Introduction Laughter is a common emotion and may rarely be a manifestation of neurological illnesses. It has been associated with cataplexy as well. Cataplexy is usually triggered by strong emotions. Gelastic syncope is an uncommon phenomenon which may be mistaken for cataplexy. We summarize 3 cases referred to the Sleep Medicine clinic for evaluation for Narcolepsy. Report of Case 55 yo male comes with 2 episodes of blacking out and falling down relating to episodes of laughter in 3 months. Patient describes loss of consciousness and no episodes of freezing. Reported 15 years of snoring and witnessed apneas along with grinding his teeth while sleeping. Polysomnogram revealed Obstructive Sleep Apnea (OSA) with an AHI of 20. 60 yo male comes with episodes of loss of consciousness over the past 6 months, including sitting in a chair, laughing, urinating, washing dishes while standing, expressing strong emotions (father’s funeral), etc. Also reports bugs crawling over his legs when trying to sleep, loud snoring and waking up choking while sleeping. Polysomnogram revealed OSA with an AHI of 20. 43 yo male comes 3 episodes of loss of consciousness, 2 of them related to laughing and the last one related to stretching his arms out. He passes out for 5-10 seconds at a time and a period of 20-30 seconds before passing out where he feels dizzy when he is unable to respond at this time, no post episode confusion. Positive on the Cataplexy Emotional Trigger Questionairre. Reported witnessed apneas, snoring and sleep talking. Polysomnogram revealed OSA, hence the Multiple Sleep Latency Testing ordered was not completed. Conclusion While the first two episodes point towards Gelastic Syncope based on symptoms, the third did warrant MSLT if there was no OSA on PSG. It is important to recognize gelastic syncope as an entity and differentiate it from cataplexy.

Abstract Introduction Flibanserin, a serotonin antagonist currently indicated for treatment of female sexual dysfunction disorder, has not heretofore been described to worsen cerebellar function. Such a case is presented. Methods A 60-year-old woman, 8 months prior to presentation, had an acute onset of fainting and hitting her head into a wall without loss of consciousness. She could not stand up, had left-sided weakness, and vomiting, with garbled, slow speech and severe headache. Findings in the emergency room showed a left cerebellar parenchymal hemorrhage of 3.2 x 3.1 x 2 cm with the epicenter at the dentate nucleus, extending medially towards midline into the cerebellar vermis, with surrounding perilesional edema extending into the middle cerebellar peduncle. Also, 5.2 cm of the hemorrhage extended from the petrous of the tentorium to the cerebellar vermis. Moreover, a ventral left thalamic hemorrhage with subependymal clot at the foramen of Monroe extended into the dependent portion of lateral ventricles without midline shift. Post one month of physical therapy, speech, walking, and coordination improved but she continued to have delayed speech and trouble getting up, with a wide stance. Results Neurologic Examination: Cranial Nerve (CN) Examination: CN XI: Sternocleidomastoid hypertrophy, horizontal titubation. Motor examination: Drift test: L pronator drift with L abductor digiti mini sign. Gait examination: heel walking, dystonic posture of L hand. Tandem gait: unstable, wide based. Cerebellar examination: Both (B) finger-to-nose dysmetria, Left > Right. Slow rapid alternating movements (RAM) L Upper Extremity (UE). Due to absent sexual desire she started 100 mg of flibanserin nightly. Maintaining this for 5 weeks, her coordination markedly worsened with poor balance and a need for a cane to ambulate. She would stumble, with a wider gait, and found climbing stairs challenging. Physical examination displayed worse cerebellar function: prominent horizontal titubation. Finger-to-nose—dysmetria L>R. Decreased RAM, L UE. Markedly positive Holmes Rebound phenomenon, Bilateral UE. Tandem gait: unstable. A week post stopping flibanserin, gait and cerebellar examination returned to baseline. Discussion The temporal correlation between the use of flibanserin and transient worsening of cerebellar function strongly suggests that this is the causative agent. Since serotonin is essential in cerebellar function, including its action on the cerebellar cortex and deep cerebellar nuclei, it strongly suggests that its action as a serotonin antagonist is the mechanism whereby flibanserin is causing cerebellar symptoms. In those on flibanserin, investigation to detect the presence of cerebellar dysfunction is warranted. Assessment for the presence of cerebellar dysfunction in those who are on anti-serotonin drugs, such as cyproheptadine and methysergide, may be worthwhile. Funding No Funding