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Neurologic disorders in pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Robert Burger, Terry Rolan, David Lardizabal, Upinder Dhand, Aarti Sarwal, Pradeep Sahota
Rarely, abnormal movements known as choreas appear during gestation, typically following the first trimester known as chorea gravidarum. The chorea is generally seen only on half of the body and is known as a hemichorea. The incidence is said to be 1:139,000 pregnancies (76). It was previously associated with rheumatic fever; however, in the United States, the virtual elimination of this disorder has made this association less likely. More often now, it is linked to systemic lupus erythematosus or anti-phospholipid antibody syndrome (77,78). The chorea typically resolves spontaneously, often after delivery. Rarely, the movements are so severe as to induce rhabdomyolysis and hyperthermia (79). Treatment is typically by using dopamine receptor blockers. Due to concerns involving the fetus, haloperidol is preferred since of all of the medications available, it is the least likely to cause harm (80). Similar choreiform movements may occur following institution of birth control pills as well. These typically resolve after discontinuation of OC pills.
Hyperkinetic Movement Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Morales-Briceno Hugo, Victor S.C. Fung, Annu Aggarwal, Philip Thompson
Hormonal chorea: Hormone replacement therapy.Pregnancy (chorea gravidarum).
Choreiform Movements
Published in K. Gupta, P. Carmichael, A. Zumla, 100 Short Cases for the MRCP, 2020
K. Gupta, P. Carmichael, A. Zumla
Apart from Huntington's and rheumatic (Sydenham's) chorea, the causes of chorea are: Chorea gravidarum.Senile chorea.Wilson's disease (other features: cirrhosis, Kayser-Fleischer rings in cornea, haemolysis).Post-encephalitis.Drug-induced (e.g. phenothiazines, L-dopa).
Sydenham’s chorea: an update on pathophysiology, clinical features and management
Published in Expert Opinion on Orphan Drugs, 2019
Luiz Paulo Bastos Vasconcelos, Marcelle Cristina Vasconcelos, Maria Do Carmo Pereira Nunes, Antonio Lucio Teixeira
Regarding recurrence of SC symptoms, 20% to 46% of patients had recurrent chorea in longitudinal studies [34,36]. Korn-Lubetzki et al. (2004) could not detect specific factors associated with SC recurrence but observed that SC recurred even in the absence of RF activity [36]. Conversely, Gurkas et al. (2016) reported that recurrence of chorea occurred mainly in patients with irregular use of antibiotic prophylaxis [37]. Pregnancy is also another known cause of recurrence of chorea in female patients with history of SC. In a case series from a movement disorders clinic, Maia et al. (2012) reported that out of 66 female patients with SC history followed for over 15 years, 20 patients became pregnant. Fifteen of these patients (23% of all female patients and 75% of pregnant patients) evolved with recurrence of chorea during pregnancy, leading to the diagnosis of chorea gravidarum. Although these numbers cannot be extrapolated to other clinical settings or the community, pregnancy has been associated with high recurrence rate of chorea [38].
Pharmacotherapy for Sydenham’s chorea: where are we and where do we need to be?
Published in Expert Opinion on Pharmacotherapy, 2023
Roberta Bovenzi, Matteo Conti, Tommaso Schirinzi
This review will provide a comprehensive analysis on the available pharmacological treatments for SC, highlighting the more urgent gaps. Moreover, as SC mostly affects young females and recurrences are reported in pregnancy (‘chorea gravidarum’), we will focus on the management of such condition in this critical phase of a woman’s life.
Chorea revealing systemic lupus erythematosus in a 13-year old boy: A case report and short review of the literature
Published in International Reviews of Immunology, 2018
E. Athanasopoulos, I. Kalaitzidou, G. Vlachaki, S. Stefanaki, A. Tzagkaraki, G. Niotakis, I. Tritou, F. Ladomenou
Although the pathophysiology of chorea in SLE has not been clearly identified, two pathogenetic pathways have been recognized: a predominant ischemic-vascular one involving large and small blood vessels, mediated by aPL, immune complexes and leuko-agglutination and a predominantly inflammatory-neurotoxic one mediated by complement activation, increased permeability of the blood-brain-barrier, intrathecal migration of autoantibodies, local production of immune complexes and pro-inflammatory cytokines and other inflammatory mediators.28,29 The first theory suggests that aPL cause ischemia in basal ganglia, either by attaching phospholipids in endothelial cells, altering the local cellular signaling and causing accumulation of platelets and thrombosis, or by affecting directly phospholipids of the platelet membranes.28 However, latest data propose that SLE chorea is not caused by ischemic thrombi, as it has recurrent characteristics, it is not combined with other thrombotic events, and neuroimaging findings cannot support this theory.30,31 The second suggested pathway involves the activation of the immune system, leading to neuronal disorders. This activation is due either to autoantibodies, mainly aPL, that seem to go through blood-brain-barrier and connect to unknown antigens in CNS, or to microthrombi that disturb local circulation of cerebral small vessels, causing disruption of the blood-brain-barrier, which normally protects CNS from plasma proteins and cells. When antibodies, mainly aPL, cross the blood-brain-barrier, they react with phospholipid containing structures in the basal ganglia, and cause neurotoxicity and loss of neuroplasticity and synaptic transition.29 Hormonal contribution may be also involved in the pathophysiology of chorea, as there are some case reports describing SLE chorea during pregnancy, called “Chorea Gravidarum.”32 All these mechanisms, however, are not well established for pediatric patients mostly due to their different developmental characteristics.33