Chorea gravidarum (CG) is the term given to chorea occurring during pregnancy. This is not an etiologically or pathologically distinct entity but rather a generic term for chorea of any cause starting during pregnancy. Therefore, CG is regarded as a syndrome rather than a specific disease entity. Chorea is an involuntary abnormal movement, characterized by abrupt, brief, nonrhythmic, nonrepetitive movement of any limb, often associated with nonpatterned facial grimaces.[1, 2, 3]
Rheumatic fever is no longer a major cause of chorea gravidarum (CG) and the pathophysiology of CG in current times is unclear. Several pathogenetic mechanisms for CG have been proposed, but none have been proven.
In regard to rheumatic fever, the pathologic changes in the brain reported in CG are similar to those found in rheumatic cardiac disease. These changes include nonspecific arteritis with endothelial swelling, perivascular lymphocytic infiltration, and petechial hemorrhages.[4] Of note, Aschoff bodies, found in the rheumatic heart disease, are not found in the brain.[5, 6] These pathologic changes in the brain are most prominent in the corpus striatum and associated with severe neuronal loss. The corpus striatum is considered to be the largest structure present in the basal ganglia. Classically, the corpus striatum is divided in two parts: dorsal striatum (caudate nucleus and putamen) and ventral striatum (nucleus accumbens and olfactory tubercle). The corpus striatum preforms a variety of different functions from cognitive process and behavior reinforcement to motor functions. It is the dorsal striatum, however, which is most significant in motor activity and commonly involved in hyperkinetic and hypokinetic movement disorders.
In CG patients with autoimmune pathology, postmortem studies show diffuse foci of small hemorrhages present throughout the brain. These hemorrhages are most evident in basal ganglia and caudate nucleus with associated widespread vasculitis.[7, 8] Presumably, as the inflammation resolves, the chorea disappears, and degenerative changes are left in small arterioles.
Another pathologic hypothesis is related to hormonal mediation, particularly estrogen, given there is an increase in chorea cases among young women on oral contraceptives. Nausuda et al reported that modification of postsynaptic dopamine receptors produces dopamine hypersensitivity in high estrogen states.[9] Lee et al suggested that estrogen augments the neuronal function by increasing the expression of active D5 receptors.[10] Estrogen acts as a dopamine agonist on the striatal D2 receptors in the medial part of corpus striatum. In normal estrogen states there does not appear to be any effect on the striatal dopamine receptor expression.[11, 12] Oral contraceptives may activate the same high estrogen state mechanism of CG leading to chorea and further supporting the role of estrogen in CG. In 1950, Beresford and Graham postulated that, “It may be that pregnancy lowers the resistance of a patient who is inherently susceptible to chorea.”[13] Therefore, it has been hypothesized that another cause of CG may be from the reactivation of previous subclinical damage to the basal ganglia during high estrogen states including pregnancy.
In 2004, Miranda et al reported of a case of chorea associated with the use of the oral contraceptives, in which anti-basal ganglia antibodies were detected, suggesting a possible immunological basis to the pathogenesis of this disorder.[14] However, the presence of antibodies in serum does not necessarily infer pathogenicity; the antibodies could be produced as part of tissue damage.[15] To demonstrate that a disorder is autoimmune, 5 criteria must be fulfilled.[16] The criteria are (1) the presence of autoantibodies, (2) the presence of antibodies in target tissue, (3) the induction of disease in an animal model by passive transfer of the antibody, (4) the induction of disease in an animal model by autoantigen immunization, and (5) improvement of clinical symptoms after removal of the antibodies with plasma exchange.
Movement disorders rarely occur during reproductive years, therefore, clinicians are not very familiar with chorea gravidarum (CG). Willson and Preece found that the overall incidence of CG was approximately 1 case per 300 deliveries. According to them, the first description of chorea with onset during pregnancy was made by Horstius in 1661. Rheumatic fever secondary to untreated streptococcal pharyngitis was a major cause of CG at the time of Willson and Preece’s publication. They noted that nearly 70% of their patients had a previous history of either rheumatic fever or chorea.[4] Since the widespread use of antibiotics for streptococcal pharyngitis, CG has become very uncommon.
Calculating the current incidence of CG is not possible given the rarity of the syndrome and lack of more recent published studies. However, a study by Zegart and Schwartz found that one patient with CG had been encountered among 139,000 deliveries in 3 major Philadelphia hospitals.[17] In general, about half the cases of CG are idiopathic, with rheumatic fever and antiphospholipid syndrome (APS) responsible for the reminder of cases.[18]
Demographics
Most patients with CG are young; the average age of onset is 22 years old.[4] Almost all reported patients have been Caucasians, although this may be due to a bias in the older literature, in which the vast majority of reported cases are among patients of European descent.
Of afflicted women, 60% previously had chorea and a family history of transient chorea is not unusual. When occurring with first pregnancies, 50% of CG cases occur in the first trimester and 30% of cases occur in the second trimester. Recurrence of CG in subsequent pregnancies may occur, particularly when associated with antiphospholipid syndrome.[4]
Chorea gravidarum (CG) seldom persists indefinitely. Without treatment, the disease abates in about one third of patients before child delivery. In almost two thirds of patients, the chorea lasts up to 6 weeks postpartum, also known as puerperium. Symptoms often dramatically improve and disappear in the days after childbirth. In some patients, however, neurological sequelae may continue in the form of various degrees of incoordination, tremor, and clumsiness.
Mortality in patients with CG is now rare[7] but, again, difficult to calculate given the scarcity of data. Willson and Preece reported a mortality rate of 12%.[4] However, this likely reflects death due to underlying rheumatic heart disease rather than CG. Beresford and Graham's 1950 analysis of CG reported that death occurred in 1.5% of pregnancies, fetal death in 3.3%, and premature labor in 6.6%,[13] However, due to the absence of a control group it is impossible to interpret this data. Additionally, advances in maternal-fetal medicine since 1950 would also likely improve these statistics.
In the case of drug-induced CG and contraceptive-induced chorea, movements typically resolve after cessation of the drug; and specific therapeutic interventions are not often needed. Individual susceptibility for adverse effects from these drugs may be due to preexisting basal ganglia abnormalities, such as prior vascular insults, Sydenham chorea, or hypoxic encephalopathy.
Fetal prognosis
In view of the paucity of CG, fetal mortality is difficult to assess. Willson and Preece mentioned two 19th-century cases of neonatal chorea. One case involved a microcephalic child with athetoid cerebral palsy. The other case was said to involve transient chorea, but the movements were not described further.[4] It is not clear that these cases were related to CG and no further data is available since their 1932 report.
There is no increased risk of spontaneous abortion in CG[17] and children are generally born healthy and there are not reports on delivery complications. There is no data to indicate significant fetal complications and the 1950 Beresford and Graham report is unclear as noted above.
Future pregnancy
It is unclear what the recurrence rate of CG is in modern times. Willson and Preece reported 21% of women with CG have recurrent chorea with subsequent pregnancies.[4] Several cases have been described in which attacks occurred in the third, fourth, and even fifth pregnancy.[19, 20]
Chorea gravidarum (CG) is a rare clinical entity often without an identifiable cause, but its early recognition is important to decrease the maternal and fetal morbidity and mortality. The diagnosis requires a detailed patient history and physical examination along with thorough laboratory evaluation.
The clinical presentation is variable as chorea can present in various forms including generalized, focal, multifocal or hemichorea. It can also be unilateral or bilateral and include upper extremities and/or lower extremities. There are many different forms of chorea including Huntington's disease, paralytic, persistent, recurrent, tetanoid, functional, maniacal, hemichorea, and chorea gravidarum.[21]
Patients may attempt to disguise chorea by incorporating movements into a mannerisms or gestures. Some patients may appear simply restless or fidgety. Some may be unaware of the abnormal movements and, thus, may not complain about chorea or abnormal movements. Additionally, stress may aggravate the movements of CG and the movements disappear during sleep. These factors may lead to misdiagnosis of the condition.
As the exact etiology of CG is not clear, getting a comprehensive history from the patient is important. A thorough past medical history including rheumatic fever, history of recent infection with group A beta-hemolytic streptococcus (GABHS), and family history of chorea also needs to be identified. A pre-pregnancy history of Sydenham’s chorea has an increased risk of development if CG.[4] Of note, there are published case reports from the early 1900s in which women with normal pregnancies before rheumatic fever developed chorea in subsequent pregnancies after having rheumatic fever.[22, 23]
Immune-mediated conditions, including antiphospholipid antibody syndrome (APS) and systemic lupus erythematosus (SLE) may also predispose patients to a higher risk of CG. Therefore, a history of dermatological and joint complaints, clotting abnormalities, and spontaneous abortions may point to these etiologies being the cause of CG.
History should also focus on reviewing prescribed medications, particularly dopamine agonists, as well as inquiring about substance abuse and illicit drug use. Prior use of oral contraceptives (OC) also helps in supporting the diagnosis of recurrence of CG. Fernando et al reported the first case linking estrogen containing oral contraceptives to chorea. Chorea may also reappear in CG patients who later take OCs or use topical estrogen.[24]
A detailed history should be obtained to rule out other diagnoses that may manifest as chorea during pregnancy such as thyrotoxicosis, Wilson’s disease, and Huntington’s disease. Though patients with these diseases may have chorea during pregnancy, they are etiologically distinct pathological process and not typically considered to be CG.
Clinical manifestations of chorea gravidarum (CG) may include the following:
Involuntary muscle movements: Typically the dance-like movements of chorea, which are rapid, purposeless, irregular, jerky movements that seem to randomly flow from one part of the body to another. These movements worsen with stress or anxiety and completely disappear during sleep. Generally, the affected limb may be hypotonic; joints are floppy, and knee jerks are pendular. Wrist and fingers assume the shape of a dinner fork with abduction of the thumb.
Facial grimacing: Involuntary movements are often associated with non-patterned grimacing of the face due to incoordination of muscles.
Milkmaid’s grip: Due to varying hand strength, when the patient tries to shake someone’s hand they may grip and release the fingers over and over again. This action appears similar to milking a cow, thus is referred to as milkmaid’s grip.
Darting tongue sign: When the patient tries to protrude his tongue, it may slide in and out uncontrollably.[25]
Dysarthria: Chorea movements may involve facial muscle leading to dysarthria. However, it should be noted that dysarthria can be present in some cases even without facial chorea.[26]
Mental status changes: Some cases of CG may present with confusion and agitation. This is more likely when the etiology of CG is related to autoimmune disease.
Neuropsychiatric symptoms: Chorea movements can be preceded by neuropsychiatric symptoms like emotional lability, mild cognitive changes, and psychosis.[27] Other clinical manifestations include personality changes, depression, chronic cognitive deficits, hypnic hallucinations, delirium, and Tourette-like symptom.[28]
The cerebral manifestation of rheumatic fever has sometimes historically been referred to as rheumatic brain disease. This may present as Sydenham’s chorea associated with mental status changes, emotional lability to hysterical traits, psychotic delusions, hallucinations, seizures, and papilledema depending on the severity of illness.[29, 30, 31] Encephalopathy associated with rheumatic fever, historically referred to as rheumatic encephalopathy, may be reflected in the EEG findings of 3–6 Hz slow waves, particularly over the frontal and central regions.[32]
The diagnosis of CG relies on a complete physical examination in which the involuntary, non-rhythmic, abrupt movements of chorea are identified during pregnancy, particularly in the first trimester. Case reports have documented dystonia as a sole presentation in the first trimester with resolution after delivery as a form of CG. Authors hypothesized that transient dystonia in these patients has a similar pathophysiology of CG due to the hyperkinetic nature of dystonia.[33]
Though CG is not a life-threatening condition, hyperthermia, rhabdomyolysis, myoglobinuria, and death have been reported in severe cases.[7]
There is evidence that chorea gravidarum (CG) is a sequela of rheumatic fever and autoimmune diseases. Although CG is a rare entity today, the etiology is most probably autoimmune in nature in industrialized nations, whereas it is rheumatic in nature in developing nations.
Causes contributing to CG include:
Lupus anticoagulant
Anticardiolipin antibody
Systemic lupus erythematosius
Vascular malformation in the basal ganglia region
Cerebrovascular disease involving the basal ganglia region
When making the diagnosis of chorea gravidarum (CG), it is important to keep in mind the diagnositc considerations and to maintain a high index of suspicion and vigilance.
See the list below:
– erythrocyte sedimentation rate (ESR), throat culture, C-reactive protein, and ASO titer as well as antineuronal antibodies See the list below:
Husby described antineuronal antibodies using an immunofluorescent technique in 46% of patients with Sydenham chorea (n = 30) compared with 14% of patients with rheumatic fever (without chorea) (n = 50) and only 1.8–4% of control subjects (n = 203). He further demonstrated a potential correlation between antibody reactivity and the clinical status, with antibody disappearance on chorea remission.[49]
Wilson disease – serum ceruloplasmin and urinary copper (24 h)
Autoimmune disease (APS, SLE, etc) – ESR, antinuclear antibody, anticardiolipin antibodies, and lupus anticoagulant assays. Coagulation times PT and aPTT.
See the list below:
– routine stroke evaluation should include risk factor screeningsSee the list below:
Hypercoagulability of pregnancy; investigations for hyperlipidemia, diabetes, valvular heart disease, hyperviscosity states, hemoglobinopathies, or congenital cerebrovascular disease (moyamoya)
In young patients with cerebral infarction, in the absence of other clear etiological causes, vasculitides and thrombophilic tendencies must be considered. Hypercoagulable testing including checking for anticardiolipin antibody, antithrombin III levels, prothrombin gene, protein S and protein C resistance, and factor V Leiden should be considered.
Usually, chorea gravidarum (CG) is manageable non-pharmacologically and traditional therapy consists of rest or seclusion and careful feeding. In mild chorea, patients are generally unaware of the involuntary movements and may have no complaints. In general, abnormal choreic movements are more distressing to the observers than to the patient. The mainstay of pharmacologic treatment is neuroleptic drugs, such as haloperidol, and steroids.
As noted previously, the declining incidence of CG in modern times reflects, in part, the declining frequency of rheumatic fever. This results in a situation in which a greater proportion of CG is secondary to other diseases such as autoimmune disorders. SLE exacerbation risk is 7 times higher during pregnancy and the first 2 months postpartum compared to nonpregnant individuals. Although a majority of patients with SLE and CG or chorea improve after starting or increasing steroid therapy, spontaneous remissions have occurred without change of steroid dose or with haloperidol therapy alone. Patients whose symptoms did not respond to steroids or haloperidol benefited from other drugs. Ichikawa et al reported morphologic alterations of an acute or relatively acute nature in the corpus callosum in at least 11 of the cases they reviewed.[7] This suggests that the response to steroid therapy may depend on whether the primary vascular lesion involving the basal ganglion is of an acute or chronic nature.
In regards to oral contraceptive pill-/estrogen-induced chorea, whether subsequent pregnancies trigger chorea in these women is not known. The mainstay of treatment consists of discontinuing the oral contraceptive pill and using a dopamine antagonist only if needed (ie, symptoms persist after discontinuing the oral contraceptive pill). In at least 2 dozen cases,[50, 9] most patients with estrogen-induced chorea were noted to be young, nulliparous women who had taken oral contraceptives for less than 4 months. A majority of these patients recovered within 2 days of stopping oral contraceptives. Of note, approximately 50% of patients had a history of Sydenham chorea, rheumatic fever, or CG.
Pharmacologic treatment
Drug treatment is indicated for patients with disabling severe chorea, when chorea interferes with the patient's health, or when the fetus is in danger due to dehydration, malnutrition, disturbed sleep, or injury.
Reserpine is potentially toxic to the fetus and is relatively contraindicated during pregnancy.
In 1972, Axley described the therapeutic value of haloperidol in rheumatic chorea.[51] In 1973, Shenker et al reported its effectiveness in Sydenham chorea.[52] Since then, haloperidol has been effective therapy for Sydenham chorea and moderate-to-severe CG.[53, 54]
Limited studies have demonstrated that risk of birth defects attributable to haloperidol is low as judged from studies of infants born to women who took haloperidol for control of hyperemesis gravidarum,[55, 56] especially if given after the first trimester when embryonic organogenesis is complete.
It is recommended that haloperidol therapy be discontinued as soon as possible to minimize the risk of tardive dyskinesia. Most common adverse reactions include extrapyramidal effects. Thus far, haloperidol has proven to be an effective, relatively safe treatment for moderate-to-severe CG.
Chlorpromazine (25–50 mg PO/IM TID/QID) either as monotherapy or in combination with diazepam (5 mg TID) has proved to be effective in ameliorating chorea.
Shannon and Fenichel suggest that pimozide has virtually no effect on norepinephrine receptors, thus in low doses and during short-term treatment has a lower risk for the appearance of tardive dyskinesia while improving Sydenham chorea symptoms.[57]
Valproic acid enhances the activity of GABA, an inhibitory neurotransmitter of the striatonigral and striatopallidal circuit, which is decreased markedly in brains of individuals with chorea. The use of sodium valproate in Sydenham chorea shows evidence of response within 10 days, with a dose of 15–20 mg/kg/d.
Pallares and Hurtado reported a large improvement in the first week of treatment of one patient using 20 mg/kg/d.[58] They suggest that the cholinergic action of carbamazepine in the striatum increases the acetylcholine level, inducing a new equilibrium in the balance of the dopaminergic and cholinergic systems.
In patients with Sydenham chorea, the dopaminergic system is hyperactive, and the cholinergic system is hypoactive. The stimulus by carbamazepine on the cholinergic system promotes a relative decrease in dopamine, similar to the action produced by neuroleptic drugs.[53, 54]
Clinical Context:
Antipsychotic and strong tranquilizer; butyrophenone used in treatment of acute psychosis, acute schizophrenia, manic phases, control of aggression, agitation, and disorganized and psychotic thinking. May be used to help treat false perceptions (eg, hallucinations, delusions), Gilles de la Tourette syndrome, and psychosis associated with dementia, depressions, or mania.
More likely to cause adverse effects such as tardive dyskinesia than most other antipsychotic drugs.
Clinical Context:
Benzisoxazole derivative, novel antipsychotic drug. Well absorbed after PO administration, has high bioavailability, and exhibits dose proportionality in therapeutic dose range, although interindividual plasma concentrations vary considerably. Food does not affect extent of absorption, thus can be administered with or without meals.
Peak plasma concentrations of parent drug reached within 1-2 h after intake. Mainly metabolized via hydroxylation and oxidative N-dealkylation. Major metabolite is 9-hydroxy-risperidone, which has similar activity to parent drug; clinical effect brought about by active moiety, namely risperidone plus 9-hydroxy-risperidone.
Hydroxylation depends on debrisoquine 4-hydroxylase (ie, metabolism of risperidone is sensitive to debrisoquine hydroxylation-type genetic polymorphism). Consequently, concentrations of parent drug and active metabolite differ substantially in extensive and poor metabolizers. However, concentration of active moiety (risperidone plus 9-hydroxy-risperidone) did not differ substantially between extensive and poor metabolizers, and elimination half-lives were similar in all subjects (approximately 20-24 h).
Rapidly distributed. Volume of distribution 1-2 L/kg. Steady-state concentrations of risperidone and active moiety were reached within 1-2 d and 5-6 d, respectively. In plasma, bound to albumin and alpha1-acid glycoprotein. Plasma protein binding of risperidone is approximately 88% and that of metabolite 77%. One wk after administration, 70% of dose excreted in urine and 14% in feces. In urine, risperidone plus 9-hydroxy-risperidone represents 35-45% of dose. Remainder is inactive metabolites.
Evaluated at dose range of 1-16 mg/d PO and compared to both placebo and haloperidol, studies indicated that risperidone is an effective antipsychotic agent improving both positive and negative symptoms.
Clinical Context:
Diphenylbutylpiperidine derivative with neuroleptic properties. Relatively nonsedating and can be administered in single daily dose.
Appears to have selective ability to block central dopaminergic receptors, although it affects norepinephrine turnover at higher doses. Extrapyramidal effects also are observed, but it appears to have fewer autonomic effects. Peak plasma level in humans occurs 3-8 h after administration, and plasma levels decrease slowly to approximately 50% of peak level at 48-72 h after dosing.
Used to suppress severe motor and phonic tics in patients with Tourette disorder whose symptoms have not responded satisfactorily to standard treatment (eg, haloperidol). Use also extended to management of manifestations of chronic schizophrenia in which main manifestations do not include excitement, agitation, or hyperactivity. Not indicated in treatment of patients with mania or acute schizophrenia.
Clinical Context:
Hypnotic and anxiolytic. At normal doses, this sleep induction does not affect breathing, blood pressure, or reflexes. When used in combination with analgesics, can help manage pain after surgery. Used for sedation for procedures (eg, CT scan) or for agitation that is interfering with ventilation.
Onset of action is 10-15 min. Metabolized to an active metabolite, trichloroethanol, which is excreted by kidney after conjugation to glucuronide salt. Plasma life is 8-64 h in neonates (mean 37 h). Protein binding is approximately 40%.
Available as supp, syr, or cap; mix syr with one-half glass (4 oz) water or fruit juice to minimize GI upset; cap should be swallowed whole followed by full glass (8 oz) of water or fruit juice.
Clinical Context:
Barbiturate mostly used as anticonvulsant. Usually used in treatment of grand mal and focal motor epilepsy. In addition, used prophylactically for febrile seizures in children. Exact mode and site of action of phenobarbital (and other barbiturates) in suppression of seizure activity unknown. Believed to work by reducing neuronal excitability and by increasing motor cortex threshold to electrical stimulation.
Use also extends to suppression of anxiety and apprehension.
Clinical Context:
Anticonvulsant whose activity may be related to increased brain concentrations of GABA. Peak serum levels occur approximately 1-4 h after single PO dose. Serum half-life typically 6-16 h. Primarily metabolized in liver to glucuronide conjugate. Elimination of valproic acid and its metabolites occur principally in urine, with minor amounts in feces and expired air.
Used as sole or adjunctive therapy in treatment of simple or complex absence seizures, including petit mal, and useful in primary generalized seizures with tonic-clonic manifestations. Also used for manic phase of depression and in migraine.
Clinical Context:
Chemically similar to cyclic antidepressants. Also manifests antimanic, antineuralgic, antidiuretic, anticholinergic, antiarrhythmic, and antipsychotic effects. Anticonvulsant action not known but may involve depressing activity in nucleus ventralis anterior of thalamus, resulting in reduction of polysynaptic responses and blocking posttetanic potentiation. Due to potentially serious blood dyscrasias, undertake benefit-to-risk evaluation before drug instituted. Peak serum levels in 4-5 h. Half-life (serum) in 12-17 h with repeated doses. Therapeutic serum levels are 4-12 mcg/mL. Metabolized in liver to active metabolite (ie, epoxide derivative) with half-life of 5-8 h. Metabolites excreted through feces and urine.
Clinical Context:
Anxiolytic sedative drug useful in symptomatic relief of anxiety and tension states. Also has adjunctive value in relief of certain neurospastic conditions. Peak blood levels reached within 1-2 h after single PO dosing. Acute half-life is 6-8 h with slower decline thereafter, possibly due to tissue storage. However, after repeated doses, blood levels increase significantly over 24-48 h.
In humans, comparable blood levels were obtained in maternal and cord blood, indicating placental transfer of drug.
Symptomatic management of mild-to-moderate degrees of anxiety in conditions dominated by tension, excitation, agitation, fear, or aggressiveness, such as may occur in psychoneurosis, anxiety reactions due to stress conditions, and anxiety states with somatic expression.
In acute alcohol withdrawal, may be useful in symptomatic relief of acute agitation, tremor, and impending acute delirium tremens.
As adjunct for relief of skeletal muscle spasm due to reflex spasm to local pathology, such as inflammation of muscle and joints or secondary to trauma; spasticity caused by upper motor neuron disorders, such as cerebral palsy and paraplegia; athetosis and rare "stiff man syndrome."
While usual daily dosages meet needs of most patients, some may require higher doses. In first few days of administration, cumulative effect may occur; therefore, increase dosage only after stabilization is apparent.
By binding to specific receptor sites, these agents appear to potentiate effects of GABA and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters.
Saher K Choudhary, MD, Director, Neurology Residency Program, Center for Neurology-Greer, Prisma Health; Affiliate Clinical Professor, University of South Carolina School of Medicine, Greenville; Locums Clinical Neurohospitalist, Greenville Memorial Hospital; Locums Neurologist in Telemedicine, Greenville Health Systems
Enrique Urrea-Mendoza, MD, Advanced Clinical Research Associate, Neuroscience Associates, Greenville Health System; Clinical Assistant Professor, University of South Carolina School of Medicine, Greenville; Instructor, Clemson University School of Health Research
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Nestor Galvez-Jimenez, MD, MSc, MHA, The Pauline M Braathen Endowed Chair in Neurology, Chairman, Department of Neurology, Program Director, Movement Disorders, Department of Neurology, Division of Medicine, Cleveland Clinic Florida
Disclosure: Nothing to disclose.
Chief Editor
Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida Morsani College of Medicine
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Bioserenity, Catalyst, Ceribell, Eisai, Jazz, LivaNova, Neurelis, Neuropace, SK Life Science Science, Sunovion, Takeda, UCB<br/>Serve(d) as a speaker or a member of a speakers bureau for: Catalyst, Jazz, LivaNova, Neurelis, SK Life Science, Stratus, UCB<br/>Received research grant from: Cerevel Therapeutics; Ovid Therapeutics; Neuropace; Jazz; SK Life Science, Xenon Pharmaceuticals, UCB, Marinus, Longboard.
Additional Contributors
Stephen T Gancher, MD, Adjunct Associate Professor, Department of Neurology, Oregon Health Sciences University
Disclosure: Nothing to disclose.
Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS, † Professor Emeritus of Neurology and Psychiatry, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Neuroscience Director, Department of Neurology, Crouse Irving Memorial Hospital
Kim, Ok; Kim, A; Seo, M W; Kweon, J Y; Ahn, H Y; Park, et al. Chorea gravidarum associated with Moyamoya disease. J Perinatal Med. 2007. 35(Suppl II):S187.
Markham CH, Ansel RD. Drugs and motor behaviour. Jarvik ME, ed. Psychopharmacology in the Practice of Medicine. NY: Appleton Century Crofts; 1977. 127-139.
Wall C, Andrews HR. On chorea in pregnancy. J Obstet Gynaecol Br. 1903. 3:540-547.
