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Acute and Chronic Chorea in Childhood Donald L Acute and Chronic Chorea in Childhood Donald L. Gilbert, MD, MS This review discusses diagnostic evaluation and management of chorea in childhood. Chorea is an involuntary, hyperkinetic movement disorder characterized by continuous, jerky, or flowing movement fragments, with irregular timing and direction. It tends to be enhanced by voluntary actions and generally causes interference with fine motor function. The diagnostic evaluation begins with accurate classification of the movement disorder followed by consideration of the time course. Most previously healthy children presenting with acute/subacute chorea have an autoimmune etiology. Chronic chorea usually occurs as part of encephalopathies or diseases causing more global neurologic symptoms. We review the management of acute/subacute and chronic choreas, with special emphasis on Sydenham chorea and benign hereditary chorea. Semin Pediatr Neurol 16:71–76 © 2009 Published by Elsevier Inc. horea is a nonpatterned, involuntary, hyperkinetic genetic chorea, will be emphasized. Paroxysmal movement Cmovement disorder. It is continuous, variable in speed, disorders involving chorea will not be discussed but are re- unpredictable in timing and direction, and flowing or jerky in viewed elsewhere.4 As the phenomenology of chorea over- appearance.1 Chorea may be accompanied by athetosis or laps in acute and chronic choreas, most features of the neu- ballism. Athetosis is also continuous but the rate is slower. rologic examination will be discussed under acute chorea. Athetosis often accompanies dystonia or occurs in symptom- atic chorea and may be referred to as choreoathetosis. Ballism designates larger amplitude, flinging, proximally generated Acute Chorea movements. It rarely occurs in isolation in children but can accompany chorea. Clinical Characteristics Anatomically, chorea classically most often results from of Acute/Subacute Chorea disturbances in the caudate or putamen.2 Occasionally, the History of Present Illness source may be thalamic/subthalamic.3 A number of neurode- In childhood, chorea is most often acquired acutely or sub- generative ataxias can also present with prominent chorea. acutely. It interferes with purposeful movements and often Because of the vulnerability of the basal ganglia and its with speech. Parents can describe the hour, day, or week of connections to a wide variety of pathologies, the differential onset and the way in which the child’s speech and purposeful diagnosis of acute and chronic chorea is very large. Genetic movements have changed. In subtle cases, parents will report and metabolic diseases, endocrine disturbances, autoim- that coordination or speech has been affected in ways that mune disorders, infections, cerebrovascular disease, neo- may not be apparent to the examiner. When the observable, plasms, neurodegenerative diseases, toxins, and trauma can choreic movements are being discussed in clinic, children all result in chorea. A detailed review of the entire spectrum with mature communication and awareness should be able to of these diseases would exceed space limitations for this ar- describe the subjective nature of the movements, that is, the ticle. This review will discuss acute and chronic chorea, em- movements are involuntary, nonsuppressible, and not per- phasizing clinical diagnosis and management. Sydenham formed in response to an urge or sensation. They may de- chorea, the most common acute/subacute acquired chorea in scribe that the movements make them clumsy and that their childhood, and benign hereditary chorea, a rare but primary speech is slurred or slow. The movements generally cause functional interference. This can be gauged by asking about difficulties with activities of daily living. From the Movement Disorders Clinics, Cincinnati Children’s Hospital Med- A careful history of possible antecedents to acute chorea is ical Center, Cincinnati, OH. critical. As the most common etiology is autoimmune and Address reprint requests to Donald L. Gilbert, MD, MS, Division of Neurol- ogy, Cincinnati Children’s Hospital Medical Center ML 11006 and Neu- poststreptococcal, a careful history of known or possible up- rology, 3333 Burnet Avenue, Cincinnati OH. E-mail: donald.gilbert@ per respiratory infections or other illnesses should be sought. cchmc.org Exposures to and doses of psychiatric and other medications, 1071-9091/09/$-see front matter © 2009 Published by Elsevier Inc. 71 doi:10.1016/j.spen.2009.03.009 72 D.L. Gilbert Table 1 Neurologic Examination in the Child With Chorea Neurologic Examination Key Findings Mental status Emotional changes may be present as part of or in response to the disease. Note that the presence of involuntary facial movements that do not match the child’s mood or meaning may confound assessment. Cranial nerve May be normal. Slurring of speech due to motor control problems of face and tongue, and not due to brainstem or cranial nerve pathology. Motor examination Bulk and reflexes may be normal; tone may be normal or low. Strength may appear weak due to motor impersistence, ie, involuntary relaxations or choreic intrusions on sustained motor output. Classic examples include “milk maid’s grip” during sustained grip and “darting tongue” during sustained tongue protrusion. Actions enhance chorea. With arms outstretched horizontally, hands pronated, and fingers spread wide, there may be hyperextension at the metacarpophalangeal joints (a dystonic posture referred to as “spooning”) and irregular distal movements. The “touchdown sign” is an inability to maintain hands and arms fully extended and supinated over head due to chorea. Additional tasks, such as talking or protruding tongue, may magnify hand/arm findings. Sensory examination Typically normal. Significant sensory hypersensitivity suggests akathisia rather than chorea. Cerebellar and gait Important and sometimes challenging to discern. Cerebellar dysfunction on finger to nose and gait/tandem gait testing should be fairly regular. In contrast, basal ganglia dysfunction results in interference due to irregularly timed choreic intrusions on the trajectory of limb movements, causing the finger to miss the target or the gait to lurch. In some diseases, cerebellar and basal ganglia dysfunction co-occur. exposure to toxins, detailed medical and developmental his- Diagnostic Approach tory, recent psychological stressors, and review of systems The critical component is identifying and classifying the should be routinely obtained. movement disorder. Once established that the problem is General and Neurologic Examination acute chorea, the history should point to a relatively limited During the process of taking the history, the clinician will number of categories of disease, and from there the testing generally observe that the child’s trunk appears restless and is can be targeted. Selected etiologies are listed in Table 2. moving continuously in a random manner that is distinct from titubation seen in ataxias. The child with acute chorea may have generalized or localized dyskinetic movements. Usually, there is prominent involvement of the face and 1 or Table 2 Etiology of Acute Chorea in Childhood: Categories both arms and hands. Irregularly flowing or jerking, contin- and Selected Examples uous movements give an appearance of restlessness. Facial Etiologic and tongue chorea may slur or slow speech. Marked asym- Category Examples metry of upper limb chorea may occur. Autoimmune Poststreptococcal, Sydenham chorea5 The general examination is important for other signs of Systemic lupus erythematosis6 illnesses, particularly those indicating autoimmune diseases Antiphospholipid antibody syndrome7 and infections. Skin, heart, joints, and lymph nodes should Other infections Herpes simplex virus,8 Mycoplasma9 be emphasized. Identifying an integral non-neurologic fea- and ture of a disease narrows the differential diagnosis of the encephalitides movement disorder. For example, the presence of joint in- Vascular/hypoxic Stroke; post cardiac transplantation— 10 flammation or a systolic cardiac murmur supports an auto- ischemic “post pump chorea” in infants Static damage in dyskinetic cerebral immune etiology. palsy, markedly exacerbated The neurologic examination should be thorough, empha- dyskinesia with febrile illness11 sizing portions of the examination related to basal ganglia Mitochondrial Mitochondrial encephalopathy with and cerebellar function. The clinician should carefully observe disease lactic acidosis and stroke (MELAS): the child’s motor system at rest as well as while performing acute basal ganglia injury12 sustained movements and common actions. Videotaping the Toxins Carbon monoxide13 examination is helpful to allow reviewing phenomenology and Iatrogenic Dopamine receptor blocking agents/ assessing severity over time. Key findings of the neurologic ex- neuroleptics/antipsychotics: acute, amination are described in Table 1. tardive, withdrawal-emergent14 Finally, it is important to note that fairly continuous, fre- Psychostimulants quent myoclonus, particularly with dystonia, may lead to a Anticonvulsants Psychogenic Conversion disorder15 movement disorder that appears identical to chorea. Acute and chronic chorea in childhood 73 Diagnostic Testing infections, based on Jones criteria.17 GABHS are Gram-posi- Laboratory Testing. A subacute course is most common tive bacteria that colonize or invade the upper respiratory and supports an inflammatory disease, most commonly post- tract. In selected cases, possibly due to molecular mimicry, streptococcal. Documenting
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