ILLUSTRATIVE CASE
Cocaine-Induced Dystonic Reaction An Unlikely Presentation of Child Neglect Jamie M. Pinto, MD,* Kavita Babu, MD,Þ and Carole Jenny, MD, MBAþ
Abstract: Child neglect can be difficult to recognize. Parental substance abuse may place a child at increased risk of neglect. This report reviews 2 cases of dystonic reaction in children after accidental exposure to cocaine in their home environments. The reports are followed by a review of proposed physiologic mechanisms for cocaine-induced dystonia and a discussion on neurological symptoms that may develop after cocaine exposure. Pediatric emergency physicians should consider cocaine exposure when a child of any age presents with abnormal movements. Dystonic reaction is an uncommon, but reported, complication of cocaine exposure in the absence of other risk factors and may be the first presentation of child neglect. Key Words: cocaine, dystonia, dystonic reaction, child neglect (Pediatr Emer Care 2013;29: 1006Y1008)
N
eglect is defined as deprivation of adequate clothing, food, medical attention, shelter, or a failure to provide supervision such that a child’s well-being is placed at risk.1 Parental substance abuse may increase a child’s risk of neglect.2,3 Data from the National Survey on Drug Use and Health show that 1.9% of women with children younger than 18 years abuse illicit drugs; more than 20% of these women abuse cocaine.4 It is well reported that cocaine use can predispose to dystonic reactions in patients taking dopamine blocking medications.5Y7 In addition, cocaine is a known, but uncommon, cause of dystonic reactions in the absence of other risk factors.8Y10 To our knowledge, currently reported cases of cocaine ingestion independently triggering dystonic reactions have all been in recreational drug users. We report here 2 cases of child neglect, which presented as dystonic reactions after accidental exposure to cocaine.
CASE 1 A previously healthy 7-year-old boy presented to the emergency department (ED) with the chief complaint of odd movements. His mother described an episode of exaggerated posturing of his extremities and rhythmic movements, during which he had no loss of consciousness and no tonic-clonic shaking. The child was also noted to have a fixed rightward gaze. The movements were involuntary, but he was aware of them and found them anxiety provoking. His pupils were dilated, and his speech was rapid with flight of ideas. The self-resolved episode lasted for 20 minutes, after which the patient appeared tired. The patient and family denied recent head trauma, fevers, headaches, nausea, vomiting, or bowel or bladder incontinence. He had no access to
From the *K. Hovnanian Children’s Hospital, Neptune, NJ; †Rhode Island Hospital; and ‡Hasbro Children’s Hospital, Warren Alpert Medical School of Brown University, Providence, RI. Disclosure: The authors declare no conflict of interest. Reprints: Jamie M. Pinto, MD, K. Hovnanian Children’s Hospital, 1945 Route 33, Neptune, NJ 07753 (e-mail: [email protected]). Copyright * 2013 by Lippincott Williams & Wilkins ISSN: 0749-5161
1006
www.pec-online.com
neuroleptics or antiemetics in his home environment. There was no family history of seizure, dystonia, or movement disorders. The parents brought the child to the hospital 6 hours after the event for evaluation. On arrival to the pediatric ED, the child had an unremarkable examination findings, including a nonfocal neurological assessment. He was afebrile, with a heart rate of 89 beats per minute and a blood pressure of 100/65 mm Hg. His magnesium level was 1.9 mEq/L, and his calcium level was 9.3 mg/dL, both within reference range. Creatine phosphokinase (CPK) was also normal (63 IU/L [normal, 41Y277 IU/L]). The patient was admitted to the hospital for further evaluation of dystonic reaction with no clear inciting cause. An electroencephalogram finding was negative for epileptiform discharges. No intracranial masses or sclerosis were identified on magnetic resonance imaging or magnetic resonance angiography of the brain. Thyroid stimulating hormone was 2.81 mU/L (normal, 0.7Y6.4 mU/L). Urine toxicology screen was positive for cocaine metabolites by immunoassay, and the presence of cocaine was confirmed by mass spectrometric analysis. Comprehensive toxicologic testing did not indicate the presence of other illicit or pharmaceutical drugs. Upon repeat questioning, parents disclosed frequent cocaine use at home. Although the 7-year-old patient noted seeing a white dust in his parents’ bedroom, in which he coslept, he denied intentionally ingesting the drug. The police found cocaine in his home. He had no further dystonic events after admission. He was discharged into the care of the state social service agency. His parents were charged with child neglect and voluntarily enrolled into a drug treatment program.
CASE 2 A 4-year-old boy was seen in his primary care physician’s office with acute dystonia after ingestion of an unknown pill. His head was rigidly turned to the right, and his right arm was extended. The physician advised transport to the ED via ambulance, but the child’s father refused transport and left the office. Instead, he took the child to a relative’s house, who eventually brought the child to the ED. At the bedside, the father reported that earlier, the child had had ‘‘an allergic reaction’’ with swollen eyes and a puffy face. He did not mention the possible ingestion, but the primary care physician had called the ED to report the visit to his office. When asked, the child said he ate ‘‘chalk.’’ In the ED, the child was afebrile, with a heart rate of 136 beats per minute and a blood pressure of 114/83 mm Hg. His neurological examination was nonfocal. A urine toxicology screen was positive for cocaine metabolites; mass spectrometric analysis confirmed the presence of cocaine. Comprehensive toxicologic testing also indicated the presence of ibuprofen but did not indicate the presence of other illicit or pharmaceutical drugs. The child was admitted to the hospital for observation. He had an elevated CPK (2130 IU/L [normal 41Y277 IU/L]), an elevated anion gap (19 [normal 3Y13]), and an elevated osmolar gap. Testing for ethanol, aspirin, acetaminophen, and toxic alcohols were unrevealing. Pediatric Emergency Care
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Volume 29, Number 9, September 2013
Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Pediatric Emergency Care
&
Volume 29, Number 9, September 2013
TABLE 1. Toxicologic Causes of Acute Dystonia Medication/Drug Class
Representative Medications
Commonly reported Antipsychotics, typical Antipsychotics, atypical Antiemetics Anticonvulsants Antidepressants Antimalarials Cocaine MDMA Uncommonly reported Buspirone Benzodiazepines Triptans Lithium
Haloperidol, chlorpromazine Quetiapine, aripiprazole Compazine, metoclopramide Carbamazepine, phenytoin Fluoxetine, bupropion Chloroquine, hydroxychloroquine
Diazepam, alprazolam Sumatriptan
MDMA indicates 3,4-methylenedioxy-N-methylamphetamine.
The patient’s hospital course was benign; his anion gap elevation and osmolar gap elevation resolved during hospitalization and CPK improved to 1926 IU/L, with no recurrence of symptoms. The police found cocaine in his home, and the patient was discharged into the care of the state social service agency.
DISCUSSION Dystonia is a common movement disorder that involves sustained, involuntary muscle contractions; however, the exact physiologic basis for dystonia remains elusive. Dystonia is a known adverse effect of multiple drugs (Table 1). It can also occur secondary to drug withdrawal (Table 2). Classically, dystonic reactions are considered hyperkinetic disorders that occur when there are alterations of the dopaminergic balance within the indirect pathway of the basal ganglia.11 It is thought that the indirect pathway has a net inhibitory effect on movement.11 Theoretically, dopamine blockade should increase the activity of the inhibitory indirect pathway. It is therefore somewhat counterintuitive that dopamine blocking agents cause dystonia. Authors theorize that dopamine blockade causes a compensatory increase in dopamine production, increased sensitivity of the postsynaptic receptor, and excessive striatal cholinergic output as the body’s adaptive response.12 Cocaine is known to inhibit the reuptake of dopamine into cells, which increases the amount of available postsynaptic dopamine.13 It can then be postulated that dystonia is the result of increased dopaminergic tone that inhibits the indirect pathway, causing a hyperkinetic state. Conversely, more current evidence suggests that dystonia might be a result of decreased, not increased, dopamine activity within the indirect pathway or from instability of normal feedback
TABLE 2. Toxicologic Causes of Acute Dystonia During Withdrawal
Cocaine-Induced Dystonic Reaction
loops within the basal ganglia.11 It can then be argued that cocaine predisposes to dystonic reaction by depleting dopamine stores and that dystonia is a result of cocaine withdrawal, not acute intoxication.8 The available evidence is inconclusive, and the exact physiologic basis of cocaine-induced dystonia is yet to be determined. Cocaine use has been associated with various movement disorders in addition to dystonia, including akathisia, chorea (colloquially called ‘‘crack dancing’’), tremor, myoclonus, and tics.14 In the pediatric population, seizure is a common presentation of symptomatic cocaine ingestion.15Y17 Although ingestion or administration may be intentional, infants and young children can be accidentally exposed to cocaine both by inhalation of vapors or by inadvertent ingestion of cocaine dust in their environment.18Y20 Both active and passive cocaine exposure by children is prevalent in certain urban settings.15,16 This is likely underestimated because children exposed to cocaine can be asymptomatic.18 A comprehensive evaluation for potential causes of dystonia was completed for the first patient, as our original index of suspicion for substance-induced dystonia was low. Once other causes of dystonia were excluded and the child had no further events, we came to the conclusion that this child’s movement disorder was caused solely by cocaine. An extensive workup was avoided in the second case, when cocaine was suspected and the exposure was confirmed. It is interesting to note that both young age and male sex, have been previously identified as risk factors for dystonia.21 Our patients’ dystonic reactions secondary to accidental cocaine ingestion represent atypical, but important, presentations of supervisory neglect resulting in bodily harm. Each child’s wellbeing was endangered both by his access to and by his ingestion of cocaine. As both cases illustrate, some parents might be reluctant to disclose a child’s exposure to cocaine, interfering with a health care provider’s ability to make the correct diagnosis and placing the child in danger of unnecessary medical evaluation. Providers must maintain a high index of suspicion for toxicologic exposure in patients with a new dystonia to be able to identify atrisk patients. Cocaine is detected on commonly available urine drug screens; however, more comprehensive testing is required to identify potential toxicologic exposures, such as haloperidol or antiemetics that may also signal supervisory neglect or criminal poisoning. These are not the first reported cases of unintentional cocaine ingestion in the pediatric literature.16,19,20 However, this is the first report of dystonic reactions from involuntary cocaine exposure outside of the newborn period.22 Pediatricians should consider cocaine exposure in the differential diagnosis for dystonic reaction at any age.
CONCLUSIONS To our knowledge, these are the first reports of dystonia secondary to accidental cocaine exposure during childhood. Pediatric ED physicians should be aware of this association and that dystonia may be the presenting symptom of child neglect. Correct diagnosis can avoid costly investigations for alternative causes of dystonia and allow for temporary foster placement of the child while the parents receive treatment and services for their substance abuse issues. REFERENCES
Medication Baclofen F-hydroxybutyric acid Amantadine * 2013 Lippincott Williams & Wilkins
1. US Department of Health and Human Services. Definitions of child abuse and neglect. Child Welfare Information Gateway Website. Available at: http://www.childwelfare.gov/systemwide/laws_policies/ statutes/define.cfm. Accessed June 6, 2012.
www.pec-online.com
Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
1007
Pediatric Emergency Care
Pinto et al
2. Chaffin M, Kelleher K, Hollenberg J. Onset of physical abuse and neglect: psychiatric, substance abuse, and social risk factors from prospective community data. Child Abuse Negl. 1996;20:191Y203. 3. Ondersma SJ. Predictors of neglect within low-SES families: the importance of substance abuse. Am J Orthopsychiatry. 2002;72: 383Y391.
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Volume 29, Number 9, September 2013
12. Marsden CD, Jenner P. The pathophysiology of extrapyramidal side-effects of neuroleptic drugs. Psychol Med. 1980;10:55Y72. 13. Weiner WJ, Rabinstein A, Levin B, et al. Cocaine-induced persistent dyskinesias. Neurology. 2001;56:964Y965. 14. Williams O. Movement disorders and substance abuse. Continuum. 2004;10:77Y87.
4. Simmons LA, Havens JR, Whiting JB, et al. Illicit drug use among women with children in the United States: 2002Y2003. Ann Epidemiol. 2009;19:187Y193.
15. Shannon M, Lacouture PG, Roa J, et al. Cocaine exposure among children seen at a pediatric hospital. Pediatrics. 1989;83:337Y342.
5. Kumor K, Sherer M, Jaffe J. Haloperidol-induced dystonia in cocaine addicts. Lancet. 1986;2:1341Y1342.
16. Mott SH, Packer RJ, Soldin SJ. Neurologic manifestations of cocaine exposure in childhood. Pediatrics. 1994;93:557Y560.
6. Hegarty AM, Lipton RB, Merriam AE, et al. Cocaine as a risk factor for acute dystonic reactions. Neurology. 1991;41:1670Y1672.
17. Ernst AA, Sanders WM. Unexpected cocaine intoxication presenting as seizures in children. Ann Emerg Med. 1989;18:774Y777.
7. Horwitz EH, van Harten PN. Acute dystonias in combined use of cocaine and neuroleptics [in Dutch]. Ned Tijdschr Geneeskd. 1994;138:2405Y2407.
18. Kharasch SJ, Glotzer D, Vinci R, et al. Unsuspected cocaine exposure in young children. Am J Dis Child. 1991;145:204Y206.
8. Choy-Kwong M, Lipton RB. Dystonia related to cocaine withdrawal: a case report and pathogenic hypothesis. Neurology. 1989;39:996Y997. 9. Farrell PE, Diehl AK. Acute dystonic reaction to crack cocaine. Ann Emerg Med. 1991;20:322. 10. Merab J. Acute dystonic reaction to cocaine. Am J Med. 1988;84:564. 11. Sanger TD. Childhood onset generalized dystonia can be modeled by increased gain in the indirect basal ganglia pathway. J. Neurol Neurosurg Psychiatry. 2003;74:1509Y1515.
1008
www.pec-online.com
19. Heidemann SM, Goetting MG. Passive inhalation of cocaine by infants. Henry Ford Hosp Med J. 1990;38:252Y254. 20. Bateman DA, Heagarty MC. Passive freebase cocaine (‘crack’) inhalation by infants and toddlers. Am J Dis Child. 1989;143:25Y27. 21. Rodnitzky R. Drug-induced movement disorders. Clin Neuropharmacol. 2002;25:142Y152. 22. Beltran RS, Coker SB. Transient dystonia of infancy, a result of intrauterine cocaine exposure? Pediatr Neurol. 1995;12:354Y356.
* 2013 Lippincott Williams & Wilkins
Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Cocaine-Induced Dystonic Reaction An Unlikely Presentation of Child Neglect Jamie M. Pinto, MD,* Kavita Babu, MD,Þ and Carole Jenny, MD, MBAþ
Abstract: Child neglect can be difficult to recognize. Parental substance abuse may place a child at increased risk of neglect. This report reviews 2 cases of dystonic reaction in children after accidental exposure to cocaine in their home environments. The reports are followed by a review of proposed physiologic mechanisms for cocaine-induced dystonia and a discussion on neurological symptoms that may develop after cocaine exposure. Pediatric emergency physicians should consider cocaine exposure when a child of any age presents with abnormal movements. Dystonic reaction is an uncommon, but reported, complication of cocaine exposure in the absence of other risk factors and may be the first presentation of child neglect. Key Words: cocaine, dystonia, dystonic reaction, child neglect (Pediatr Emer Care 2013;29: 1006Y1008)
N
eglect is defined as deprivation of adequate clothing, food, medical attention, shelter, or a failure to provide supervision such that a child’s well-being is placed at risk.1 Parental substance abuse may increase a child’s risk of neglect.2,3 Data from the National Survey on Drug Use and Health show that 1.9% of women with children younger than 18 years abuse illicit drugs; more than 20% of these women abuse cocaine.4 It is well reported that cocaine use can predispose to dystonic reactions in patients taking dopamine blocking medications.5Y7 In addition, cocaine is a known, but uncommon, cause of dystonic reactions in the absence of other risk factors.8Y10 To our knowledge, currently reported cases of cocaine ingestion independently triggering dystonic reactions have all been in recreational drug users. We report here 2 cases of child neglect, which presented as dystonic reactions after accidental exposure to cocaine.
CASE 1 A previously healthy 7-year-old boy presented to the emergency department (ED) with the chief complaint of odd movements. His mother described an episode of exaggerated posturing of his extremities and rhythmic movements, during which he had no loss of consciousness and no tonic-clonic shaking. The child was also noted to have a fixed rightward gaze. The movements were involuntary, but he was aware of them and found them anxiety provoking. His pupils were dilated, and his speech was rapid with flight of ideas. The self-resolved episode lasted for 20 minutes, after which the patient appeared tired. The patient and family denied recent head trauma, fevers, headaches, nausea, vomiting, or bowel or bladder incontinence. He had no access to
From the *K. Hovnanian Children’s Hospital, Neptune, NJ; †Rhode Island Hospital; and ‡Hasbro Children’s Hospital, Warren Alpert Medical School of Brown University, Providence, RI. Disclosure: The authors declare no conflict of interest. Reprints: Jamie M. Pinto, MD, K. Hovnanian Children’s Hospital, 1945 Route 33, Neptune, NJ 07753 (e-mail: [email protected]). Copyright * 2013 by Lippincott Williams & Wilkins ISSN: 0749-5161
1006
www.pec-online.com
neuroleptics or antiemetics in his home environment. There was no family history of seizure, dystonia, or movement disorders. The parents brought the child to the hospital 6 hours after the event for evaluation. On arrival to the pediatric ED, the child had an unremarkable examination findings, including a nonfocal neurological assessment. He was afebrile, with a heart rate of 89 beats per minute and a blood pressure of 100/65 mm Hg. His magnesium level was 1.9 mEq/L, and his calcium level was 9.3 mg/dL, both within reference range. Creatine phosphokinase (CPK) was also normal (63 IU/L [normal, 41Y277 IU/L]). The patient was admitted to the hospital for further evaluation of dystonic reaction with no clear inciting cause. An electroencephalogram finding was negative for epileptiform discharges. No intracranial masses or sclerosis were identified on magnetic resonance imaging or magnetic resonance angiography of the brain. Thyroid stimulating hormone was 2.81 mU/L (normal, 0.7Y6.4 mU/L). Urine toxicology screen was positive for cocaine metabolites by immunoassay, and the presence of cocaine was confirmed by mass spectrometric analysis. Comprehensive toxicologic testing did not indicate the presence of other illicit or pharmaceutical drugs. Upon repeat questioning, parents disclosed frequent cocaine use at home. Although the 7-year-old patient noted seeing a white dust in his parents’ bedroom, in which he coslept, he denied intentionally ingesting the drug. The police found cocaine in his home. He had no further dystonic events after admission. He was discharged into the care of the state social service agency. His parents were charged with child neglect and voluntarily enrolled into a drug treatment program.
CASE 2 A 4-year-old boy was seen in his primary care physician’s office with acute dystonia after ingestion of an unknown pill. His head was rigidly turned to the right, and his right arm was extended. The physician advised transport to the ED via ambulance, but the child’s father refused transport and left the office. Instead, he took the child to a relative’s house, who eventually brought the child to the ED. At the bedside, the father reported that earlier, the child had had ‘‘an allergic reaction’’ with swollen eyes and a puffy face. He did not mention the possible ingestion, but the primary care physician had called the ED to report the visit to his office. When asked, the child said he ate ‘‘chalk.’’ In the ED, the child was afebrile, with a heart rate of 136 beats per minute and a blood pressure of 114/83 mm Hg. His neurological examination was nonfocal. A urine toxicology screen was positive for cocaine metabolites; mass spectrometric analysis confirmed the presence of cocaine. Comprehensive toxicologic testing also indicated the presence of ibuprofen but did not indicate the presence of other illicit or pharmaceutical drugs. The child was admitted to the hospital for observation. He had an elevated CPK (2130 IU/L [normal 41Y277 IU/L]), an elevated anion gap (19 [normal 3Y13]), and an elevated osmolar gap. Testing for ethanol, aspirin, acetaminophen, and toxic alcohols were unrevealing. Pediatric Emergency Care
&
Volume 29, Number 9, September 2013
Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Pediatric Emergency Care
&
Volume 29, Number 9, September 2013
TABLE 1. Toxicologic Causes of Acute Dystonia Medication/Drug Class
Representative Medications
Commonly reported Antipsychotics, typical Antipsychotics, atypical Antiemetics Anticonvulsants Antidepressants Antimalarials Cocaine MDMA Uncommonly reported Buspirone Benzodiazepines Triptans Lithium
Haloperidol, chlorpromazine Quetiapine, aripiprazole Compazine, metoclopramide Carbamazepine, phenytoin Fluoxetine, bupropion Chloroquine, hydroxychloroquine
Diazepam, alprazolam Sumatriptan
MDMA indicates 3,4-methylenedioxy-N-methylamphetamine.
The patient’s hospital course was benign; his anion gap elevation and osmolar gap elevation resolved during hospitalization and CPK improved to 1926 IU/L, with no recurrence of symptoms. The police found cocaine in his home, and the patient was discharged into the care of the state social service agency.
DISCUSSION Dystonia is a common movement disorder that involves sustained, involuntary muscle contractions; however, the exact physiologic basis for dystonia remains elusive. Dystonia is a known adverse effect of multiple drugs (Table 1). It can also occur secondary to drug withdrawal (Table 2). Classically, dystonic reactions are considered hyperkinetic disorders that occur when there are alterations of the dopaminergic balance within the indirect pathway of the basal ganglia.11 It is thought that the indirect pathway has a net inhibitory effect on movement.11 Theoretically, dopamine blockade should increase the activity of the inhibitory indirect pathway. It is therefore somewhat counterintuitive that dopamine blocking agents cause dystonia. Authors theorize that dopamine blockade causes a compensatory increase in dopamine production, increased sensitivity of the postsynaptic receptor, and excessive striatal cholinergic output as the body’s adaptive response.12 Cocaine is known to inhibit the reuptake of dopamine into cells, which increases the amount of available postsynaptic dopamine.13 It can then be postulated that dystonia is the result of increased dopaminergic tone that inhibits the indirect pathway, causing a hyperkinetic state. Conversely, more current evidence suggests that dystonia might be a result of decreased, not increased, dopamine activity within the indirect pathway or from instability of normal feedback
TABLE 2. Toxicologic Causes of Acute Dystonia During Withdrawal
Cocaine-Induced Dystonic Reaction
loops within the basal ganglia.11 It can then be argued that cocaine predisposes to dystonic reaction by depleting dopamine stores and that dystonia is a result of cocaine withdrawal, not acute intoxication.8 The available evidence is inconclusive, and the exact physiologic basis of cocaine-induced dystonia is yet to be determined. Cocaine use has been associated with various movement disorders in addition to dystonia, including akathisia, chorea (colloquially called ‘‘crack dancing’’), tremor, myoclonus, and tics.14 In the pediatric population, seizure is a common presentation of symptomatic cocaine ingestion.15Y17 Although ingestion or administration may be intentional, infants and young children can be accidentally exposed to cocaine both by inhalation of vapors or by inadvertent ingestion of cocaine dust in their environment.18Y20 Both active and passive cocaine exposure by children is prevalent in certain urban settings.15,16 This is likely underestimated because children exposed to cocaine can be asymptomatic.18 A comprehensive evaluation for potential causes of dystonia was completed for the first patient, as our original index of suspicion for substance-induced dystonia was low. Once other causes of dystonia were excluded and the child had no further events, we came to the conclusion that this child’s movement disorder was caused solely by cocaine. An extensive workup was avoided in the second case, when cocaine was suspected and the exposure was confirmed. It is interesting to note that both young age and male sex, have been previously identified as risk factors for dystonia.21 Our patients’ dystonic reactions secondary to accidental cocaine ingestion represent atypical, but important, presentations of supervisory neglect resulting in bodily harm. Each child’s wellbeing was endangered both by his access to and by his ingestion of cocaine. As both cases illustrate, some parents might be reluctant to disclose a child’s exposure to cocaine, interfering with a health care provider’s ability to make the correct diagnosis and placing the child in danger of unnecessary medical evaluation. Providers must maintain a high index of suspicion for toxicologic exposure in patients with a new dystonia to be able to identify atrisk patients. Cocaine is detected on commonly available urine drug screens; however, more comprehensive testing is required to identify potential toxicologic exposures, such as haloperidol or antiemetics that may also signal supervisory neglect or criminal poisoning. These are not the first reported cases of unintentional cocaine ingestion in the pediatric literature.16,19,20 However, this is the first report of dystonic reactions from involuntary cocaine exposure outside of the newborn period.22 Pediatricians should consider cocaine exposure in the differential diagnosis for dystonic reaction at any age.
CONCLUSIONS To our knowledge, these are the first reports of dystonia secondary to accidental cocaine exposure during childhood. Pediatric ED physicians should be aware of this association and that dystonia may be the presenting symptom of child neglect. Correct diagnosis can avoid costly investigations for alternative causes of dystonia and allow for temporary foster placement of the child while the parents receive treatment and services for their substance abuse issues. REFERENCES
Medication Baclofen F-hydroxybutyric acid Amantadine * 2013 Lippincott Williams & Wilkins
1. US Department of Health and Human Services. Definitions of child abuse and neglect. Child Welfare Information Gateway Website. Available at: http://www.childwelfare.gov/systemwide/laws_policies/ statutes/define.cfm. Accessed June 6, 2012.
www.pec-online.com
Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
1007
Pediatric Emergency Care
Pinto et al
2. Chaffin M, Kelleher K, Hollenberg J. Onset of physical abuse and neglect: psychiatric, substance abuse, and social risk factors from prospective community data. Child Abuse Negl. 1996;20:191Y203. 3. Ondersma SJ. Predictors of neglect within low-SES families: the importance of substance abuse. Am J Orthopsychiatry. 2002;72: 383Y391.
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Volume 29, Number 9, September 2013
12. Marsden CD, Jenner P. The pathophysiology of extrapyramidal side-effects of neuroleptic drugs. Psychol Med. 1980;10:55Y72. 13. Weiner WJ, Rabinstein A, Levin B, et al. Cocaine-induced persistent dyskinesias. Neurology. 2001;56:964Y965. 14. Williams O. Movement disorders and substance abuse. Continuum. 2004;10:77Y87.
4. Simmons LA, Havens JR, Whiting JB, et al. Illicit drug use among women with children in the United States: 2002Y2003. Ann Epidemiol. 2009;19:187Y193.
15. Shannon M, Lacouture PG, Roa J, et al. Cocaine exposure among children seen at a pediatric hospital. Pediatrics. 1989;83:337Y342.
5. Kumor K, Sherer M, Jaffe J. Haloperidol-induced dystonia in cocaine addicts. Lancet. 1986;2:1341Y1342.
16. Mott SH, Packer RJ, Soldin SJ. Neurologic manifestations of cocaine exposure in childhood. Pediatrics. 1994;93:557Y560.
6. Hegarty AM, Lipton RB, Merriam AE, et al. Cocaine as a risk factor for acute dystonic reactions. Neurology. 1991;41:1670Y1672.
17. Ernst AA, Sanders WM. Unexpected cocaine intoxication presenting as seizures in children. Ann Emerg Med. 1989;18:774Y777.
7. Horwitz EH, van Harten PN. Acute dystonias in combined use of cocaine and neuroleptics [in Dutch]. Ned Tijdschr Geneeskd. 1994;138:2405Y2407.
18. Kharasch SJ, Glotzer D, Vinci R, et al. Unsuspected cocaine exposure in young children. Am J Dis Child. 1991;145:204Y206.
8. Choy-Kwong M, Lipton RB. Dystonia related to cocaine withdrawal: a case report and pathogenic hypothesis. Neurology. 1989;39:996Y997. 9. Farrell PE, Diehl AK. Acute dystonic reaction to crack cocaine. Ann Emerg Med. 1991;20:322. 10. Merab J. Acute dystonic reaction to cocaine. Am J Med. 1988;84:564. 11. Sanger TD. Childhood onset generalized dystonia can be modeled by increased gain in the indirect basal ganglia pathway. J. Neurol Neurosurg Psychiatry. 2003;74:1509Y1515.
1008
www.pec-online.com
19. Heidemann SM, Goetting MG. Passive inhalation of cocaine by infants. Henry Ford Hosp Med J. 1990;38:252Y254. 20. Bateman DA, Heagarty MC. Passive freebase cocaine (‘crack’) inhalation by infants and toddlers. Am J Dis Child. 1989;143:25Y27. 21. Rodnitzky R. Drug-induced movement disorders. Clin Neuropharmacol. 2002;25:142Y152. 22. Beltran RS, Coker SB. Transient dystonia of infancy, a result of intrauterine cocaine exposure? Pediatr Neurol. 1995;12:354Y356.
* 2013 Lippincott Williams & Wilkins
Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
