Neurologic Manifestations of Cocaine Exposure in Childhood

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Neurologic

Manifestations

of Cocaine

Exposure

in Childhood

Stephen H. Mott, MD*, Roger

J.

Packer, MD*; and Steven

J.

Soldin, PhD

ABSTRACT. Objective. To describe the neurologic manifestations of cocaine exposure in children and

ado-lescents as the neurologic effects of cocaine have been

described in adults and neonates.

Methods. During 1-year period, 41 children between

the ages of 2 months and 18 years who had been exposed to cocaine, were examined in the emergency department at the Children’s National Medical Center. Cocaine ex-posure was documented on urine samples; all were con-firmed by urine gas chromatographic/mass spectrometric analysis.

Results. Nineteen (46%) of 41 had neurologic

abnor-malities, including seizures (7), obtundation (6), delirium (4), dizziness (1), drooling (1), and ataxia (1). In 14 others, the neurologic effects of cocaine were difficult to deter-mine because of other concomitant medical conditions, including head injuries and severe abdominal or chest trauma. Two major age-related patterns were seen: (a) in each child <5 years of age, seizures and obtundation; and (b) in 11 older children, delirium (3), dizziness (1),

drool-ing (2), and lethargy (4). Seizures, occurring at ages 12

months to 8 years, were focal with secondary generaliza-tion in three and generalized in four. They were associ-ated with fever in two children. Six children had no fur-ther seizures, and one developed a mixed-seizure

disorder. Passive intoxication while being in a room in which “crack” was smoked was the most likely cause of exposure for young victims. Multiple drug abuse was not documented in any child with neurologic impairment.

Conclusions. 1) Cocaine exposure is common in

chil-dren in our urban setting 2) neurologic manifestations

frequently occur; 3) in children 8 years of age or younger,

“passive” ingestion/inhalation is associated with focal and generalized seizures without evidence of structural brain injury; 4) cocaine may lower seizure threshold in children predisposed to seizures; 5) in children >8 years

of age, manifestations are similar to those in adults; 6) trauma and motor vehicle accidents were seen in the ado-lescent age group exposed to cocaine; and 7) urine toxi-cological study in cocaine exposure is recommended in all first-time seizures as well as first-time febrile seizures.

Pediatrics 1994;93:557-560; cocaine exposure, passive

in-toxication, neurologic impairment, seizure, obtundation,

delirium, dizziness, drooling, ataxia, trauma.

During the past decade there has been a dramatic

increase in the use of cocaine in the United States) The

adverse neurologic consequences of cocaine have

been well documented in the adult, adolescent, and

Received for publication Dec 21, 1992; accepted Aug 13, 1993.

From the Departments of *Neurology, IPediatrics, and §Clinical

Labora-tory, Children’s National Medical Center, The George Washington

Univer-sity, Washington, DC.

Reprint requests to (S.H.M.) Neurology Dept. Children’s National Medical

Center, 111 Michigan Aye, NW, Washington, DC 20010.

Acad-emy of Pediatrics.

neonatal populations.3-’ Adult and adolescent

neu-rologic complications include cerebrovascular

acci-dents, seizures, and alterations in mental status such

as delirium and obtundation.2 During the perinatal

period, cocaine exposure has been associated with

in-creases in spontaneous abortion, abruptio placentae,

premature labor, and intrauterine growth

retarda-tion.3 Neonates exposed to cocaine in utero may

de-velop cerebral infarction, hemorrhage, and seizures.4

The neurologic effects of cocaine in infants and older

children have been poorly documented. To document

the frequency and character of the neurologic

corn-plications in a pediatric population, we reviewed

co-caine exposures seen at our institution during a 1-year

period.

MATERIALS AND METHODS

During a 12-month period (January 1, 1990 through December

31, 1990), the records of all patients examined with toxicology

screens positive for cocaine in the emergency department at the

Children’s National Medical Center were reviewed. Urine toxicol-ogy screens were obtained in the emergency department at the discretion of the treating physician. Patients between the ages of 2 months and 21 years were included in the study; infants <2 months of age were excluded from analysis because the study was investigating the neurologic manifestations of cocaine outside the neonatal and adult periods of life.

The urine samples obtained were studied using the Abbott ADx fluorescent polarization immunoassay technique.5 Drugs screened

for included cocaine, amphetamines, phencyclidine, marijuana,

benzodiazepines, and opiates. The screening cutoff limit was 80 pg/L for benzoylecgonine, the major metabolite of cocaine.5 All positive samples were sent for gas chromatographic-mass spec-trometric confirmation. For a positive result by mass spectroscopy, at least 50 pg/L of cocaine had to be present in the urine.

The clinical status of each patient at the time of positive urine cocaine was retrospectively reviewed, as was the patient’s subse-quent clinical course.

RESULTS

During the 12-month period, 1345 urine toxicology

screens were sent to the laboratory at the Childrens

National Medical Center and 41 patients were found

to have a cocaine-positive urine sample. During this

period, 56 000 children were examined in the

emer-gency department. Of the 41, 14 patients could not be

examined for purely cocaine-related neurologic

tox-icity due to coexistent medical conditions

confound-ing evaluation of neurologic status. Nine of the 14 had

gunshot wounds to the head or neck, many of whom

were in shock. Four of the 14 were in motor vehicle

accidents that resulted in alterations in mental status.

One of the 14 suffered a head injury secondary to an

altercation.

Nineteen of the remaining 27 (70%) had neurologic

abnormality by history or examination. For the other

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previ-558 NEUROLOGIC MANIFESTATION OF COCAINE EXPOSURE

ous history of drug ingestion (2), chest pain (1), falling

episodes (2), depression (1), cyanosis (1), and a

sexu-ally transmitted disease (1). Multiple drug abuse was

documented in two of the patients screened for drug

ingestion, but cocaine was the only abnormality

found in the remaining 25 patients including the 19

with neurologic involvement. The neurologic

abnor-malities listed in Table 1 included seizures in 7 (37%)

of 19, obtundation in 6 (32%) of 19, delirium in 4

(21 %) of 19, dizziness in I (5%) of 19, and drooling

in 2 (1 1 %) of 19. For purposes of this review,

chil-dren who had seizures and obtundation were

con-sidered to be obtunded secondary to the seizure

rather than drug exposure.

Nine of the 19 children were 8 years of age. Their

neurologic abnormalities included seizures in 7(78%)

of 9 and obtundation/ataxia in 2 (22%) of 9. In the 10

children >8 years of age, neurologic abnormalities

in-cluded obtundation in 4 (40%) of 10, delirium in 3

(30%)

of 10, dizziness in I (10%) of 10, and drooling

in 2 (20%) of 10.23

Seizures were the single most common neurologic

manifestation of cocaine exposure (Table 2).

Convul-sions, occurring at ages 12 months to 8 years, were

focal with secondary generalization in three patients

and generalized in four others. In two patients, they

were associated with fever, although in one child the

highest documented fever was 101#{176}F.In the two

pa-tients with seizures associated with fever, aged 13 and

59 months, there was no family history of febrile

sei-zures nor history of previous seizures in the patient.

Most of the seizures were brief and stopped before

arrival in the emergency department. One child was given phenobarbital on arrival at the emergency

de-partment, whereas the others were not treated. Two

patients had prior neurologic difficulties, cerebral

palsy in one and developmental delay in the other.

The results of neurologic examinations after seizures

were normal in all patients except those children with

known preexisting neurologic deficits. Two children

have developed epilepsy; one was the child with

known mental retardation and the other has had

difficult-to-control seizures since the convulsion,

tern-porally related to cocaine. Subsequent evaluation has

not determined an etiology for the seizure disorder. In the patients >8 years of age, varying degrees of

alterations in consciousness were noted (Table 3).

Although quite marked at times, the alterations in

consciousness tended to be brief and self-limited.

Cerebellar ataxia was the only focal neurologic

find-ing associated with obtundation. All symptoms

ulti-mately resolved, most within 6 hours. However,

two patients required 24 hours for full neurologic

recovery.

TABLE 1. Neurolog ic Manifestation s (Total)

Type No. Age Range Children

<8y Children >8y Seizures Obtundation Delirium Dizziness Drooling 7 6 4 I 2

12 mo-8 y

5 mo-18 y

16-19 y 18 y 16-18 y 7 2 0 0 0 0 4 4 1 2

The route of exposure to cocaine was unclear in

many patients. Patients >8 years of age often initially

denied using illicit drugs. In the children 8 years of

age, especially the toddlers, there was no evidence of

clear-cut ingestion, because no history could be

elic-ited of cocaine being left on the floor or within reach

of the child, and gastric lavage was not routinely

per-formed. On repeat questioning, most of the children

<5 years who were neurologically compromised were

found to have been in a room where cocaine was

be-ing smoked before the onset of neurologic difficulties.

DISCUSSION

Exposure to cocaine is a relatively frequent

occur-rence in our urban setting, which is the primary

re-ferral source for pediatric patients in the Washington,

DC area. Given the retrospective nature of this study,

we can not assess the incidence of cocaine exposure

in the population served by the Childrens National

Medical Center, or more exactly how often exposed

children suffer neurologic compromise. However, in

those children identified by toxicology screens,

neu-rologic symptoms were frequent and age-related.

Seventy percent of children with positive urine

screens, who could be examined, had neurologic

dys-function. This may be an underestimation because

children with coexisting head injuries were excluded

from our analysis, and it is conceivable that cocaine,

with its known neuropsychiatric consequences, was a

contributing factor in their resultant injuries and acts

of violence (auto accident, gun shot wounds, etc).

Although the neurologic manifestations of cocaine

toxicity were seen in all age groups, there seems to be

an age-related spectrum of neurologic effects.

Ado-lescents in our series typically displayed alterations in

consciousness without seizures or cerebrovascular

events. In other reports, adolescents, similar to adults,

typically displayed alterations in mental status,

in-cluding delirium, stupor, or coma. Cocaine may

ac-count for as many as 8% of first-time convulsions in

adult studies; death has been cited secondary to

ter-minal status epilepticus in one patient.9’1#{176} Although

occurrence is low, cerebral infarctions and

hemor-rhages have been cited as well.2

In this study, seizures seem to be the most common

manifestation of cocaine exposure in the younger

chil-dren (Table 2). The literature describing the

neuro-logic manifestations of cocaine exposure in early

childhood (outside the perinatal period) has been

sparse. Intracranial hemorrhages, infarctions, and

sei-zures have been reported primarily in the neonatal

112 Electroencephalographic abnormalities

noted in neonates have included generalized bursts of

spikes and sharp waves termed “cerebral irritation”

by Doberczak et al.13 Legido et a114 found that infants

of cocaine-abusing mothers had more sleep spindle

activity than expected during quiet sleep, as well as

decreased total quiet sleep pattern, as compared with

controls.

Previous case reports cite cocaine-related seizures

in pre-adolescents. Ernst and Sanders reported four

patients, ages ranging from 4 months to 3 years, with

seizures.15 Dinnies et aU6 described three children

be-tween 15 and 20 months with seizures. Rivkin and

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Outcome

Fever Normal

None Normal

None Resolved None Resolved None Recovery during

24 h Nonfocal Normal

5 mo Lethargy

16 y Combative, delirious

18 y Obtunded

18 y Agitated 18 y Dizzy, ataxic

18 y Obtunded, drooling,

twitching

16 y Agitated, ataxic,

drooling

10 mo Obtunded, crawling

in circles

18 y Drowsy, obtunded

19 y Delirious

15 y Obtunded

Cerebellar, ataxic None None None None

1. Office of National Drug Control Policy. National Drug Control Strategy.

Washington, DC: Executive Office of the President; September 1989

2. Mody CK, Miller BL, McIntyre HB, Cobb 5K, Goldberg MA. Neurologic

complications of cocaine abuse. Neurology. 1988;38:1189-1193

3. Chasnoff U, Bussey ME, Savich R, Stack C. Perinatal cerebral infarction

and maternal cocaine use. JPediatr. 1986;108:456-459

4. Volpe J. Effect of cocaine use on the fetus. N Engl IMed. 1992;6:399-407

5. Soldin SJ, Morales AJ, D’Angelo U, Bogema SC, Hicks JM. The

impor-tance of lowering the cut-off concentrations for urine screening and

confirmatory tests for benzoylecgonine/cocaine. Chin Chem. 1991;

51:993

6. Rich JA, Singer DE. Cocaine-related symptoms in patients presenting to

an urban emergency department. Ann Emerg Med. 1991;20:616-621

7. Hicks JM, Morales A, Soldin SJ. Drugs of abuse in a pediatric outpatient population. Clin Chem. 1990;36:1256-1257

8. Rifai N, Morales A, MacDonald MG, Soldin Si. Cocaine prevalence in a

neonatal intensive care unit. Clin Chem. 1990;36:1025

9. Pascual-Leone A, Dhuna A, Altafullah I, Anderson D. Cocaine-induced

seizures. Neurology. 1990;40:404-407

10. Wetti CV, Wright R. Death caused by recreational cocaine use. JAMA.

1979;241 :2519-2522

1 1. Spires MC, Gordon EF, Choudhori M, Maldonado E, Chan R.

Intra-cranial hemorrhage in a neonate following prenatal cocaine exposure.

Pediatr Neurol. 1989;5:324-326

12. Kramer LD, Locke GE, Ogunyemi A, Nelson L. Neonatal

cocaine-related seizures. JChild Neurol. 1990;5:60-64

13. Doberczak TM, Shanzer 5, Snie RT, Kandall SR. Neonatal neurologic

TABLE 2. Neurologic Manifestation: Seizures

Age Symptoms PMH* Associated Outcome

Findings

23 mo L focal with secondary generalization; 1 mm Neg None No subsequent seizures

12 mo Generalized tonic-clonic Neg None No subsequent seizures

13 mo 2 R focals; then one generalized Neg Fever 101#{176}F Given phenobarbital

35 mo L focal; then one generalized Developmental delay; calcification on CT;

previous seizure with cocaine

Hyperreflexia; hypertonia

No subsequent seizures

59 mo 5-mm general tonic-clonic Neg 102#{176}F No subsequent seizures

25 mo 30-s generalized Neg None Poorly controlled seizures

8 y Mixed seizures Mental retardation;

cerebral palsy

None Occasional seizures

* PMH, past medical history; L, left; R, right; Neg, negative; CT, computed tomographic scan.

TABLE 3. Neurologic Manifestation: Others

Age Symptoms Associated

_______

Findings Normal Resolved during 24 h Resolved during 24 h Resolved Resolved

Cilmor&7 discussed a 9-month-old case with

gener-alized tonic-clonic seizures and cocaine-positive

urine. The reason for the relationship between

sei-zures in young children and cocaine remains

specu-lative. In two cases in our series, fever was an

asso-ciated finding, and one hypothesis is that the

cumulative effects of illness, fever, and cocaine

pro-yoked the seizure. Two children were

developmen-tally and neurologically handicapped before their

sei-zures, raising the possibility that cocaine lowered the

seizure threshold in these patients. A second

possi-bility is that the developmental vulnerability of the

central nervous system in this age group predisposes

the younger child to seizures rather than other

neu-rologic manifestations of cocaine toxicity. The

short-term outcomes of children in our series with

con-vulsions were good for the most part. Seizures

generally did not require prolonged anticonvulsant

therapy and were self-limited in all but one child.

Within 6 hours of the convulsion, all patients had

returned to their preseizure baseline neurologic

sta-tus. Two of the seven patients subsequently

devel-oped epilepsy, one with known preexisting mental

retardation.

In children 8 years of age, the manner in which

the child was exposed to cocaine is unclear. Oral

in-gestion by an infant playing with food from a

previ-ous night’s party where cocaine powder was used,17

and passive inhalation by an infant in a closet within

which their parents were free-basing have been

cited.16 Conway et a118 reported a 13-month-old who

chewed a used cocaine packet. Chaney et a!19 reported

oral ingestion in a nursing infant because the mother

had used cocaine as a topical anesthetic for her nipple

soreness. Bateman and Heagarty2#{176} reported four

well-documented cases of passive inhalation by patients

being in the same closed space in which cocaine was

being free-based. In this study, passive inhalation was

the most probable mode of cocaine intoxication in the

patient <8 years of age; although this is difficult to

prove. Patients in our series did not have gastric

la-vage to rule out oral ingestion.

In summary, there seems to be a

neurodevelopmen-tal symptomatology to the effects of cocaine on the

central nervous system. This study reveals seizures as

the major manifestation of cocaine neurotoxicity in

the young patient outside the neonatal period. The

adolescents had alterations in mental status, as

re-ported in adult studies. The reason for the difference

in symptomatology is unclear. In our setting, a drug

screen is an essential part of an initial work-up for

first-time afebrile seizures and possibly febrile

sei-zures. Future, prospective studies are needed to

de-fine the incidence of cocaine exposure in children and

resultant neurologic sequelae.

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560 NEUROLOGIC MANIFESTATION OF COCAINE EXPOSURE

and electroencephalographic effects of intrauterine cocaine exposure. IPediatr. 1988;113:354-358

14. Legido A, Clancy R, Spitzer A, Finnegan L. Electroencephalographic

and behavioral-state studies in infants of cocaine-addicted mothers.

AJDC. 1992;146:748-752

15. Ernst AA, Sanders WM. Unexpected cocaine intoxication presenting as

seizures in children. Ann Emerg Med. 1989;18:774-777

16. Dinnies JD, Darr CD, Saulys AJ. Cocaine toxicity in toddlers. AJDC.

1990;144:743-744

17. Rivkin M, Gilmore HE. Generalized seizures in an infant due to

environmentally acquired cocaine. Pediatrics. 1989;84:1 100-1102

18. Conway EE, Jr., Mezey AP, Powers K. Status epilepticus following the

oral ingestion of cocaine in an infant. Pediatr Energ Care. 1990;6:

189-190

19. Chaney NE, Ranke J, Wadlington WB. Cocaine convulsions in a

breast-feeding baby. JPediatr. 1988;112:134-135

20. Bateman DA, Heagarty MC. Passive freebase cocaine (‘crack’)

inhala-tion by infants and toddlers. AJDC. 1989;143:25-27

MINNESOTA

TAKES

CONTROVERSIAL

STEPS

TO REFORM

HEALTH CARE

When Minnesota legislators last spring passed health legislation that included a tax on health care providers, many physicians thought the state had gone too far.

As the state begins to implement the law, however (physicians will begin paying

the tax in 1994), those same physicians are realizing that their troubles may have

just begun.

The tax is only one part of a larger health reform package that promises to change the way Minnesota physicians practice. Under the law, for example, the state will

assign physicians to some patients. The law also requires the state to develop

practice parameters and controls on technology ...

Beginning in 1994, physicians will pay a 2% income tax on their gross revenues. The tax, which wifi not be levied on Medicare or Medicaid services or on physicians employed by managed care providers, will help pay for health insurance for the

state’s approximately 400,000 uninsured.

Many physicians opposed the legislation because it will cut into their pay ...

And to achieve its goal of reducing health care costs by 10% a year for five years, the state will develop and implement practice parameters in an attempt to avoid

ineffective treatment.

Doyle E. Minnesota takes controversial steps to reform health care. ACP Observer. December 1992, p. 8.

Noted by J.F.L., MD

(5)

1994;93;557

Pediatrics

Stephen H. Mott, Roger J. Packer and Steven J. Soldin