Brandt, T.

Hamann, Gerhard F.

Strupp, M.

English

Universität München: Elektronischen Publikationen

Short Reports
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Eur Neurol 2000;43:181–182
Combined Amphetamine and Cocaine Abuse
Caused Mesencephalic Ischemia in a 16-Year-Old
Boy – Due to Vasospasm?
M. Strupp, G.F. Hamann, T. Brandt
Department of Neurology, University of Munich,
Klinikum Grosshadern, Munich, Germany 
Both the relationship between cocaine or amphetamine abuse
and stroke as well as the pathomechanism of cocaine/amphetamine-
induced stroke are still unclear. Whereas a recent study showed no
association between cocaine abuse and ischemic stroke in young
patients [1], others have described cocaine- or amphetamine-related
strokes [2–5]. Several pathomechanisms have been discussed in the
literature: cocaine-associated cerebral vasculitis [6], cocaine-associ-
ated cardiomyopathy leading to embolic stroke [2, 7, 8] or vasospasm
[3]. We report on a young patient who used both drugs and subse-
quently suffered an ischemic lesion, which was most likely caused by
vasospasm due to the combined abuse of both drugs.
Case Report
A 16-year-old, previously healthy schoolboy was admitted to our
emergency unit complaining of unsteadiness and double vision,
which had begun 3 days prior to admission. The patient had no risk
factors for atherosclerosis (normal blood pressure, no smoking, no
diabetes mellitus), no history of migraine and no family history of
stroke. He reported that his symptoms started 5 min after intranasal
inhalation of a small amount of ‘amphetamine’ (see below). He had a
1-year history of regular marihuana abuse. Since the patient still had
some of the drug, we were able to analyze it by ligand assay and high-
pressure liquid chromatography: it contained amphetamine and
cocaine, i.e. the amphetamine had been ‘cut’ with cocaine.
The neurological examination on admission revealed a left-sided
internuclear ophthalmoplegia. Further, the patient had incomplete
fascicular paresis of the left oculomotor nerve (with moderate ptosis
and weakness of the inferior oblique muscle) and saccadic vertical
smooth pursuit. His blood pressure was normal. He steadily im-
proved and became symptom free 3 weeks after symptom onset.
After discharge he did not use any psychostimulants (follow-up time
6 months).
Cranial MRI was performed on admission. The T2-weighted
images showed a left-sided hyperintense lesion near the midline of
the mesencephalon (fig. 1). Follow-up MRI 12 days after symptom
Fig. 1. A left-sided hyperintense lesion near the midline of the mes-
encephalon close to the oculomotor nucleus was found on admission
on T2-weighted axial images. Follow-up MRI 12 days after symptom
onset demonstrated that the lesion had become much smaller and
that there was contrast enhancement (not shown).
onset revealed that the lesion had become much smaller. There were
no abnormalities in the T1-weighted and intra-/extracranial MR
angiography images, no contrast enhancement and no evidence of
bleeding. Extra- and transcranial Doppler/duplex sonography, trans-
esophageal echocardiography, electrocardiography, chest roentgeno-
graphy, 24-hour ECG Holter monitoring, lumbar puncture, visually
and somatosensory-evoked potentials and the results of laboratory
examinations [including blood sedimentation rate, antinuclear and
anticytoplasmatic antibodies, coagulation tests (AT-III, protein C
and S, factor V Leiden)] were normal, i.e. there was no evidence of
other causes of ischemic stroke such as cocaine/amphetamine-
induced vasculitis or dissection.
181
182 Short Reports
Discussion
This case indicates that (1) the ischemic lesion was most likely
caused by the acute and combined action of cocaine and amphet-
amine (this is strongly supported by the close temporal relationship
between intake of the drug and onset of the symptoms) and (2) vaso-
spasm due to the synergistic effects of both drugs is the most probable
pathomechanism in this case, since we found no evidence of other
causes of cocaine/amphetamine-induced ischemia (see above).
While we are aware that in our case vasospasm as the pathome-
chanism was not proved by angiography, an angiographic study in
rabbits clearly showed that cocaine or amphetamine alone caused
little or no basilar artery spasm even at high doses, but coadministra-
tion of both produced definite basilar artery vasospasm, caused by a
synergistic vasoconstrictive effect [9]. This synergism can be ex-
plained pharmacologically: amphetamine causes the release of epi-
nephrine and norepinephrine, while cocaine prevents the reuptake of
both, thereby sensitizing the arterioles to sympathomimetic neuro-
transmitters. Thus, the combination of these drugs may be harmful,
even in small amounts.
Acknowledgements
We thank Ms. J. Benson for copy-editing the text.
References
1 Qureshi AI, Akbar MS, Czander E, Safdar K, Janssen RS, Frankel MR:
Crack cocaine use and stroke in young patients. Neurology 1997;48:341–
345.
2 Levine SR, Welch KM: Cocaine and stroke. Stroke 1988;19:779–783.
3 Martinez N, Diez Tejedor E, Frank A: Vasospasm/thrombus in cerebral
ischemia related to cocaine abuse. Stroke 1996;27:147–148.
4 Petty GW, Brust JC, Tatemichi TK, Barr ML: Embolic stroke after smok-
ing ‘crack’ cocaine. Stroke 1990;21:1632–1635.
5 Lambrecht GL, Malbrain ML, Chew SL, Baeck E, Verbraeken H: Intranas-
al caffeine and amphetamine causing stroke. Acta Neurol Belg 1993;93:
146–149.
6 Fredericks RK, Lefkowitz DS, Challa VR, Troost BT: Cerebral vasculitis
associated with cocaine abuse. Stroke 1991;22:1437–1439.
7 Sauer CM: Recurrent embolic stroke and cocaine-related cardiomyopathy.
Stroke 1991;22:1203–1205.
8 Kaufman MJ, Levin JM, Ross MH, Lange N, Rose SL, Kukes TJ, Mendel-
son JH, Lukas SE, Cohen BM, Renshaw PF: Cocaine-induced cerebral
vasoconstriction detected in humans with magnetic resonance angiogra-
phy. JAMA 1998;279:376–380.
9 Wang AM, Suojanen JN, Colucci VM, Rumbaugh CL, Hollenberg NK:
Cocaine- and methamphetamine-induced acute cerebral vasospasm: An
angiographic study in rabbits. AJNR Am J Neuroradiol 1990;11:1141–
1146.
Priv.-Doz. Dr. M. Strupp, MD, Department of Neurology
University of Munich, Klinikum Grosshadern, Marchioninistrasse 15
D–81366 Munich (Germany)
Tel. +49 89 7095 2571, Fax +49 89 7095 5584
E-Mail mstrupp@nefo.med.uni-muenchen.de


Combined amphetamine and cocaine abuse caused mesencephalic ischemia in a 16-year-old boy - Due to vasospasm?

M. Strupp

G.F. Hamann

T. Brandt

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Combined Amphetamine and Cocaine Abuse Caused Mesencephalic Ischemia in a 16-Year-Old Boy – Due to Vasospasm?

Open Access LMU ( Ludwig-Maximilians-Univ. München)

Short ReportsABCFax + 41 61 306 12 34E-Mail karger@karger.chwww.karger.com© 2000 S. Karger AG, BaselAccessible online at:www.karger.com/journals/eneEur Neurol 2000;43:181–182Combined Amphetamine and Cocaine AbuseCaused Mesencephalic Ischemia in a 16-Year-OldBoy – Due to Vasospasm?M. Strupp, G.F. Hamann, T. BrandtDepartment of Neurology, University of Munich,Klinikum Grosshadern, Munich, Germany Both the relationship between cocaine or amphetamine abuseand stroke as well as the pathomechanism of cocaine/amphetamine-induced stroke are still unclear. Whereas a recent study showed noassociation between cocaine abuse and ischemic stroke in youngpatients [1], others have described cocaine- or amphetamine-relatedstrokes [2–5]. Several pathomechanisms have been discussed in theliterature: cocaine-associated cerebral vasculitis [6], cocaine-associ-ated cardiomyopathy leading to embolic stroke [2, 7, 8] or vasospasm[3]. We report on a young patient who used both drugs and subse-quently suffered an ischemic lesion, which was most likely caused byvasospasm due to the combined abuse of both drugs.Case ReportA 16-year-old, previously healthy schoolboy was admitted to ouremergency unit complaining of unsteadiness and double vision,which had begun 3 days prior to admission. The patient had no riskfactors for atherosclerosis (normal blood pressure, no smoking, nodiabetes mellitus), no history of migraine and no family history ofstroke. He reported that his symptoms started 5 min after intranasalinhalation of a small amount of ‘amphetamine’ (see below). He had a1-year history of regular marihuana abuse. Since the patient still hadsome of the drug, we were able to analyze it by ligand assay and high-pressure liquid chromatography: it contained amphetamine andcocaine, i.e. the amphetamine had been ‘cut’ with cocaine.The neurological examination on admission revealed a left-sidedinternuclear ophthalmoplegia. Further, the patient had incompletefascicular paresis of the left oculomotor nerve (with moderate ptosisand weakness of the inferior oblique muscle) and saccadic verticalsmooth pursuit. His blood pressure was normal. He steadily im-proved and became symptom free 3 weeks after symptom onset.After discharge he did not use any psychostimulants (follow-up time6 months).Cranial MRI was performed on admission. The T2-weightedimages showed a left-sided hyperintense lesion near the midline ofthe mesencephalon (fig. 1). Follow-up MRI 12 days after symptomFig. 1. A left-sided hyperintense lesion near the midline of the mes-encephalon close to the oculomotor nucleus was found on admissionon T2-weighted axial images. Follow-up MRI 12 days after symptomonset demonstrated that the lesion had become much smaller andthat there was contrast enhancement (not shown).onset revealed that the lesion had become much smaller. There wereno abnormalities in the T1-weighted and intra-/extracranial MRangiography images, no contrast enhancement and no evidence ofbleeding. Extra- and transcranial Doppler/duplex sonography, trans-esophageal echocardiography, electrocardiography, chest roentgeno-graphy, 24-hour ECG Holter monitoring, lumbar puncture, visuallyand somatosensory-evoked potentials and the results of laboratoryexaminations [including blood sedimentation rate, antinuclear andanticytoplasmatic antibodies, coagulation tests (AT-III, protein Cand S, factor V Leiden)] were normal, i.e. there was no evidence ofother causes of ischemic stroke such as cocaine/amphetamine-induced vasculitis or dissection.181182 Short ReportsDiscussionThis case indicates that (1) the ischemic lesion was most likelycaused by the acute and combined action of cocaine and amphet-amine (this is strongly supported by the close temporal relationshipbetween intake of the drug and onset of the symptoms) and (2) vaso-spasm due to the synergistic effects of both drugs is the most probablepathomechanism in this case, since we found no evidence of othercauses of cocaine/amphetamine-induced ischemia (see above).While we are aware that in our case vasospasm as the pathome-chanism was not proved by angiography, an angiographic study inrabbits clearly showed that cocaine or amphetamine alone causedlittle or no basilar artery spasm even at high doses, but coadministra-tion of both produced definite basilar artery vasospasm, caused by asynergistic vasoconstrictive effect [9]. This synergism can be ex-plained pharmacologically: amphetamine causes the release of epi-nephrine and norepinephrine, while cocaine prevents the reuptake ofboth, thereby sensitizing the arterioles to sympathomimetic neuro-transmitters. Thus, the combination of these drugs may be harmful,even in small amounts.AcknowledgementsWe thank Ms. J. Benson for copy-editing the text.References1 Qureshi AI, Akbar MS, Czander E, Safdar K, Janssen RS, Frankel MR:Crack cocaine use and stroke in young patients. Neurology 1997;48:341–345.2 Levine SR, Welch KM: Cocaine and stroke. Stroke 1988;19:779–783.3 Martinez N, Diez Tejedor E, Frank A: Vasospasm/thrombus in cerebralischemia related to cocaine abuse. Stroke 1996;27:147–148.4 Petty GW, Brust JC, Tatemichi TK, Barr ML: Embolic stroke after smok-ing ‘crack’ cocaine. Stroke 1990;21:1632–1635.5 Lambrecht GL, Malbrain ML, Chew SL, Baeck E, Verbraeken H: Intranas-al caffeine and amphetamine causing stroke. Acta Neurol Belg 1993;93:146–149.6 Fredericks RK, Lefkowitz DS, Challa VR, Troost BT: Cerebral vasculitisassociated with cocaine abuse. Stroke 1991;22:1437–1439.7 Sauer CM: Recurrent embolic stroke and cocaine-related cardiomyopathy.Stroke 1991;22:1203–1205.8 Kaufman MJ, Levin JM, Ross MH, Lange N, Rose SL, Kukes TJ, Mendel-son JH, Lukas SE, Cohen BM, Renshaw PF: Cocaine-induced cerebralvasoconstriction detected in humans with magnetic resonance angiogra-phy. JAMA 1998;279:376–380.9 Wang AM, Suojanen JN, Colucci VM, Rumbaugh CL, Hollenberg NK:Cocaine- and methamphetamine-induced acute cerebral vasospasm: Anangiographic study in rabbits. AJNR Am J Neuroradiol 1990;11:1141–1146.Priv.-Doz. Dr. M. Strupp, MD, Department of NeurologyUniversity of Munich, Klinikum Grosshadern, Marchioninistrasse 15D–81366 Munich (Germany)Tel. +49 89 7095 2571, Fax +49 89 7095 5584E-Mail mstrupp@nefo.med.uni-muenchen.de

A: Vasospasm/thrombus in cerebral ischemia related to cocaine abuse.

Frankel MR: Crack cocaine use and stroke in young patients.

Intranasal caffeine and amphetamine causing stroke. Acta Neurol Belg 1993;93:

KM: Cocaine and stroke.

ML: Embolic stroke after smoking ‘crack’ cocaine. Stroke

NK: Cocaine- and methamphetamine-induced acute cerebral vasospasm: An angiographic study in rabbits.

Recurrent embolic stroke and cocaine-related cardiomyopathy.

Renshaw PF: Cocaine-induced cerebral vasoconstriction detected in humans with magnetic resonance angiography.

Troost BT: Cerebral vasculitis associated with cocaine abuse.

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Combined amphetamine and cocaine abuse caused mesencephalic ischemia in a 16-year-old boy - Due to vasospasm?

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