CASE REPORT

Spontaneous Intracerebral Hemorrhage Related to
Methamphetamine Abuse
Autopsy Findings and Clinical Correlation
Shawn M. McGee, MD,* Deanna N. McGee, PharmD, BCPS,† and Michael B. McGee, MD‡

Abstract: A healthy 31-year-old male abstinent from drug abuse
during his recent incarceration developed slurred speech, a severe
headache, and left-sided hemiparesis prior to his eventual death 9.5
hours after inhalation of methamphetamine. On postmortem examination, inspection of the brain revealed bilateral subarachnoid
hemorrhage, with a prominent intralobar hemorrhage centered
within the right frontal cerebral hemisphere. No evidence of vasculitis, infarction, intraventricular hemorrhage, or ruptured aneurysm
could be observed. While this is not the first report of a methamphetamine-related stroke, this report describes the autopsy findings
of an intracerebral hemorrhage secondary to methamphetamine
abuse on autopsy and compares the findings and antemortem history
to previously reported methamphetamine cerebral vascular deaths.
Key Words: methamphetamine, autopsy, cerebral vascular
accident, hemorrhagic stroke, ischemic stroke
(Am J Forensic Med Pathol 2004;25: 334 –337)

M

ethamphetamine (MA) is the most commonly abused
drug of patients presenting to emergency departments
in the western United States,1 with MA-related deaths having
a greater than 2-fold increase in several US cities since the
early 1990s.2 Consequently, the results of MA abuse have
become important entities to understand clinically and pathologically. A problem seen with the abuse of MA is spontaneous
cerebral vascular accidents (CVAs), illustrated by an increasing
amount of case reports and case series described in the last
decade. Overall, CVAs make up a smaller percentage of MA-

Manuscript received November 15, 2003; accepted February 4, 2004.
From the *University of Minnesota School of Medicine, Minneapolis,
Minnesota; the †Department of Pharmacy, Hennepin County Medical
Center, Minneapolis, Minnesota; and the ‡Ramsey County Medical
Examiner’s Office, St. Paul, Minnesota.
Reprints: Michael B. McGee, MD, Ramsey County Medical Examiner’s
Office, 300 E. University Ave., St. Paul, MN 55101. E-mail:
mmcgee1@mn.rr.com.
Copyright © 2004 by Lippincott Williams & Wilkins
ISSN: 0195-7910/04/2504-0334
DOI: 10.1097/01.paf.0000137206.16785.2f

334

related deaths as compared with homicides, poisonings, and
accidents due to the drug.3,4 Nonetheless, the incidence of MA
abuse is growing, especially in younger age groups, and identification of CVAs secondary to MA in emergency departments
and at autopsy has an increasing significance.
The majority of previous reports discussing MA-related
CVAs have emphasized and studied the clinical and/or the
radiographic findings, with less attention paid to pathologic
findings on autopsy. This report follows the progression of a
cerebral hemorrhage in a distinct timeframe within an otherwise
healthy male with an unremarkable history of abusing MA.

CASE REPORT
A 31-year-old male smoked and then snorted MA
(“crank”) with 2 of his male acquaintances at approximately
5:00 PM. Statements later provided to the police estimated the
amount of drug ingested to be between 0.25 and 0.50 g. Ten
to fifteen minutes after ingesting the drug, the subject began
to complain of a “mean headache,” followed by nausea and
vomiting. Upon arrival at a second residence, the subject
elected to “sleep off” the effects of the drug in the back of an
automobile. An acquaintance monitored his welfare throughout the evening hours. During these visits, the subject complained that the left side of his body felt numb, his speech was
noted to be slurred, and he repeatedly fell from the seat upon
which he was lying onto the floor. When an offer was made
to take him to a nearby medical facility, the subject declined,
stating that he had been released from a correctional facility
earlier that week and a condition of his parole was to abstain
from using controlled substances. He was subsequently discovered dead within the automobile at 2:30 AM the following
morning, approximately 9.5 hours after ingestion of MA.
Police and paramedics were summoned to the scene of death.
Scene investigation revealed the subject lying supine in
a parked automobile, with only the left side of the body
clothed. The subject’s right arm and right leg had been pulled
out of his shirt and pants, respectively. Examination of the
body at the scene revealed no evidence of trauma. The body
was cool to the touch, with rigor present and fixed. Livor was
appropriate in its distribution.

The American Journal of Forensic Medicine and Pathology • Volume 25, Number 4, December 2004

The American Journal of Forensic Medicine and Pathology • Volume 25, Number 4, December 2004

At postmortem examination, the body of a 31-year-old
male was observed. No evidence of acute traumatic injuries
was noted at the time of the external or internal examination.
Inspection of the heart revealed a normal coronary vasculature system with no evidence of coronary vessel disease. On
examination of the brain, cerebral edema was observed, with
a weight of 1480 g. The cerebral hemispheres appeared
asymmetric with a right to left midline shift. Subarachnoid
hemorrhage (SAH) was present over the cerebral convexities
bilaterally. On sectioning of the cerebral hemispheres, an
intracerebral hemorrhage (ICH) was noted lateral to the basal
ganglia and extending to involve the lateral aspect of the
putamen, as well as the claustrum, external capsule, insula,
and into the superior longitudinal fasiculus of the right
cerebral hemisphere, covering an area that measures 3.5 cm
by 4.5 cm (Fig. 1). No evidence of intraventricular hemorrhage, infarction, aneurismal rupture, or arterial venous malformation could be appreciated. Microscopic sections revealed fresh appearing hemorrhage, with no evidence of
inflammation or vasculitis noted.
Toxicology analysis performed on specimens collected
at the time of the postmortem examination revealed a negative blood ethanol and serum screen. A urine screen was
positive for MA, amphetamine, and THC. Confirmatory testing revealed a blood MA level of 300 ng/mL, with a blood
amphetamine level of 30 ng/mL.

DISCUSSION
There are limited reports of autopsy findings in patients
with CVAs secondary to MA abuse.5,6 Postmortem examination in these reports describes either an ICH or cerebral
infarction (Table 1). In the literature, amphetamine and MArelated CVAs are predominantly hemorrhagic strokes.5,7–12
Paradoxically, hemorrhagic strokes account for less than one

FIGURE 1. Intracerebral hemorrhage measuring 3.5 ⫻ 4.5 cm
in the right cerebral hemisphere.
© 2004 Lippincott Williams & Wilkins

ICH and MA Abuse

fourth of CVAs in the general population.13 MA-related ICHs
have been reported in all cerebral lobes, with the majority
involving the frontal lobe, as seen in our case. Grossly, these
ICHs are indistinguishable from those caused by other amphetamines and cocaine.14 –16 As in our case, a proportion of
amphetamine- and MA-related ICHs have also been found to
have a SAH.5,8,17 In some cases, MA-related ICHs have been
attributed to the disturbance of arterial venous malformations18 or ruptured cerebral aneurysms,19 resulting in an ICH
seen in the distribution of the affected cerebral artery.
Ischemic strokes attributed to MA abuse are described
in the literature as having infarctions involving the cerebral
hemispheres, the brainstem, or both.6,20,21 The majority of
infarctions are described as secondary to acutely organized
thrombus in cerebral vessels affected by necrosis associated
with vasculitis. Cerebral vasculitis is the most commonly
described histologic and radiologic finding in abusers of MA
with either hemorrhagic or ischemic strokes.5,6,10,11,17,22 Histologic analysis of persons suffering from CVAs associated
with MA-related cerebral vasculitis shows necrotic lesions
seen in small and large cerebral arteries, with moderate to
extensive medial necrosis with the presence of minimal
inflammatory cells.5,6 Citron et al22 noted that amphetaminerelated vasculitis could be histologically characterized as
necrotizing angiitis in multiple organs, including the neurologic system, with a resemblance to periarteritis nodosa.
Radiographically, cerebral vasculitis associated with MA is
best described on arteriography of cerebral vessels, which
shows a diffusely pronounced irregularity of flow with arterial narrowing and cerebral artery beading.6,11,12,21
The anatomic and histologic description of MA-related
CVAs may lend knowledge about the physiology behind the
type of stroke that results. Vasculitis and subsequent arterial
narrowing secondary to long-term exposure to MA with an
acute vascular spasm have frequently been postulated to have
led to a cerebral ischemic event.6,21 In the case of patients
suffering a spontaneous ICH without vasculitis or vessel
malformations, few theories have been proposed about its
pathophysiology. Studies have indicated that spontaneous
nontraumatic ICHs are most commonly secondary to hypertensive disease.23 With MA known to increase both systolic
and diastolic blood pressures with dosages slightly higher
than the therapeutic dose (5–25 mg),24 it is quite probable that
an ICH secondary to hypertension can occur acutely at very
elevated doses of MA, as in the case of our patient (250 –500
mg; Table 1). More often, the advent of spontaneous MArelated ICHs is most likely secondary to gradual vessel
weakening with repeated drug abuse and an acute elevated
blood pressure at the time of ingesting MA.
Etiologic differentiations between hemorrhagic and
ischemic strokes have been previously examined by the
method of MA ingestion. CVAs have occurred with all
modes of MA ingestion, including oral intake, inhalation, and

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McGee et al

The American Journal of Forensic Medicine and Pathology • Volume 25, Number 4, December 2004

TABLE 1. Autopsy Findings and Clinical History of Reported Methamphetamine (MA)-Related Cerebral Vascular Accidents
Report/Series, Year

Autopsy Findings

Mode of MA
Ingestion

Length of MA
Abuse

Dosage
Used

Bostwick et al.,
19806
Shibata et al., 19915

Cerebral infarction with vasculitis

intravenous injection

multiple years

not given

9 days

Intracerebral hemorrhage (ICH) &
subarachnoid hemorrhage (SAH)
with vasculitis
ICH & SAH without vasculitis

intravenous injection

1 year

not given

inhaled

under 1 year

up to 0.5
gram

51 hours;
respiratory arrest
at 13 hours
9.5 hours

McGee et al., 2003

intravenous injection.17,20,21,25 Reports have contemplated
whether ischemic strokes are associated to the inhalation of
MA, while oral and intravenous injection show a predilection
for cerebral hemorrhage.6,8,14,21 The deceased in our case
inhaled MA and suffered from a fatal ICH and SAH without
evidence of infarction or vasculitis (Table 1). Although our
findings do not correlate with previous reports, Yen et al25
have shown that MA inhalers may be susceptible to either
hemorrhagic or ischemic strokes.
The longevity of MA abuse prior to a stroke may
indicate the type of CVA that results. Few reports and series
have detailed the patient’s past medical history to include
long-term illicit drug abuse. The majority of patients with
long-term abuse of MA in these reports are described as
having vasculitic changes demonstrated on cerebral angiography. Similar to the inflammatory changes described in
animal studies with long-term exposure to increased levels of
cocaine,26 the examiner would expect a patient to develop
vasculitis over a extended period of time secondary to another
sympathomimetic, such as MA. In the 2 previous reports
describing autopsy findings, both deceased had vasculitis,
with one suffering from a subsequent cerebral infarct after
abuse of MA for close to a decade.6 The second deceased had
an ICH with an indeterminate history of MA abuse until 1
year previously (Table 1).5 The deceased described in our
report had no acute history of abusing MA and suffered from
an ICH, without histologically appreciating vasculitis (Table
1). Although more studies are needed, within these 3 patients
the duration of MA abuse seems to have an impact on the
formation of vessel inflammation and subsequently the type
of CVA secondary to the drug.
Patients suffering from MA-related ICHs and a concomitant SAH have a decreased time to death when compared
with ischemic strokes. This may seem inherent since ICHs,
regardless of their cause or association, end in death 45% of
the time compared with 12% for cerebral infarcts.13 Still, the
mortality of MA-related ICHs is even greater when a concomitant SAH is taken into consideration. Studies have
shown that up to 15% of patients die before they receive
medical attention and another 10% die within 24 hours after

336

Time to Death

the onset of a SAH.27–29 With the majority of MA-related
CVAs attributed to ICHs and the deceptively low average age
of patients presenting with stroke symptoms secondary to
MA (approximately 30 years old), information is needed
regarding the time to death. The 2 previous case reports
describing autopsy findings have calculated the time span
from MA ingestion to death in a hospital as 2 and 9 days
(Table 1).5,6 In these reports, both patients had a deterioration
of neurologic status proceeding to a comatose state, with
eventual respiratory arrest or brain death. The deceased in our
case showed acutely deteriorating physical and neurologic
findings consistent with the location of the ICH, which
progressed to fatality 9.5 hours after MA inhalation (Table 1).
The deceased previously described by Shibata et al,5 suffering an ICH, died 51 hours after MA injection with appropriate medical intervention, but respiratory arrest was reported
to have occurred at 13 hours after MA ingestion. Both the
deceased in our case and the deceased described in this report
suffered a fatal arrest secondary to an ICH and SAH in a
shorter time span (9.5 and 13 hours) when compared with an
ischemic stroke without a SAH (9 days).
Death secondary to a CVA in young persons are tragic
and sometimes misleading due to the relative infrequency of
strokes in a younger age group. With the resurgence of MA
abuse, CVAs related to MA as the cause of nontraumatic
neurologic deficits and respiratory distress in younger patients have become higher on the differential diagnosis in
emergency departments30 and need to be correctly identified
on postmortem examinations. In this case, the deceased
suffered from a fatal spontaneous ICH and SAH without
evidence of vasculitis less than 10 hours after inhalation of
MA. Although the etiology of the CVA cannot be deduced by
method of ingestion alone, our deceased’s short-term exposure to MA, decreased time to death, and dosage of MA may
help to suggest an ICH on to postmortem examination.
Further understanding of spontaneous ICHs related to MA
abuse will require diligent surveillance and detailed anatomic
description on further postmortem examinations with clinical
correlation.
© 2004 Lippincott Williams & Wilkins

The American Journal of Forensic Medicine and Pathology • Volume 25, Number 4, December 2004

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