Igor
Mikityansky, MD and PL Westesson, MD, PhD, DDS
Clinical
Presentation: A
29-year-old female presents with right-sided hemiparesis after
repeated cocaine use on her honeymoon.
Radiological
Findings: On
the head MRI there are three small areas of increased signal
on DWI with decreased ADC which are located in the left anterior
thalamus, the genu of internal capsule, and to the left of
the anterior commissure. The head MRA demonstrates irregularity
of the M-1 segment of left MCA.
Figure
1: (From top to bottom) T1 post (A), T2 post (B), FLAIR (C),
DWI (D), ADC (E), EDC (F) sequences demonstrate infarcts in the left
genu of internal capsule. Note that lesions
have high signal on T2, FLAIR, DWI, EDC, low on ADC, and
not seen on T1.
Figure
2: A collapsed view and 3DTOF images demonstrate irregularity
of the M-1 segment (arrow) of left MCA suggestive of vasculitic
changes in the person of this age.
Diagnosis: Cocaine induced vasculitis; infarcts
Discussion: Cocaine,
benzoylethylecgonine, is weakly antimuscarinic and highly lipid
soluable alkaloid that gets absorbed rapidly across mucous membranes.
It achieves brain:plasma ratio 5:1 with a half-life of 1 hour.
In the CNS cocaine blocks reuptake carrier of monoamines, thus
potentiating their effects. Increased activity of noradrenergic
sympathetic system results invasoconstriction and secondary rise
in blood pressure, tachycardia, increased cardiac output, mydriasis,
hyperglycemia, and hyperthermia [1].
The onset of action depends on the route of administration. Inhalation
of the “free base”, or “crack,” results in
high CNS levels in 8-10 seconds, while “snorting” causes
CNS effects in 3-5 minutes. Although the chemical half-life of cocaine
is around 1 hr, a typical “high” lasts 15-30 minutes
and requires repeated dosing for desired effect [1].
Cocaine induced neurologic pathology includes ischemic infarctions,
intracerebral, subarachnoid and intraventricular hemorrhages, and
cerebral vasculitis. Although majority of drug-related ischemic infarctions
usually occur in MCA territory, cocaine characteristically causes
infarcts in cerebrum, thalamus, brainstem, cerebellum and retina.
About 80% of strokes caused by the base cocaine use are hemorrhagic,
while alkaloidal cocaine has even distribution of hemorrhagic and
ischemic strokes [2].
While only 4% of all strokes occur in people less than 45 years-old,
up to 30% of them are drug-related. Estimated risk of stroke in cocaine
and/or amphetamine users after controlling for other risk factors
is 6.5 times higher than general population, with hemorrhagic stroke
risk 9.6 times higher and ischemic 4.5 times above the general population
[3]. About 85-90% of drug-related strokes occur in 4th and 5th decades,
however they can be seen at any age. There is equal gender distribution.
While time interval between drug use and stroke onset can be as long
as one week, risk for stroke is highest within 3-6 hour after drug
use [2].
There are several etiologic components of the cocaine induced strokes.
Dose dependent systemic vasoconstriction causing acute arterial hypertension
is considered to be one of the causes of the hemorrhagic strokes.
It has been suggested that preexisting vascular pathology such as
aneurisms or AVMs are more likely to bleed earlier and at smaller
sizes in cocaine abusers than in nonusers. [4] Some hypothesize that
chronic cocaine use causes accelerated atherosclerotic changes that
may predispose to thrombosis. [5] Increased platelet aggregation
and cardiomyopathy as a source of emboli have been implicated in
cocaine related strokes [2]. A cocaine-induced cerebral vasculitis
was considered to be the cause for strokes, but could only be demonstrated
in rare cases [4].
In cocaine users T1WI can demonstrate
decrease in gray matter concentration in orbitofrontal, insular,
cingulate regions as well as in temporal
cortex. On T2WI users without serebrovascular symptoms have severe
increase in frequency of severe T2 hyperintense lesions in cerebral
and insular white matter as well as transient occlusion of arteries
in MCA territory causing small infarctions. Hemorrhagic lesions have
decreased signal on T2* GRE. DWI may show restricted diffusion. Post-contrast
images may demonstrate enhancement in the subacute infarcts. MRA
can demonstrate arterial spasm and/or vasculitis [2].
Differential considerations include hypertensive hemorrhages in basal
ganglia, vascular malformations, intratumoral hemorrhage, and dural
sinus thrombosis with hemorrhagic infarct [2].
References:
Fessler RD,
et al. The neurovascular complications of cocaine.
Surg Neurol (1997) 47:339-45.
