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A Neurological Analog of the Dynamic EKG?
Fluctuating Aphasia in a Cocaine User
Hood-Medland E., Kravitz R., Aronowitz P.
University of California, Davis Medical Center; Sacramento, CA
Labs and Imaging
Cocaine use has been shown to have a strong
association with ischemic stroke in young adults.
Proposed mechanisms include increased sympathetic
drive, increased atherosclerosis, vasculitis, and
vasospasm. Patients generally present with focal
neurologic deficits, with infarcts most commonly
found in the MCA territory.
Case Presentation
History of Present Illness:
A 28-year-old man brought in by a friend to the
emergency department for altered mental status and an
episode of vision loss in the right eye.
• 3 days ago – in usual health
• Morning of presentation – communicating by
phone with friend, unable to give directions.
Complained of vision loss in right eye.
• Prior to presentation - his friend picked him up
from his house, and he was ‘insensible.’
• Friend brought patient to emergency department
Past Medical History/Past Surgical History:
Non-ischemic cardiomyopathy
Congestive Heart Failure with Reduced Ejection
Social History:
Cocaine and Methamphetamine use
Carvedilol, Lisinopril, Furosemide
Physical exam:
Vital signs were significant for tachycardia and
tachypnea. Benign heart, lung, and abdominal
examination. On neurologic examination, he cycled
from normal language function to expressive aphasia
to global aphasia back to normal language function
over the course of a few minutes, without other
neurologic deficits
Left: MRI/MRA showing infarct of left peri-sylvian region,
Meyer’s loop, and Wernicke’s area, with no vasculitis.
Right: CTA without evidence of vessel stenosis or
Pertinent Laboratory Studies
Other Investigative Studies
All within normal
Mild kidney injury
Elevated total bilirubin
Urine toxicology
EF 30%
No thrombus or
No epileptiform activity
(+) Cocaine
(-) Amphetamines
Hospital Course
• Admitting differential diagnosis: stroke, seizure, drug intoxication
• The patient was noted to have infarct on MRI/MRA. Neurology was
consulted, and advised CTA, which showed no evidence of vessel stenosis
or vasospasm. EEG showed no epileptiform activity.
• Despite the negative CTA, cerebral vasospasm was posited as the etiology
of ischemic stroke; and dual anti-platelet therapy was withheld.
• After working with speech therapy, his symptoms resolved by hospital day
13, and he was discharged home in good condition.
This patient presented in an unusual fashion, as his
symptoms cycled rapidly from normal to aphasic over
a span of minutes, with no sensory or motor deficits.
Fluctuating symptoms suggested a reversible etiology
such as seizure or vasospasm rather than a fixed defect
such as embolism or vessel thrombosis. Ischemic
stroke in young adults is rising in prevalence, with
cocaine as a putative etiology in at-risk patients. One
mechanism of cocaine-associated stroke is cerebral
vasospasm. Although vasospasm was not apparent on
CT angiography, transitory alterations in vessel
physiology may not be visible on later imaging. We
believe this patient’s presentation of rapidly
fluctuating aphasia was due to cerebral vasospasm
from cocaine use not unlike that sometimes seen in
coronary vasospasm with dynamic EKG changes or
fluctuating chest pain. In this case, fluctuating aphasia
as detected by a careful neurologic exam may have
been the neurologic analog of dynamic EKG changes
in cardiology.
Fluctuating neurological changes may be a
neurologic analogue of dynamic EKG changes
in cardiology in patients experiencing cocaineinduced vasospasm of cerebral vessels.
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