Baylor University Medical Center Proceedings July 2017 - 356

pressure was within normal limits without treatment, and his
neurological examination was within normal limits.

Figure 2. A CT scan of the head reveals low attenuation areas in both occipital
lobes, more so on the left, and punctate hemorrhages in the left occipital lobe.
This result is consistent with vasogenic edema.

(Figure 2). The patient was started on nicardipine. Magnetic
resonance imaging (MRI) of his head with gadolinium contrast
showed multifocal areas of abnormal T2 ﬂuid-attenuated inversion recovery signal; gyriform enhancement; restricted diﬀusion
in the superior parietal lobes, both occipital lobes, and both
cerebellar hemispheres; and minimal hemorrhage in the left
superior parietal lobe consistent with atypical PRES (Figure 3).
The patient eventually reported that prior to admission he had
abused kratom (amount unknown) and had taken six tablets of
dextroamphetamine; he was unwilling to provide more detail
about the use of these drugs. He was hospitalized for 5 days. His
headache steadily improved, and a CT scan on the day before
discharge was unchanged. On the day of discharge, his blood

DISCUSSION
Although kratom has been used as an herbal remedy for
many years in Southeast Asia, published investigations of it
have been limited to case reports and small trials. Kratom's
toxic eﬀects include dry mouth, changes in urination, nausea,
vomiting, and weight loss. Serious complications, such as seizures and coma, have been reported. The eﬀects of kratom are
dose dependent. Small doses produce cocaine-like eﬀects; larger
doses cause morphine-like sedative eﬀects. Kratom users report
increased work capacity, alertness, sociability, and sometimes
increased sexual desire (2). Mitragynine and 7-hydroxymitragynine are the two alkaloids responsible for the eﬀects of kratom
and act as full agonists at μ-subtype opioid receptors (Figure
1). Pharmacological activities are mainly mediated via opioid
receptors and neuronal Ca++ channels with a dominant eﬀect at
neuromuscular junctions and not in skeletal muscles or somatic
nerves (2). In one small trial, pharmacokinetics demonstrated
a terminal half-life of about 1 day (3).
PRES is a distinct clinical syndrome with characteristic radiographic abnormalities on CT and MRI. It has developed
in patients with hypertensive encephalopathy, eclampsia, and
disorders treated with cytotoxic or immunosuppressive drugs.
The initial clinical series reported in 1996 included 13 women
and 2 men with ages ranging from 15 to 62 years (4). Twelve of
these patients had hypertension (systolic blood pressure range
142 to 200 mm Hg), eight had elevated creatinines (range 1.5
to 16.1 mg/dL), three were taking cyclosporine, and three were
taking tacrolimus. CT and MRI showed extensive white matter
changes consistent with edema in the posterior regions of both
cerebral hemispheres. Although the pathogenesis of PRES is
not fully understood, abnormal cerebral blood ﬂow regulation
likely contributes to its development (5). As the arterial blood
pressure rises, this pressure change could cause blood-brain bar-

Figure 3. MRI T2 fluid-attenuated inversion recovery images of (a) the cerebellum, (b) occipital regions, and (c) frontoparietal lobes.
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Baylor University Medical Center Proceedings

Volume 30, Number 3

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