Baylor University Medical Center Proceedings July 2017 - 355

Posterior reversible leukoencephalopathy syndrome after
kratom ingestion
Austin Castillo, BS, J. Drew Payne, DO, and Kenneth Nugent, MD

Posterior reversible encephalopathy syndrome has been associated with
hypertension, preeclampsia, cancer chemotherapy, and drugs of abuse,
such as amphetamine and methamphetamine. We report a young man
who suddenly developed severe headache, disorientation, and aphasia
following ingestion of kratom and Adderall. Computed tomography and
magnetic resonance imaging of his head revealed foci of vasogenic
edema in the posterior occipital lobes, frontal lobes, and brainstem. In
addition, he had a small area of hemorrhage in the left posterior occipital
lobe. Lumbar puncture revealed an increased number of red blood cells
but no other abnormalities. His initial blood pressure was elevated but
returned to normal during hospitalization. This case suggests that kratom
can cause posterior reversible encephalopathy syndrome and needs to be
considered when patients present to emergency centers with headaches,
confusion, and visual disturbances.

itragyna speciosa (kratom) is a tropical evergreen
tree native to Southeast Asia. It is a member of the
Rubiaceae family (Ulbricht) and contains the psychoactive compounds mitragynine (C23H30N2O4,
molecular weight 398.49) and 7-hydoxymitragynine (7-HMG)
(Figure 1) (1). Kratom leaves have traditionally been used in
Southeast Asia to treat chronic pain or opioid withdrawal, although no scientiﬁc evidence supports this use. Over the past
years, kratom plant use has increased in the United States due
to its psychoactive and opioid-like activity, and the leaves are
used for recreation and for self-medicated opioid withdrawal
treatment. We report a patient with posterior reversible leukoencephalopathy syndrome (PRES) possibly related to kratom.
CASE PRESENTATION
A 22-year-old man presented with a severe headache ("absolute worse pounding") that had started earlier that morning. His
headache was described as throbbing (10/10), mostly in the back
of his head, and unrelieved by acetaminophen. He also reported
mild confusion, dizziness, and disorientation. The patient was
prescribed ﬂuoxetine for depression and quetiapine for insomnia. He occasionally misused dextroamphetamine and marijuana. His blood pressure was 180/105 mm Hg, heart rate 53
beats per minute, and respiratory rate 16 breaths per minute. He
was alert and oriented but uncomfortable. His Glasgow coma

Proc (Bayl Univ Med Cent) 2017;30(3):355-357

Figure 1. 7-hydroxymitragynine (7-HMG).

scale score was 15. His white blood cell count was 12.8 k/μL,
hemoglobin 17.1 g/dL, and platelet count 247 k/μL. The serum
sodium was 136 mEq/L, potassium 3.6 mEq/L, chloride 101
mEq/L, blood urea nitrogen 12 mg/dL, and creatinine 0.9 mg/
dL. The prothrombin time was 11.6 sec. A computed tomography (CT) scan of the head revealed a possible occipital intraparenchymal hemorrhage. A lumbar puncture was performed,
and the cerebrospinal ﬂuid had 1500 red blood cells/mm3, 0
white blood cells/mm3, glucose 65 mg/dL, protein 21 mg/dL,
and a negative Gram stain.
The patient was then transferred to our facility; during his
initial interview he was confused, disoriented to place and time,
and aphasic. He had photophobia. His systolic pressure varied
from 160 mm Hg to 100 mm Hg. His pupils were equal, round,
and reactive to light. Motor examination and coordination were
normal. His Glasgow coma scale score was 14. His drug screen
was positive for amphetamine, benzodiazepine (lorazepam given
in local emergency room), cannabinoids, and opiates (morphine
given in local emergency room). His urine was not tested for kratom. A repeat CT scan of the head revealed bilateral low-density
changes consistent with edema in both cerebellar hemispheres,
in both occipital lobes, and in both parietal lobes consistent
with PRES and a left occipitoparietal intraparenchymal bleed
From the Department of Internal Medicine, Texas Tech University Health Sciences
Center, Lubbock, Texas.
Corresponding author: J. Drew Payne, DO, Department of Internal Medicine,
Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX
79430 (e-mail: drew.payne@ttuhsc.edu).
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