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Abstract Details

A Curious Case of Cocaine-Induced Hypokalemic Periodic Paralysis Mimicking Guillain-Barre Syndrome
Autoimmune Neurology
P10 - Poster Session 10 (8:00 AM-9:00 AM)
6-003

Cocaine inhibits the reuptake of monoamines at the synaptic cleft to prolong sympathetic output. This adrenergic hyperresponsiveness mimics thyrotoxicosis as it replicates sodium/potassium ATPase hyperactivity, causing a cellular influx of potassium (hypokalemia), hyperpolarization, and sodium channel inactivation that presents as sudden, painless muscle weakness and paralysis.

To describe a rare cause of progressive ascending paralysis resembling Guillain-Barre Syndrome (GBS).
Consent obtained from patient.

A 30-year-old female with no past medical history was evaluated in the ED for acute lower extremity weakness that ascended to the upper extremities within < 12 hours. Labs were significant for hypokalemia at 1.6, elevated inflammatory markers, elevated Free T4 at 2.58, and low TSH at < 0.015. Urine drug screen was positive for cannabis and cocaine. Serum toxicology was negative. MRI of the T-spine and L-spine were unremarkable. Lumbar puncture was unremarkable.

Cranial nerves were intact. Strength was 1/5 throughout, including at the neck. Flaccid tone. Lower extremity reflexes were 2+. Negative Babinski. Positive Hoffman bilaterally. Preserved sensation.

The patient was admitted to the ICU, intubated for impending respiratory distress, and treated with IVIg. MRI of the C-spine was unremarkable. Further labs demonstrated elevated Free T3 at 7.13 and positive anti-TPO antibodies, significant for Grave’s disease. Urine labs were substantial for distal RTA. Anti-SSA and SSB antibodies were positive, indicating likely Sjogren’s syndrome (SS). Ganglioside panel was negative. Potassium was aggressively repleted. By day 1, the patient was moving all four extremities, and IVIg was discontinued. By day 2, she was successfully extubated. She was ambulating without difficulty on discharge.

Secondary hypokalemic periodic paralysis may mimic Guillain Barre syndrome (GBS), a life-threatening demyelinating neuropathy that presents as rapidly progressive, symmetric, ascending paralysis or paresthesia with loss of reflexes. In our case, cocaine was the most plausible trigger for hypokalemia.

Authors/Disclosures
Elizabeth Gene Baumann, MD (Memorial Hospital West)
PRESENTER
Dr. Baumann has nothing to disclose.
Hassnain Ali Rizvi, DO (Memorial Healthcare Systems) Dr. Rizvi has nothing to disclose.
Amaris Alayon, MD Ms. Alayon has nothing to disclose.
Tyler Kendall, MD Dr. Kendall has nothing to disclose.
Sydney Margaret Shaffer, MD (Memorial Healthcare System) Dr. Shaffer has nothing to disclose.
Stephan Mouhanna, MD Dr. Mouhanna has nothing to disclose.
Sean T. Kenniff, MD (Memorial Neuroscience Institute) Dr. Kenniff has nothing to disclose.