Background: Sporadic hemiplegic migraine (SHM) is an unusual migraine syndrome characterized by recurrent transient attacks of unilateral weakness or paralysis as part of the migraine aura. Underlying mutations have been detected in the CACNA1A, ATP1A2, SCN1A, and PRRT2 genes. SHM is a genetically and clinically heterogeneous condition.
Case Presentation: We present a 13-year-old German girl with SHM with a known mutation in the ATP1A2 gene. She presented to our emergency department with headache, somnolence, confusion, nausea, vomiting, photophobia, and a hemiparesis of the left arm and leg (1/5 BMRC) as well as a paresis of the left side of the face. A cranial magnetic resonance imaging (MRI) revealed cortical edema and the EEG showed unilateral slowing of the corresponding hemisphere.
Initial treatment consisted of antiedematous therapy and intravenous levetiracetam but her symptoms persisted. On day 8, a continuous nimodipine infusion was initiated. Nimodipine has pleiotropic mechanisms of action with one being its L-type calcium channel–mediated vasodilation of vascular smooth muscle cells to relax arteries. Because of one reported case of deterioration of symptoms, our patient was carefully monitored on the ICU. After starting the infusion, the symptoms of our patient improved rapidly. After 12 hours, the Babinski sign disappeared, her vigilance, vision, speech, and orientation improved, and the patient regained motor control over her left body side (3–4/5 BMRC). The abnormal cortical signal in the T1 sequences in her MRI improved.
Result: Apart from moderate bradycardia and arterial hypotension during sleep, when we had to reduce the initial dose of 50 to 25 mg/h, there were no unwarranted effects. We conclude that nimodipine is an effective option in the management for prolonged SHM attack in our patient.
Conclusion: Despite earlier cautioning reports, nimodipine might be a treatment option for prolonged attacks in patients with hemiplegic migraine.
