Case Presentation: An 87-year-old woman with a history of pancreatic cancer status post distal pancreatectomy/splenectomy/partial colectomy, chronic kidney disease, hepatocellular carcinoma, and diabetes was admitted following sudden onset of new, uncontrollable bilateral upper extremity shaking and facial twitching. Symptoms started the night before and became progressively worse with dyspnea, nausea, and bilateral lower extremity tremors leading to ambulatory dysfunction. Prior to admission, the patient received three doses of levofloxacin for a urinary tract infection. In the ED, she was believed to be in status epilepticus and received lorazepam with no improvement. The shaking events worsened with outstretched hands. CT revealed no acute intracranial abnormality. Upon examination by neurology, the patient was determined to have non-rhythmic, low-amplitude twitching aggravated by talking and arm extension. There was no loss of consciousness or abnormal sensation, but she experienced solid and liquid dysphagia due to her shaking. Neurology suspected her episodes were due to levofloxacin-induced myoclonus. Levofloxacin was replaced with piperacillin-tazobactam, and her symptoms improved, beginning in her face and extending to her extremities. Within 48 hours, she was steady on her feet and ready for discharge with her caregiver.
Discussion: This case demonstrates myoclonus as a lesser known but serious adverse effect of levofloxacin. The mechanism behind levofloxacin-induced myoclonus is suspected to be neurotransmitter imbalances in NMDA receptor overexcitation and GABA receptor inhibition. They compete with and displace GABA from its receptor sites, which causes a hyperexcitable neuronal state and the resulting acute twitching presentation. Although it is considered a rare reaction, patients with ongoing renal complications are at an increased risk of experiencing these events and the other severe adverse effects of levofloxacin. There is limited data regarding fluoroquinolone-induced myoclonus; where large studies cite central nervous symptoms and neuropsychiatric adverse events, case reports have noted myoclonus among movement-based events. Our patient was at increased risk considering her known chronic kidney disease, given 87% of levofloxacin is renally cleared and that the half-life ranges from 27-35 hours with renal impairment compared to six to eight hours in healthy adults. According to a literature review summarizing fluoroquinolone-induced movement disorders, half of the cases reviewed occurred in patients with renal or hepatic dysfunction. The onset of movement-related effects from fluoroquinolones typically occurred within five days after drug administration and resolved within seven days after discontinuation among these patients. This is crucial for providers to consider, as impaired kidney function compromises drug biotransformation pathways, causing unwanted accumulation and toxicity. As a result, at-risk patients may need further monitoring.
Conclusions: Even though myoclonus is reversible, physicians must be aware of this severe uncommon reaction from levofloxacin and other fluoroquinolones, particularly among high-risk patients with renal and liver conditions. Providers may opt to reevaluate its implementation in medical practice based on these adverse events. Ultimately, the issue remains that there is minimal data showing evidence of myoclonus as a side effect despite its recurrence in recent cases around the world.