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Cefepime-induced encephalopathy and myoclonus

T. Rasameesoraj, X.x. Yu, A. Ahmed, H. Fernandez (Cleveland, OH, USA)

Meeting: 2017 International Congress

Abstract Number: 859

Keywords: Myoclonus: Clinical features, Myoclonus: Etiology and Pathogenesis

Session Information

Date: Wednesday, June 7, 2017

Session Title: Myoclonus

Session Time: 1:15pm-2:45pm

Location: Exhibit Hall C

Objective: To raise awareness of cephalosporin-induced encephalopathy and myoclonus.

Background: Myoclonus occurs in 15% of antibiotic-associated encephalopathy, especially with penicillins and cephalosporins. Cefepime and ceftazidime are the most commonly implicated.

Methods: Case report with video prior to and post cefepime discontinuation.

Results: We report an 85-year-old man who was admitted for encephalopathy and myoclonus. He has complex medical history of recurrent scalp squamous cell carcinoma invading the skull with intracranial extension, requiring multiple excisions, craniectomies, cranioplasties, and radiations. Prior to his current admission, he developed intermittent right arm jerking. EEG and MRI could not be performed due to his  scalp wound and mechanical heart valve. He was empirically treated with gabapentin for focal seizures, which was later switched to pregabalin. Levetiracetam was then added due to persistent symptoms. Since the CT of the brain raised the possibility of  infection, he was then treated with cefepime for possible cerebritis. Within few days, he became encephalopathic, had difficulty speaking and developed bilateral upper extremity jerking. On exam, while  afebrile, he was encephalopathic but able to follow some simple commands with perseveration. He had  spasticity, hyperreflexia on the lower extremities with sustained clonus, and proximal weakness. Indeed, there was postural and action-induced myoclonus along with asterixis. Tactile and auditory stimuli  did not trigger myoclonus. Levetiracetam dose was decreased, pregabalin was discontinued, divalproex sodium was added for myoclonus treatment without success. Finally, cefepime was discontinued after a negative CSF culture. Within 24 hours after discontinuing cefepime, his  mental status improved, and myoclonic frequency diminished. Complete resolution of encephalopathy and myoclonus was noted within 36 hours.

Conclusions: Cephalosporin-associated neurotoxicity is an under-recognized, highly reversible cause that should be considered as a differential in patients with encephalopathy and myoclonus. Early recognition may help decrease morbidity and mortality. Unfortunately, as in this illustrative case, it is often seen in an ICU setting, with multiple co-morbidities and concurrent psychotropic medications, making it a diagnostic challenge.

References: Bhattacharyya S, Darby R, Raibagkar P, et al. Antibiotic-associated encephalopathy. Neurology 2016;86:1-9.

Grill MF, Maganti RK. Neurotoxic effects associated with antibiotic use: management considerations. Br J Clin Pharmacol 2011;72:381-393.

To cite this abstract in AMA style:

T. Rasameesoraj, X.x. Yu, A. Ahmed, H. Fernandez. Cefepime-induced encephalopathy and myoclonus [abstract]. Mov Disord. 2017; 32 (suppl 2). https://www.mdsabstracts.org/abstract/cefepime-induced-encephalopathy-and-myoclonus/. Accessed July 12, 2025.
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