Related Experiment Video
Updated: Apr 17, 2026
05:26
Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
9.8K
Creatine phosphokinase elevation exacerbated by levetiracetam therapy
Julia E Isaacson1, Dongwhoon J Choe2, Michael J Doherty3
1Dartmouth College, Department of Psychological & Brain Sciences, Maynard Street, Hanover, NH 03755, USA.
Epilepsy & Behavior Case Reports
|February 11, 2015
Summary
Levetiracetam, an epilepsy medication, can cause elevated creatine phosphokinase (CPK) levels. Discontinuing levetiracetam (LEV) led to normalized CPK, suggesting it as a cause for persistent elevations post-seizure.
Area of Science:
- Neurology
- Clinical Pharmacology
Background:
- Epilepsy management often involves antiepileptic drugs.
- Levetiracetam (LEV) is a commonly prescribed antiepileptic medication.
- Elevated creatine phosphokinase (CPK) can occur post-seizure, but other causes must be considered.
Purpose of the Study:
- To investigate the potential association between levetiracetam therapy and unexplained elevations in creatine phosphokinase (CPK) levels.
- To determine the effect of levetiracetam discontinuation on CPK levels in a patient with epilepsy.
Main Methods:
- Case report of a 19-year-old male with epilepsy.
- Administration of levetiracetam as additional therapy.
- Monitoring of creatine phosphokinase (CPK) levels.
- Observation of CPK levels following levetiracetam discontinuation.
Main Results:
- A significant increase in creatine phosphokinase (CPK) was observed after initiating levetiracetam.
- The CPK elevation could not be solely attributed to renal dysfunction or rhabdomyolysis.
- Discontinuation of levetiracetam resulted in a rapid normalization of CPK levels.
Conclusions:
- Levetiracetam (LEV) should be considered as a potential cause for persistent creatine phosphokinase (CPK) elevations in patients following convulsive seizures.
- Monitoring CPK levels and considering drug-induced effects is crucial in epilepsy management.
- This case highlights a potential adverse effect of levetiracetam on muscle enzymes.
Related Concept Videos
01:20Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein
1.2K
Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
1.2K
01:20Antiepileptic Drugs: Potassium Channel Activators
1.0K
Ezocgabine or retigabine, an antiepileptic drug of remarkable efficacy, has revolutionized the management of seizures. It is a potassium channel activator, explicitly targeting the family of Q subtype potassium channels. It enhances the transmembrane potassium currents, regulating neuronal excitability. This action stabilizes the resting membrane potential, a pivotal factor in mitigating the hyperexcitability that characterizes epilepsy.
Ezogabine has gained approval as an adjunctive treatment...
Ezogabine has gained approval as an adjunctive treatment...
1.0K
01:24Muscle Recovery and Fatigue
5.1K
Muscle fatigue refers to the decline in a muscle's ability to maintain the force of contraction after prolonged activity. It primarily stems from changes within muscle fibers. Even before experiencing muscle fatigue, one may feel tired and have the urge to stop the activity. This response, known as central fatigue, occurs due to changes in the central nervous system, namely the brain and spinal cord. While there is no single mechanism that induces fatigue, it may serve as a protective...
5.1K
01:14Antiepileptic Drugs: Glutamate Antagonists
1.3K
Glutamate is a fundamental neurotransmitter in the central nervous system, playing a vital role in neuronal communication and various cognitive processes. Glutamate stands as the principal excitatory neurotransmitter in the brain. Its presence is crucial for the communication between neurons, underpinning essential processes such as synaptic transmission, neuronal excitability, and plasticity. These functions are vital for higher-order cognitive processes, including learning and memory. The...
1.3K
01:29Hepatic Encephalopathy
2
DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic...
2
01:22Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test
266
In clinical practice, the direct measurement of hepatic blood flow to evaluate liver function presents significant challenges due to the intricate and specialized nature of the necessary techniques. Consequently, healthcare professionals often rely on empirical estimates derived from thorough patient examinations and liver function tests to gauge liver health. Among the tools at their disposal, the Child–Pugh and MELD scoring systems stand out for their ability to categorize and assess...
266