Gabapentin and pregabalin toxicity can manifest as myoclonus. While myoclonus can present in multiple ways – focal or multifocal, positive, negative, and rest, cortical or subcortical – it most often occurs in a positive or rest, multifocal, and subcortical fashion. Abstract Gabapentin (GBP) and pregabalin (PGB) are FDA approved for adjunctive treatment of partial seizures and for treatment of post-herpetic neuralgia. Both drugs are primarily eliminated by renal excretion. However, PGB or GBP induced myoclonus has only been reported infrequently in case reports/series. It is not discussed with patients and its sudden occurrence can lead to anxiety because Gabapentin is Food and Drug Administration-approved for treating postherpetic neuralgia and neuropathic pain due to its efficacy and tolerability, with minimal drug interactions and adverse effects. However, it may rarely cause acute onset myoclonus, which should be communicated to the patient and diligently observed by the clinician Abstract A wide variety of drugs can cause myoclonus. To illustrate this, we first discuss two personally observed cases, one presenting with generalized, but facial-predominant, myoclonus that was induced by amantadine; and the other presenting with propriospinal myoclonus triggered by an antibiotic. We then review the literature on drugs that may cause myoclonus, extracting the corresponding LEARNING POINTS Gabapentin is used as an anti-epileptic and for neuropathic pain. Adverse effects with gabapentin include severe myopathy, severe myoclonus, neutropenia, hypoglycaemia episodes and altered consciousness. Gabapentin is renally excreted; dose adjustments are required to prevent accumulation and toxicity. Gabapentin toxicity can be manifested with symptoms such as myoclonus, [4] hypoglycemia, [5] and altered sensorium. [6] Modalities for treatment of cases of gabapentin toxicity have not been extensively investigated, but there has been a report of effective treatment and recovery by hemodialysis [7] in a patient with suspected gabapentin Gabapentin and pregabalin toxicity can manifest as myoclonus. While myoclonus can present in multiple ways – focal or multifocal, positive, negative, and rest, cortical or subcortical – it most often occurs in a positive or rest, multifocal, and subcortical fashion. In a study which included two cases of myoclonus associated with gabapentin toxicity in the setting of renal disease, the patients settled with HD and peritoneal dialysis (PD). Myoclonic activity may occur as a complication of gabapentin toxicity, especially with acute kidney injury or end-stage renal disease. We report 2 cases of myoclonic activity associated with gabapentin toxicity in the setting of renal disease which resolved with discontinuation of gabapentin and treatment with hemodialysis and peritoneal dialysis. Acute hyperkinetic movement disorders such as multifocal or segmental myoclonus in elderly patients warrant a prompt review of recent drug history, especially gabapentin, even in the background of normal renal function. In the cases reported, both HD and PD were effective in treating myoclonic activity in acute and chronic renal dysfunction. Gabapentin requires renal dosing in patients with chronic kidney disease and in patients at risk for developing AKI. In cases of symptomatic gabapentin-induced toxicity, dialysis should be instituted. Background: Myoclonus may be linked to a variety of causes, including epilepsy, postanoxic brain injury, metabolic encephalopathies and focal central nervous system lesions. Various drugs also have been reported to induce myoclonus. Gabapentin-induced myoclonus has been reported previously, especially in cases with impaired renal function or epilepsy. These medications can cause lethargy or agitation in overdose, increase risk of death combined with opioids, and manifest a withdrawal syndrome. This topic will discuss the evaluation and management of gabapentinoid poisoning and withdrawal. A summary table to facilitate emergency management is provided (table 1). Myoclonus is a rare side effect of gabapentin (GBP) and has been reported in patients with preexisting myoclonus, mental retardation, chronic static encephalopathy, diffuse brain damage, impaired renal function, or end stage renal disease. We report Background: Gabapentin (GBP)-induced movement disorders (MDs) are under-recognized adverse drug reactions. They are commonly not discussed with patients, and their sudden occurrence can lead to misdiagnosis. This literature review aims to evaluate the clinical–epidemiological profile, pathological mechanisms, and management of GBP-associated MD. Methods: Two reviewers identified and assessed Gabapentin is the first-line treatment for painful diabetic polyneuropathy. [2] Gabapentin is primarily excreted from the kidneys and the clearance of gabapentin is altered in patients with deranged renal function. [3] Gabapentin toxicity can be manifested with symptoms such as myoclonus, [4] hypoglycemia, [5] and altered sensorium. [6] Conclusion: Pregabalin- and gabapentin-induced negative myoclonus can develop even in patients with normal renal function. Physicians should keep in mind the possibility of patients developing negative myoclonus under treatment of pregabalin or gabapentin even in short period of time and with low dosage, and in the normal range of renal function. Gabapentin and pregabalin toxicity can manifest as myoclonus. While myoclonus can present in multiple ways – focal or multifocal, positive, negative, and rest, cortical or subcortical – it most often occurs in a positive or rest, multifocal, and subcortical fashion. This case report highlights the potential for gabapentin to induce myoclonus in patients with renal dysfunction, demonstrating the need for careful monitoring and appropriate dosing adjustments. Two cases are presented where patients developed myoclonic activity associated with gabapentin toxicity, leading to hemodialysis and peritoneal dialysis as effective treatments in the context of acute Conclusions Myoclonus is a well-reported complication of gabapentin toxicity especially in patients with renal impairment. As gabapentin is solely excreted by the kidneys, renal dose adjustment is recommended in the literature. However, patients with CKD remain at risk of life-threatening neurotoxic adverse events even with appropriate dosing
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