Abstracts

Rationale: Gabapentin (GBP) and pregabalin (PGB) are FDA approved for adjunctive treatment of partial seizures and the treatment of post-herpetic neuralgia. PGB is also approved for the management of diabetic neuropathy and fibromyalgia. GBP and PGB are chemical analogs of gamma-aminobutyric acid (GABA) and have similar mechanisms of action by binding to voltage-gated calcium channels and reducing the release of neurotransmitters.Both drugs are primarily eliminated by renal excretion. Clearance is highly correlated with renal function, and patients with poor renal clearance require a dose adjustment to prevent elevated plasma concentrations and common side effects like confusion, dizziness, and somnolence.However, PGB or GBP induced myoclonus has rarely been reported in case reports/series (Table 1) and is unknown to most clinicians. It is not discussed with patients, and its sudden occurrence can lead to anxiety because of “seizure-like” nature. Also, first-contact physicians might treat it as seizures, leading to unnecessary tests and aggressive management. It is frequently encountered in association with renal insufficiency in reported literature and clinical practice. We describe a series of five patients who developed myoclonus on PGB/GBP in association with renal dysfunction and one patient with epilepsy without renal dysfunction. Methods: We reviewed medical records of patients who had myoclonus because of PGB or GBP seen by Neurology service between January & May 2017 in inpatient or outpatient setting at our tertiary care setting were reviewed. Results: We identified five patients who were on either GBP or PGB or both who developed likely subcortical myoclonus in the setting of renal insufficiency and one patient who developed myoclonus independent of renal dysfunction (Table 2). While four patients had worsening of renal function at baseline chronic medication dose, one with known end stage renal disease had introduction of GBP at a “usual” starting dose. In contrast, Patient #6 with controlled generalized epilepsy likely had cortical myoclonus and an impaired awareness seizure due to the introduction of narrow-spectrum PGB to her baseline GBP. Conclusions: Our series suggests that PGB/GBP induced myoclonus is commonly seen but rarely documented or discussed in patients in various clinical settings with or without renal insufficiency, and is independent of the severity of the renal failure. However, this is a reversible side effect of medication, and it resolves either by discontinuing the medication, removing the medication with hemodialysis or by improvement of renal dysfunction. The type of myoclonus is dependent on the comorbidity, either renal dysfunction or epilepsy, and should be managed accordingly. With a high index of suspicion, aggressive testing and treatment for other possible conditions like seizures (in non-epilepsy patients) or CNS infections can be avoided. In patients with renal failure and with decreased physiological renal clearance such as the elderly, GBP or PGB dose initiation and changes should be conservative and they should be counseled on this particular side-effect. Funding: None