Encephalopathy describes a spectrum of brain dysfunction resulting from metabolic imbalances, infections, toxins, or organ failure. Patients are commonly presented with confusion, altered consciousness, tremors, myoclonus, or asterixis. This case report highlights an uncommon cause of metabolic encephalopathy, underscoring the importance of thorough clinical evaluation and early recognition to guide effective treatment and improve outcomes. Case Presentation A 44-year-old female with a history of bullous emphysema-type COPD, insulin-dependent type 2 diabetes complicated with neuropathy, schizoaffective disorder, and cocaine use disorder presented with acute on chronic hypercapnic respiratory failure secondary to a COPD exacerbation and community-acquired pneumonia. She reported dry cough and dyspnea after running out of home oxygen. On admission, she was alert and oriented with bilateral wheezes and mild lower extremity edema. She was subsequently placed on a BIPAP machine and received empiric treatment with cefepime and azithromycin, as well as a prednisone taper. Additionally, she restarted her home medications, including gabapentin for diabetic neuropathy, which was increased from her home dose of 600 mg TID to 900 mg TID. Within 48 hours of admission, the patient developed new-onset diffuse tremors consistent with asterixis, stuttering speech, and functional impairment. She would drop objects due to uncontrollable shaking. Neurologic workup, including thyroid function and urine toxicology, was unremarkable. Her respiratory status improved, with no ongoing hypoxia or worsening hypercapnia. Given the timing of symptom onset after resuming gabapentin, and absence of similar symptoms during prior hypercapnic episodes, gabapentin-induced myoclonus was suspected. The dose was reduced, resulting in resolution of symptoms. This case underscores the importance of recognizing gabapentin-induced movement disorders, especially in patients with respiratory compromise, where hypercapnia may exacerbate neurotoxic drug effects. Discussion Gabapentin-induced myoclonus is a rare but clinically significant adverse effect, particularly in patients with underlying respiratory compromise. In the setting of hypercapnia, reduced clearance of carbon dioxide can exacerbate central nervous system sensitivity to neuroactive drugs like gabapentin. Myoclonus in this context may be misattributed to metabolic encephalopathy or seizure activity, delaying appropriate treatment. Recognizing gabapentin as a potential cause is essential, especially in patients with renal impairment or chronic lung disease. Discontinuation often leads to symptom resolution. This highlights the importance of thorough medication review in patients presenting with myoclonus and altered mental status, particularly when respiratory dysfunction is present. Medication changes can often be overlooked in the setting of acute illness, and it is crucial to consider them in the differential diagnosis.

Mr. Dhiraj Narayana Tadikamalla is a motivated professional affiliated with Wayne State University School of Medicine, Canton, USA. He is actively engaged in medical research and academic initiatives, with a particular interest in sharing scientific findings through poster presentations in virtual platforms. Mr. Tadikamalla demonstrates a strong commitment to advancing medical knowledge and fostering collaborative learning within the healthcare and research community. His dedication to scholarly work and evidence-based practices highlights his passion for contributing meaningfully to medical science