Pregabalin has favorable effects on several types of neurological pain, but can cause side-effects including dizziness, somnolence and delirium. Delirium presents as two variants in terms of psychomotor disturbance: the hyperactive type, showing agitation and vigilance; and the hypoactive type, showing lethargy and decreased motor activity. Patients with delirium associated with pregabalin therapy have been reported to experience hyperactive delirium. Here, we report the case of a 68-year-old patient with insidious hypoactive delirium caused by pregabalin therapy for postherpetic neuralgia. Delirium improved after discontinuation of pregabalin. Hypoactive delirium is considered to be more common than the hyperactive type in older adults, and is likely to be overlooked. Attention should thus be paid to latent cases of hypoactive delirium associated with pregabalin therapy in elderly individuals.Delirium is an acute state of confusion and is common among elderly individuals.1,2 Delirium has two variants in terms of psychomotor disturbance: the hyperactive type, associated with agitation and vigilance; and the hypoactive type, showing lethargy and decreased motor activity, and individuals often experience switching between variants. [1][2][3] Pregabalin is an analog of gabapentin, and binds to the a 2 -d protein subunit of voltage-gated calcium channels, and not to gamma amino butyric acid receptor, in the central nervous system. 4 Pregabalin is effective in the treatment of neuropathic pain associated with diabetic neuropathy, fibromyalgia and postherpetic neuralgia. [4][5][6] We report the case of a patient who developed insidious hypoactive delirium induced by pregabalin therapy.
Case reportThe patient was a 68-year-old man who had been treated in March 2007 for dementia and anorexia. He was subsequently diagnosed with panhypopituitarism caused by pituitary sarcoidosis. Symptoms improved after initiating treatment with prednisolone and levothyroxine in September 2007. He developed herpes zoster on the left neck and shoulder in September 2010, and 25 mg of pregabalin had been administered for postherpetic neuralgia since August 2011. His wife reported that he was free from any signs of cognitive function decline or appetite loss before the initiation of pregabalin therapy. The dose of pregabalin was initially increased by 25 mg every 2 weeks, and had been maintained at 100 mg since September 2011. Around that time, he felt lethargic, and motor activity, attentiveness and cognitive function showed rapid disruption. He suffered from these symptoms for 3 months, before being admitted to Niigata University Medical & Dental Hospital, Niigata, Japan, in February 2012.On admission, he showed lethargy, hallucinations and decreased motor activity. He did not have a sense of insecurity or other complaint related to depression. The results of blood testing, including testing of thyroid function, cerebrospinal fluid analysis and levels of various autoantibodies, were all normal on admission. Neurological examination ...