Sir,A 45-year-old man, ASA physical status I, diagnosed with post-burn contracture of the right elbow joint, was scheduled for contracture release with split skin grafting. Examination showed a calm and cooperative man with unremarkable airway, chest, and cardiac findings. Patient was shifted to the preoperative room and monitoring of electrocardiogram, pulse oximetry, and blood pressure was started. Patient was administered oxygen via ventimask. Ranitidine 50 mg and metoclopramide 10 mg intravenous (IV) were administered as premedication. After 5 min, the patient developed an uneasy sensation, appeared restless and agitated, and exhibited movements of the arms and legs (crossing and uncrossing of the legs). He expressed a desire to move around and wanted to remove his IV cannula. He was immediately administered midazolam 1.5 mg IV. The symptoms subsided. He was monitored in recovery room for 30 min and subsequently shifted to the operation theater. General anesthesia was administered as per the standard protocol of our institute and the rest of the procedure proceeded uneventfully.Drug-induced akathisia (DIA) is often difficult to diagnose and may present with varying grades of severity. It is defined as a psychoneuromotor phenomenon in which the patient may describe an unpleasant feeling of inner restlessness or tension referable most commonly to the lower limbs, along with a desire to get up and walk, an inability to think clearly, and a feeling of anxiety. Most common offending agents are neuroleptic anti-psychotic medication or withdrawal from any physical addiction, e.g. benzodiazepinewithdrawal syndrome.[1]The objective motor components include restlessness of the lower limbs in the form of rocking foot to foot, crossing and uncrossing of legs, and pacing.[1] Positron Emission Topography studies show D2 receptor occupancy in the striatum plays a role and noradrenergic and serotonergic systems also appear to be involved.[2] Interestingly, metoclopramide acts, in part, via presynaptic dopamine receptor antagonism, and an overactive adrenergic system secondary to presynaptic dopamine receptor block in key parts of the brain and spinal cord may be the possible mechanism of DIA.[2] Metoclopramide has been linked to akathisia in many reports and the incidence of restlessness reported after IV administration of drug is 20–25%.[3] The diagnosis of DIA is largely clinical. There are no relevant laboratory tests in making the diagnosis, as these patients may present in different ways, the condition may also mimic other clinical syndromes, or the symptoms may be masked by preoperative medication.[4] Once the diagnosis is made, the offending drug (in our case, metoclopramide) should be promptly withdrawn.Benzodiazepines, β-blockers, α2-agonists, opioids, and anti-cholinergics have all been used to treat akathisia.[5] Benzodiazepines are more effective in easing the symptoms of akathisia, but they are associated with higher sedation rates.[6]Our case highlights the importance of prompt recognition and treatment of metclopramide-induced akathisia. We believe that drugs commonly administered in the perioperative period have the potential of inducing akathisia.