doi:10.1684/epd.2014.0626 Epileptic Disord, Vol. 16, No. 1, March 2014 107 Correspondence: Donald W Gross 2E3.19 Walter Mackenzie Health Sciences Centre, 8440 112 St NW, Edmonton T6G 2B7, Canada <donald.gross@ualberta.ca> Clinical commentary with video sequences Epileptic Disord 2014; 16 (1): 107-11 Alcohol-responsive epilepsia partialis continua Trevor A Steve, Donald W Gross Division of Neurology, Department of Medicine, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Canada ABSTRACT – Epilepsia partialis continua is typically associated with lesions of the cerebral cortex. However, subcortical lesions can also cause this condition. We present a patient with epilepsia partialis continua who failed to respond to conventional anticonvulsant medications but experienced a dramatic transient response to alcohol and a subsequent response to primidone. This pattern of sensitivity, which is similar to that seen in essen- tial tremor, has led to the hypothesis that the two disorders are associated with pathology within the same anatomical network. A new pathophys- iological model is thus proposed for the occurrence of epilepsia partialis continua in both cortical and subcortical disease processes. [Published with video sequences] Key words: epilepsia partialis continua, myoclonus, essential tremor, tremor Epilepsia partialis continua (EPC) is defined as “continuous muscle jerks of cortical origin” (Cockerell et al., 1996). Patients with EPC suffer from infrequent generalised seizures and medically intractable myoclonic jerks. The most com- mon causes of EPC are Rasmussen’s encephalitis, tumours, stroke, and focal cortical dysplasia. The pathophysiology of EPC is incompletely understood (Guerrini, 2009). It is typically associated with lesions in the contralateral cerebral cortex (Cockerell et al., 1996). How- ever, subcortical pathology can also cause EPC (Juul-Jensen and Denny- Brown, 1966). The role of subcortical structures in maintaining cortical epileptic activity remains unclear. Presently, “no single mechanism” has been proposed to account for the occurrence of EPC with both cortical and subcortical lesions (Guerrini, 2009). Essential tremor (ET) consists of postural-kinetic hand tremor and variable involvement of other body regions. A striking feature in ET is a dramatic temporary response of the tremor to alcohol. Many patients also experience a moder- ate to marked improvement with primidone (Elble, 2009). The patho- physiology of ET is believed to involve “tremorogenic oscillation and synchrony in motor networks”, involving the inferior olive, cere- bellum, and cerebral cortex (Elble, 2009). We report a case of EPC which was alcohol and primidone responsive. Given the similarities of pharmacological sensitivity, we hypothesize overlap in the anatom- ical network involved in ET and EPC.