Stroke has become the common causes of epilepsy after middle age. indicate that the risk of PSE may be influenced for instance by statin treatment. Third studies are emerging regarding the treatment and prognosis of PSE. Levetiracetam and lamotrigine may be well tolerated treatment options and seizure freedom is achieved in at least a similar proportion of patients as in other epilepsies. Furthermore new animal models such as photothrombotic stroke gives hope of a more clear understanding of PSE epileptogenesis in the near future. In summary PSE shows indications of maturing into an independent epilepsy research field. This review summarizes recent advances in our understanding of PSE and provides an update on management issues such as diagnosis AED selection and prognosis. Finally future research challenges in the field are outlined. 2005 Syvertsen 2015]. Over the last decade or so there have been remarkable improvements in the management of stroke with advances in emergency revascularisation being paralleled by raised ambitions in secondary prophylaxis rehabilitation and management of nonmotor sequelae such as fatigue. Poststroke epilepsy (PSE) thereby occurs in an optimistic medical context but advances in management of poststroke seizures have not quite matched those seen in other stroke treatment domains. In fact guidance was until recently scarce for neurologists pondering relatively fundamental management issues such as when to treat whom with what. Fortunately there seems to be a growing research interest in PSE. This is perhaps part of a general trend in the epilepsy field of increased focus on aetiology. Traditionally patients with structural-metabolic epilepsy of widely different origins from developmental tumours to stroke were studied under the NPI-2358 umbrella term NPI-2358 of ‘partial epilepsy’. Although pathways of epileptogenesis may converge it is clear that structural-metabolic epilepsies of different aetiologies occur in different contexts medically and demographically and that management considerations differ in a 30-year old with a low-grade glioma from a 60-year old with hemiparesis and atrial fibrillation. For clinicians and patients the focus on aetiology is therefore good news. Better stratification of patients in studies according NPI-2358 to underlying aetiology is likely to result in more relevant knowledge and improved management. This review aims to summarize some of the recent advances in PSE research and address some important NPI-2358 questions clinicians are likely to face such as risk factors for PSE after stroke the incidence of PSE in the setting of modern stroke care and an update on current management of PSE. Not all advances have been based on new scientific data. Also covered are policy documents from the International League Against Epilepsy (ILAE) on the definition of acute symptomatic seizures and the definition of epilepsy [Beghi 2010; Fisher 2014] which have spread expert practice and brought valuable structure to the management of PSE. Epileptogenesis early and late seizures PSE shares features with other forms of structural-metabolic epilepsy. As in for instance post-traumatic epilepsy there is often a latent phase after the insult during which the brain is thought to undergo NPI-2358 epileptogenesis and acquire a predisposition for seizures. Among proposed epileptogenic mechanisms are inflammation and remodelling of synaptic networks perhaps influenced by NPI-2358 genetic susceptibility TEAD4 [Silverman 2002; Pitkanen 2015]. Historically PSE has been difficult to model in rodents and pet researchers have as a result mainly centered on types of epilepsy after injury electric powered kindling chemoconvulsant-induced position epilepticus (SE) or cortical shots of irritants such as for example tetanustoxin or ferrous chloride. Fairly recently photothrombotic heart stroke has been set up being a model for PSE in rodents [Kelly 2001; Pitkanen 2007] therefore whether PSE differs from other styles of obtained epilepsy in the standard systems of epileptogenesis will likely be elucidated soon. The principles of latency and epileptogenesis form a significant basis for scientific understanding of the idea of early past due seizures. Early seizures take place soon after a stroke and so are regarded as consequences of regional metabolic disturbances which have not necessarily changed neuronal systems but possess produced them epileptic in nature. Later seizures take place when epileptogenesis is certainly postulated to possess occurred and the mind has obtained a predisposition for seizures [Silverman 2002]..