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| NI FEATURE: THE EDITORIAL DEBATE II-- PROS AND CONS |
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| Year : 2018 | Volume
: 66
| Issue : 4 | Page : 949-951 |
Early post-stroke seizures with first-ever stroke
Lakshmi Narasimhan Ranganathan, Shubha Subramanian, Guhan Ramamurthy, MM Arun Shivaraman
Department of Neurology, Institute of Neurology, Madras Medical College, Chennai, Tamil Nadu, India
| Date of Web Publication | 18-Jul-2018 |
Correspondence Address:
Dr. Lakshmi Narasimhan Ranganathan
Department of Neurology, Institute of Neurology, Madras Medical College, Chennai, Tamil Nadu
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.237004
How to cite this article:
Ranganathan LN, Subramanian S, Ramamurthy G, Arun Shivaraman M M. Early post-stroke seizures with first-ever stroke. Neurol India 2018;66:949-51 |
The article in focus describes early post stroke seizures in a sample of Egyptian patients with first ever stroke.[1] Although a literature search reveals multitude of articles on post stroke seizures, there is no consensus among them. Thus, differences exist starting right from the terminology, classification of post stroke seizures, functional outcome, treatment guidelines.
The classification of post stroke seizure based on time of occurrence is varying and conflicting. The post stroke seizures were initially classified as early and late onset seizures with an arbitrary cut off point of 2 weeks; and, a few of the studies classified a subtype of the early onset seizures as immediate, if the seizure occurred within first 24 hours of stroke.[2]Recurrent seizures were those occurring at least 2 weeks after the initial seizure; and, the presence of 2 or more than 2 seizure episodes was considered as multiple seizures.[3] The other studies concur with the authors' view that the peak of early onset seizure is the first 24 hours, and that of late onset seizures is 6-12 months.[4]
The International League Against Epilepsy (ILAE) classifies post stroke seizure into acute symptomatic seizures (ASS), when seizures manifest within a week; and, unprovoked s eizures (US), when seizures manifest after one week. As per the present ILAE practical clinical definition of epilepsy (given by Fischer et al.,), even the presence of one unprovoked seizure due to stroke is regarded as post stroke epilepsy.[5],[6] The authors of the study in focus have chosen to go with the older terminology and it would have been prudent to mention the change in the terminology as well as the cut off points of the time of occurrence of the seizure to avoid confusion.[1]
The sample size of the present study was based on the incidence rate of 9%, as reported by Bladin et al., in a large prospective multicenter study of seizures in acute stroke.[7] There is a wide variation in the incidence and long term cumulative risk of post stroke seizures. This is due to differences in the study cohorts regarding the stroke etiology as well as its severity; and, in the study methodology like the follow up time, outcome measures as well as the definitions of early and late seizures,[8] as explained by the authors. For example, early seizures were associated with an increased risk of post stroke epilepsy in the Copenhagen stroke study.[9] Since many of the seizures in this study were seizures occurring within 2 weeks, some of them, in fact, could have been stratified as late seizures (and unprovoked seizures), according to the current definition.[10]
The pathogenesis of early onset seizures was attributed to cortical hyperexcitability by the authors. The pathogenesis of early onset seizures of ischemic and haemorrhagic stroke differ. The mechanisms involved in the epileptogenesis of early onset ischemic post stroke seizures are the lowering of seizure threshold due to local ionic shifts, the release of high levels of excitotoxic neurotransmitters, and the presence of global hypoperfusion, the hippocampus being the most vulnerable site to undergo ischemic changes.[2] The pathogenetic mechanisms of early seizures following the occurrence of intracerebral haemorrhage are the direct stimulant effects of blood degradation products, and the existence of extracellular glutamate toxicity.[7],[11] The fact that the incidence of seizures increases hierarchically from pure acute ischemic stroke to ischemic stroke with haemorrhagic transformation to pure haemorrhagic stroke suggests the role of blood products in the epileptogenesis of early post stroke seizures. The structural aftermath of stroke, the gliosis and the meningeal cicatrisation contribute to the pathogenesis of late onset seizures. On the other hand, the physiological changes occurring after the neuronal injury of stroke contribute to the pathogenesis of early onset seizures [Figure 1].[10]
Other than the risk factors described by the authors, namely intracerebral haemorrhage, the large size of the lesion, and the cortical site of haemorrhage or ischemia, hyponatremia at the stroke onset has been described as an independent predictor of early post stroke seizures.[12] In the case of haemorrhagic stroke, it would be beneficial to also calculate the hematoma volume because ganglionic haemorrhages (having lesser chance of causing post stroke seizures), if large, can extend into the cortical area, thereby increasing the chance of causing a post stroke seizure.[2] In a study done by Dhanuka et al., hematomas could be divided into a large (>30 ml) and a small (0-29 ml) sized hematoma based upon their volume.
It would be interesting to look into the semiology of post stroke seizures to assess if it has any impact on the functional outcome or treatment options. The seizure semiology in the early onset seizures is characteristically that of focal onset (with or without secondary generalisation); while, the late onset seizures generally present with a generalised tonic-clonic seizure semiology.[4] The other presentations that may be possible with post stroke seizures include atypical seizures and status epilepticus (focal/generalised).[3] Status epilepticus as a presentation of early post stroke seizures does not predict the subsequent development of epilepsy. Although the immediate prognosis of such patients is poor, the independent effect of status epilepticus on the subsequent functional outcome is controversial.[11],[13],[14]
It is worthwhile to look for electroencephalographic changes (EEG) changes in this scenario, as patients with periodic lateralizing epileptiform discharges (PLEDS), bilateral independent PLEDS and focal spikes after stroke are especially prone to developing seizures.[15] Focal slowing, diffuse slowing and normal findings on EEG were associated with a relatively lower risk of having a subsequent seizure.
There has been no mention of the treatment guidelines in the original article in focus.[1] According to the European Stroke Organisation guidelines, there are no recommendations of primary as well as secondary anti-epileptic (AED) prophylaxis in ASS due to its low recurrence rate. In the case of US, there is no recommendation for the administration of primary AED prophylaxis; therefore, only secondary AED prophylaxis is recommended, based on observational studies, due to the risk of recurrence.[16] This lack of proper guidelines and recommendation is due to the paucity of large scale randomized control trials.[5] Despite this lacuna, in actual clinical practice, prophylactic AEDs are frequently given. The early post stroke seizures, even the recurrent ones, are well controlled with a single anticonvulsant.[17] The traditional choices for post stroke seizures have been carbamazepine and phenytoin [2] but recent studies support the use of levetiracetam, lamotrigine and gabapentin in early post stroke seizures especially in the elderly population.[18],[19] A few studies advocate a short term treatment of early post stroke seizures if multiple seizures occur or even after a single seizure had occurred in the cases having an intracerebral hematoma or haemorrhagic transformation [Figure 2].[20],[21] | Figure 2: Summary of post stroke seizures. AED: Antiepileptic drugs; PSE: Post-stroke epilepsy
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The surgical treatment of intractable epilepsy, after an ischemic cerebrovascular event has taken place, is a valuable means of controlling seizures but is less often considered as a therapeutic option due to the vulnerabilities present in the affected population related to the advanced age of the subjects. In lobar haemorrhage with early onset seizures, an arteriovenous malformation should be thought of. Seizures associated with subarachnoid haemorrhage usually occur at the time of onset of stroke.[22]
With the advent of newer revascularisation techniques like thrombolysis and stroke thrombectomy, an increased incidence of reperfusion injury is a distinct possibility. In this situation, post stroke epilepsy would, in all likelihood, emerge as an important entity. On the contrary, in patients with pre-stroke epilepsy, establishing the link between the seizures occurring in the adults and the subsequent development of cardiovascular events would be an intriguing and a challenging endeavour to undertake.[8]
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[Figure 1], [Figure 2]
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