Deans' stroke musings: Does treatment with t-PA increase the risk of developing epilepsy after stroke?

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, August 15, 2015

Does treatment with t-PA increase the risk of developing epilepsy after stroke?

I guess the answer is no.
http://www.ncbi.nlm.nih.gov/pubmed/26205634

Keller L¹, Hobohm C, Zeynalova S, Classen J, Baum P.

Author information

Abstract

Patients suffering from ischemic stroke carry an enhanced risk of developing secondary epilepsy. We sought to clarify whether thrombolytic treatment with recombinant tissue plasminogen activator (t-PA) is independently associated with post-stroke epilepsy (PSE). In this observational study, data from 302 stroke patients treated at a single academic neurological department were analyzed retrospectively. Median follow-up was 42 months (maximum 80). Variables included presence of comorbidity, stroke severity, neurological presentation, complications, infarct characteristics, and treatment with t-PA. After univariate analyses, a multivariate analysis was performed to create a model of factors that were significantly associated with PSE, including treatment with t-PA. 13.9 % of patients developed PSE during follow-up. Multivariate analysis identified 5 independent factors for PSE: low Barthel Index at discharge; hemianopia; infection acquired during the hospital stay; involvement of the temporal lobe; involvement of the perirolandic cortex. While the incidence of PSE was higher in patients treated with t-PA (20.6 vs. 10.7 %, univariate analysis; p = 0.020), the effect was lost after adjusting for several factors associated with t-PA treatment [odds ratio for PSE after treatment with t-PA 1.3 (95 % CI 0.6-2.9), p = 0.489]. This study failed to identify treatment with t-PA as an independent risk factor for PSE.