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.

Thursday, June 27, 2024

What is the Risk of Poststroke Epilepsy?

 You're that incompetent and out-of-date, not reading previous research? Which is why we need a complete database of all stroke research and rehab protocols so survivors can train their medical staff in what needs to be done to recover.

Wasted research dollars that should have used to prevent post-stroke epilepsy

The latest here:

What is the Risk of Poststroke Epilepsy?

Ebbesen MQB, Dreier JW, Andersen G, Johnsen SP, Christensen J. Stroke and Risk of Epilepsy: A Danish Nationwide Register-Based Study. Stroke. 2024.

Stroke is a major cause of new-onset epilepsy in adults,1 especially in people aged 60 years and older.2 Published estimates of poststroke epilepsy risk, however, are heterogeneous, likely reflecting variable stroke and epilepsy classification accuracies in population-based cohorts, variable follow-up duration and attrition rates, and different statistical methods used to derive risk estimates. For example, crude incidences obtained from Kaplan-Meier estimates of the survival function tend to inflate risks in the presence of competing events such as death.3 This study, therefore, aimed to determine the short- and long-term risk of poststroke epilepsy while accounting for death as a competing risk.

The authors defined a population-based cohort from Danish nationwide registries. Strokes occurring between 2004-2018 were identified from the Danish Stroke Registry, which captures all acute strokes treated in hospital departments, whereas strokes occurring before 2004 and epilepsy cases were identified from the Danish National Patient Register, which contains International Classification of Diseases (ICD) codes from inpatient hospital discharge diagnoses (since 1977) and diagnoses from outpatient and emergency department visits (since 1995). The stroke group was defined from individuals who experienced a first-ever stroke between April 2004 and December 2018, without prior epilepsy. Individuals in the stroke group were matched with up to 10 reference people without prior epilepsy or stroke (i.e., the control group) on age, sex, and calendar time. Poststroke epilepsy was defined from ICD codes for epilepsy recorded at least 14 days after stroke to distinguish it from early seizures. The authors included 101,034 people in the stroke group and 1,010,333 people in the control group.

At two years, the cumulative incidence of epilepsy reached 3.5% (95% confidence interval [CI]: 3.4, 3.7%) in the stroke group vs 0.2% (95% CI: 0.1, 0.2%) in the control group, which at 10 years increased to 5.8% (95% CI: 5.6, 5.9%) in the stroke group vs 0.7% (95% CI: 0.7, 0.7%) in the control group. Poststroke epilepsy risk was higher in people with intracerebral haemorrhage as compared to those with ischemic stroke (12.5% [95% CI: 11.7, 13.2%] vs 5.1% [95% CI: 4.9, 5.3%] at 10 years). Poststroke epilepsy risk also increased with higher stroke severity and cortical involvement. Seizures within 14 days of stroke occurred in 0.6% of people with ischemic stroke and 2.2% of people with intracerebral haemorrhage, and early seizures increased the risk of poststroke epilepsy. As expected, risk estimates were higher when derived from the Kaplan-Meier estimates as compared to cumulative incidence functions that accounted for competing death risk.

This study is interesting and relevant to clinicians and researchers in stroke medicine for two main reasons. First, the authors report results which elegantly replicate prior studies that suggested not all strokes are equal when it comes to seizure risk. The first externally validated prognostic model of late (>7 days) seizures after ischemic stroke (the SeLECT score) was published in 20184 and included five clinical predictors: stroke severity, cortical involvement, early seizures, large artery atherosclerotic aetiology, and territory of middle cerebral artery involvement. In this study, the overall 5-year risk of late seizure after stroke was 8% (95% CI: 6, 9%), while people with the highest SeLECT score had a markedly high predicted 5-year risk of 83% (95% CI: 62, 93%). Both studies confirm that achieving accurate stratification of poststroke epilepsy risk is feasible.

Second, this study reports precise and reasonably accurate estimates of poststroke epilepsy risk in the general Danish population using a large prospective cohort. Producing valid estimates of poststroke epilepsy risk is a first step towards understanding the natural history of the disease, which can then be used for clinical decisions (e.g., offering closer follow-up), public health advocacy (e.g., campaigning for better resources to support people with poststroke epilepsy), research advocacy (e.g., influencing resources invested in poststroke epilepsy research), and future research questions (e.g., sample size calculation for clinical trials of interventions to prevent poststroke epilepsy). These estimates, however, may not be generalizable and need replication in other populations which might be subject to differences in factors known to influence poststroke epilepsy risk, like access to acute stroke care and stroke etiology.

Beyond stratifying and estimating risk, the optimal clinical management of people with higher poststroke epilepsy risk remains unclear. How can poststroke epilepsy risk stratification be designed and implemented? What could be the effect on routine care and patient-reported outcomes? Should stroke survivors undergo routine assessments (e.g., electroencephalogram) or monitoring (e.g., actigraphy)? Can patients with higher risk be included in trials of interventions to prevent epilepsy onset (e.g., the registered trial Exploring the Preventive Effect of Mitochondrial Protective Agent Idebenone on Post-stroke Epilepsy; clinicaltrials.gov ID: NCT05987397)? These are only a few of the persisting knowledge gaps that still need to be addressed in poststroke epilepsy research.

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