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. Author manuscript; available in PMC: 2018 Nov 1.
Published in final edited form as: J Clin Neurophysiol. 2017 Nov;34(6):512–519. doi: 10.1097/WNP.0000000000000371

Table 2.

Cox proportional hazard regression analysis for any new activation-related epileptiform abnormality in 449 people with epilepsy aged 1 year or older who had at least one EEG

Factors N (%) Crude HR (95% CI) Adjusted HR* (95% CI)

Age at EEG**
1–19 years 2.3 (1.6– 3.4) 1.8 (1.1– 2.9)
≥20 years 1.0 (referent) 1.0 (referent)
Gender
Male 238 (53%) 1.0 (referent) 1
Female 211 (47%) 1.1 (0.9–1.5)
Sleep done**
No 1.0 (referent) 1.0 (referent)
Yes 1.8 (1.3– 2.7) 2.7 (1.8– 4.2)
Photic stimulation done**
No 1.0 (referent) 1.0 (referent)
Yes 0.9 (0.6– 1.4) 0.8 (0.5– 1.6)
Hyperventilation done**
No 1.0 (referent) 1.0 (referent)
Yes 1.0 (0.7– 1.4) 1.2 (0.7– 2.1)
Etiology^
Genetic 83 (18.5%) 1.0 (referent) 1.0 (referent)
Prenatal/developmental 55 (12.2%) 0.6 (0.4–0.9) 0.5 (0.3–1.02)
Postnatal symptomatic 104 (23.2%) 0.3 (0.2–0.5) 0.3 (0.1–0.5)
Unknown 207 (46.1%) 0.5 (0.4–0.7) 0.4 (0.3–0.7)
Status epilepticus
No 438 (97.6%) 1.0 (referent) 1
Yes 11 (2.4%) 0.4 (0.1–1.6)
*

accounting for the number of seizures during each of the first five years of follow up (categorized as none, one, two or more, or unknown).

**

Time–dependent variable The status of each EEG with regard to use of any activation technique (i.e., sleep, photic stimulation, hyperventilation). It is not possible to give the N for all the variables because the time dependent covariates change over time. Therefore, we provide the remaining variables that are not time dependent.

^

Genetic etiology includes epilepsy formerly classified as idiopathic (e.g. idiopathic generalized, N=67, 80.7%; idiopathic focal, N=16, 19.3%).

HR= Hazard Ratio; 95% CI= 95% Confidence Interval;

1

Factor not included in the model;