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Childhood-onset epilepsy appeared to accelerate brain aging by about 10 years, a small prospective study in Finland suggested.

Over about 55 years of follow-up, people with childhood-onset epilepsy had greater rates of cognitive changes and more amyloid plaques, reported Matti Sillanpää, MD, PhD, of the University of Turku in Finland, and colleagues, at the American Epilepsy Society annual meeting, which is being held in Chicago and online.

Signs of brain aging were more advanced in people with focal than generalized epilepsy and in people with active epilepsy. No participant had dementia.

"Various aspects of cognitive and brain aging processes can be abnormal in persons with uncomplicated childhood-onset epilepsies as they enter their 60s, even for those whose epilepsy remitted many years ago," co-author Bruce Hermann, PhD, of University of Wisconsin 木瓜直播 School in Madison, told 木瓜直播.

"As some clinical and brain changes were found to be associated with health and lifestyle factors -- such as hypertension, education, and lifetime drug load -- greater attention to treatable factors earlier in life may benefit patients as they age," Hermann added.

The researchers compared 51 people with childhood-onset epilepsy with 52 matched controls without epilepsy, evaluating them in 2012 and 2017. Retention over the 5-year interval was 80% for the epilepsy group and 88% for controls, leaving 41 and 46 people in each group, respectively, in 2017.

Participants were diagnosed with childhood-onset epilepsy at about age 5, and mean age of people in the epilepsy group at follow-up was about 63. Amyloid was assessed by 11C-Pittsburgh compound B (PIB) PET.

A total of 32 people in the epilepsy group were in remission for 10 years or more; nine people had active epilepsy that persisted for decades.

Neurologic signs were significantly more common in people with childhood epilepsy not in remission (P=0.015), with cerebellar signs the most frequent abnormality (P<0.001). Neurologic signs in general (P=0.008) and cerebellar signs in particular (P=0.018) were more common in focal than in generalized epilepsy.

In 2012, 22% of people with childhood-onset epilepsy had amyloid plaques versus 7% of controls. By 2017, those percentages increased to 33% and 11%, respectively. There was no difference in the presence of amyloid plaques among people with active epilepsy compared with people in remission.

In the 5-year interval from 2012 to 2017, using a common threshold of meaningful cognitive change (z < -1.5) corrected for demographics and practice, the childhood-onset epilepsy group showed significant (P<0.05) prospective declines versus controls on measures of verbal reasoning, immediate recall, and set-shifting. People with active epilepsy showed additional significant (P<0.05) adverse declines in delayed memory and object naming, compared with controls and with people in remission.

Peripheral neuropathy occurred particularly in people with active epilepsy who had a higher lifetime phenytoin (Dilantin) load. MRI hippocampal atrophy in people with childhood-onset epilepsy was associated with arterial hypertension (P=0.017). MRI white matter abnormalities were linked with an absence of vocational education (P=0.011).

"Our results suggest it is important for those with childhood-onset epilepsy to work to achieve seizure control but it's also vital that they pay attention to risk and resilience factors for healthy brain and cognitive aging, including a healthy diet, exercise, and social activity, as well as treating high blood pressure, high cholesterol, and high blood glucose levels," Hermann said.

"We do not know yet if people with childhood-onset epilepsy who have amyloid plaques are more likely to develop Alzheimer's disease, a critical question we will be studying in the future," he added.

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