Intracerebral hemorrhage increases risk of dementia onset

By Scott Baltic

NEW YORK (Reuters Health) - There is a substantial risk of incident dementia following spontaneous intracerebral hemorrhage (ICH), a risk that is higher in patients with lobar ICH than non-lobar ICH, according to a new report by French and U.S. researchers.

Their prospective observational cohort study is the first to show these findings and to use a "prospective and rigorous design" to focus on dementia, the researchers note in an article online April 28 in Lancet Neurology.

The study also shows for the first time that disseminated superficial siderosis is a strong risk factor for new-onset dementia following ICH. This suggests that "underlying cerebral amyloid angiopathy might contribute to the risk of dementia after intracerebral hemorrhage," the researchers say.

In a cohort of 218 ICH survivors (54% men, median age 67.5), the researchers found that the cumulative incidence rate of new-onset dementia reached 28.3% by four years after ICH. The incidence rates for lobar and non-lobar ICH at four years were 35.1% and 20.2%, respectively.

In the 63 patients with new-onset dementia, the median time between ICH and diagnosis of dementia was 12 months.

Multivariable analysis showed that disseminated superficial siderosis, increasing cortical atrophy score, a higher number of cerebral microbleeds, and older age were risk factors for new-onset dementia.

Their results, according to the researchers, show that the risk factors for new-onset dementia after ICH are already present when ICH occurs, suggesting that a process of ongoing cognitive impairment takes place, rather than dementia induced by ICH itself.

They concluded that prevention of ICH might therefore not be adequate to prevent dementia, "which underlines the need to promote closer collaboration between memory centers and stroke units to identify patients at high risk of developing dementia."

"Appropriate preventive strategies should focus on preventing the accumulation of so-called 'silent' hemorrhagic lesions such as brain microbleeds or superficial siderosis," corresponding author Dr. Charlotte Cordonnier of Lille University Hospital, Lille, France, told Reuters Health by email. Such measures would include blood pressure management and avoiding antithrombotic agents, especially when used as primary prevention, she added.

"Prevention is also information," Dr. Cordonnier said, for both patients and physicians. "When everybody is aware of a potential complication and works as a team to fight this possible cognitive decline, then the level of care is always better." One example she suggested was planning regular cognitive follow-ups so as to identify cognitive decline and its nature early on.

Finally, Dr. Cordonnier said, these findings suggest that "the link between neurodegenerative lesions and hemorrhagic lesions may be stronger than with ischemic lesions."

"The sample size is relatively small, but large enough to suggest that lobar location of hemorrhage and the presence of specific radiological features such as cortical atrophy and superficial siderosis are associates of new dementia, suggesting that risk may relate in part to the presence of underlying cerebral amyloid angiopathy," Dr. Sarah Pendlebury, of John Radcliffe Hospital, Oxford University, Oxford, England, told Reuters Health by email.

The study, she continued, adds to the literature on post-stroke dementia, which includes relatively few studies specifically on hemorrhagic stroke, particularly with reference to location of bleeding and other radiological features, and in which pre-stroke dementia has been excluded.

"The findings will facilitate identification of patients at high dementia risk after intracerebral hemorrhage," Dr. Pendlebury concluded.

The trial was funded by two French government ministries and a French regional research consortium. The investigators reported no personal funding in connection with this research.

SOURCE: http://bit.ly/1SOz15J

Lancet Neurol 2016.

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