Children who suffer emotional neglect may have a higher risk of chronic cerebral infarction as adults, an observational study found.
Overall, adults who had moderately high levels of self-reported physical or emotional adversity in childhood were more than twice as likely to have chronic cerebral infarctions as those who reported moderately low levels of childhood adversity, according to Robert S. Wilson, PhD, of Rush University Medical Center in Chicago, and colleagues.
However, emotional neglect was the only specific form of childhood adversity that was significantly associated with pathologically proven cerebral infarction in an analysis adjusted for age at death, sex, and education (OR 1.23, 95% CI 1.14 to 1.33, P<0.001), researchers reported in the Sept. 19 issue of Neurology.
"This was unexpected, given the interrelatedness of different forms of childhood maltreatment," researchers said.
The other subgroups of childhood adversity that Wilson and colleagues examined were parental intimidation, parental violence, family turmoil, and financial need.
Although it is not clear why childhood emotional neglect is associated with adult cerebral infarcts, researchers suggested that such neglect could lead to poor self-care. But in every adjusted model, the risk associated with emotional neglect remained, they pointed out.
When they adjusted for vascular risk factors such as diabetes, smoking, and physical activity, for example, the odds ratio of having chronic cerebral infarction when one had high levels of emotional neglect was 1.25 (95% CI 1.15 to 1.35).
And the risk remained when researchers further adjusted for systolic and diastolic blood pressure and body mass index (OR 1.23, 95% CI 1.14 to 1.33), as well as when adjusted for both childhood and adult socioeconomic status (OR 1.23, 95% CI 1.14 to 1.34).
Wilson and colleagues also noted that poor self-care might manifest as arterial disease, but they found that the risk of cerebral infarction was not associated with postmortem analysis of atherosclerosis or arteriolosclerosis.
The study included 1,040 people from the Rush Memory and Aging Project, an ongoing longitudinal clinical-pathologic cohort study that began in 1997 and included people 55 and older.
During a mean of 3.5 years of follow-up, 257 people died. The current analysis is based on 192 of them who had a complete neuropathologic examination.
About two-thirds of the cohort were women and the mean age at death was 88.5.
Participants reported emotional and physical trauma that occurred during the first 18 years of their lives. Adversity scores ranged from 0 to 31, with a mean score of 8.3.
Overall, higher levels of adversity in childhood increased the risk of of cerebral infarction in adulthood (OR 1.10, 95% CI 1.05 to 1.15).
Those with a moderately high adversity score (12) had a 2.2 times higher likelihood of cerebral infarction than those with a moderately low score (3.5).
In the subgroup of emotional neglect, those with moderately high levels of adversity (score of 6) had a 2.83-fold increased risk of infarction compared with those with moderately low levels of adversity (score of 1).
Emotional neglect was significantly associated with various gross and microscopic subtypes of infarction, including gross subcortical and gross cortical, gross subcortical lacunar and gross subcortical nonlacunar, and microscopic cortical. It was not associated with microscopic subcortical.
"The results add to a growing body of evidence suggesting a link between traumatic childhood experiences and physical illness in adulthood," wrote Kevin M. Barrett, MD, MSc, and James F. Meschia, MD, from the Mayo Clinic in Jacksonville, Fla., in an accompanying editorial.
Barrett and Meschia noted some evidence linking shortened telomeres on chromosomes with childhood trauma. Truncated telomeres are believed to age more quickly than telomeres of appropriate length.
"It is interesting to speculate ... that for those who have survived childhood trauma, it might be possible to mitigate the adverse biological effects of that trauma by preserving telomere length," they said.
They added that some preliminary evidence indicates that physical activity and statins could positively effect telomere length.
Wilson and colleagues noted that their study had several limitations including the retrospective nature of childhood adversity, the potential underestimation of microscopic infarcts as they were examined in only one hemisphere, and the incomplete data on cause of death.
The study received funding from the National Institutes of Health.
Wilson reported no conflicts of interest, as did all but one co-author, who reported relationships with Schering-Plough, Medivation, Gerson Lehman Group, and Danone.
The editorialists reported they had no relevant disclosures.