Abstract
Background: Several studies have shown that well-known cerebrovascular risk factors are associated with a higher incidence of white matter lesions (WML). The knowledge of the role of alcohol in the development of WML still is poor. The aim of this study is to investigate the prevalence of WML in younger alcohol addicts. Well-known and potential risk factors for WML were taken into account. Methods: N=100 patients aged 25-60 years (mean age 44 years) fulfilling the diagnostic criteria of alcohol dependency (ICD F10.2) were examined with 1,5 Tesla magnetic resonance imaging according to a standard protocol concerning localization and dissemination of WML. All patients were voluntary in-patients. Data concerning medical history, education, occupation, exposure to toxic substances, nutrition, smoking, laboratory values, vitamin levels, ApoE-genotype, parameters of alcohol dependency and consumption of other drugs than alcohol were collected. Results: WML could be found in 39 patients. 34 had subcortical focal WML (≤ 5 mm), 13 periventricular WML (twelve patients ≤ 5 mm, one patient 6-10 mm). 26 had exclusively subcortical WML, five had exclusively periventricular WML and eight had WML of both localizations. Significant positive associations were found to higher age, higher amount of daily alcohol consumption, lower haematocrit and lower creatine kinase. There was a trend towards more frequent malnutrition, less frequent consumption of dairy products and a lower haemoglobin level in patients with WML. Patients in the fifth decade of life had significantly more often WML and reported significantly higher levels of daily alcohol consumption. Well-known cerebrovascular risk factors were not associated with WML. Conclusion: Our data suggest that the amount and the duration of higher alcohol consumption, in combination with higher age, are possible risk factors for WML as early as from the fifth decade of life. Most of the patients had subcortical WML. These are known to be associated to cerebrovascular risk f actors rather than to higher age. Nutrition might play a role in the development of WML. Consumption of dairy products might have a protective effect. The significantly lower levels for haematocrit and creatine kinase and the trend towards lower haemoglobin levels might be the consequence of an alcohol induced diabetes insipidus. We can support the assumption that there is an association between changes in blood count and brain morphology, reported by other authors. Moreover we can support the thesis that higher alcohol consumption is a risk factor for a higher vulnerability of the cerebral white matter. We assume that higher alcohol consumption accelerates aging processes of the brain and increases the risk for preterm WML.
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