Frontal Dysfunction and Frontal Cortical Synapse Loss in Alcoholism –The Main Cause of Alcohol Dementia?

TLDR: A consistent pattern of synapse loss in the superior laminae of the frontal cortical area 10 of Brodman in heavy drinkers, not related to liver disease or possible previous mental disease, seems to be a plausible main cause of the alcoholic frontal symptomatology and alcoholic dementia.

Abstract: Alcoholics often develop personality and behavioural changes, social and personal neglect, confabulation, lack of insight, empathy and emotional control. Such symptoms would increase the risk of engagement in and exposure to acts of violence and criminal activities carrying a risk of physical damage including head trauma and violent death. This was the case in at least 4 of the studied cases. A structural basis for such frontal lobe symptoms was looked for in a forensic material of 18 alcoholics, compared with an age-matched control group with regard to liver disease, brain changes of the Wernicke-Korsakoff type and cortical, especially frontal cortical changes. The salient finding was a consistent pattern of synapse loss in the superior laminae of the frontal cortical area 10 of Brodman in heavy drinkers, not related to liver disease or possible previous mental disease. The synapse loss is more likely related to alcohol, possibly mediated through vitamin B deficiency. Brain stem lesions as a source of additional symptoms cannot be dismissed. This pattern of synapse loss in alcoholism has not been described previously. The cortical changes are closely similar to those found in frontotemporal dementia, and seem to be a plausible main cause of the alcoholic frontal symptomatology and alcoholic dementia.