A Case: A 60-year old male lobbyist got lost several times while driving in places that should have been familiar to him. His wife said he made poor financial decisions and seemed confused at times.
He used to be a “heavy drinker,” but because drinking had interfered with his work, he had stopped eight years previously. Except for mild high blood pressure, his health was good. His only medication was a prescription diuretic, and he had no history of illicit substance use. He had a normal American diet and took a multivitamin daily.
Neurobehavioral examination revealed frontal lobe brain dysfunction, with an abnormal clock drawing and other tests. His short term memory was within normal limits for his age and education. His MMSE was 27. Physical examination showed some instability walking. His muscle control in fine, precise movements was also abnormal.
Blood tests were all normal. His brain MRI showed mild atrophy in his frontal lobes and cerebellum.
His diagnosis was early alcohol-related dementia.
Alcohol-related Dementia May Appear Years After Drinking Stopped
It’s generally accepted that moderate consumption of alcohol does not increase the risk for Alzheimer’s dementia. Alcohol may even reduce the risk, although that’s not universally accepted. On the other hand, the damage was done by alcohol, as in the case described, may not become apparent until years after stopping alcohol use.
No one knows for sure exactly how the delayed effect comes about. At least two theories have been proposed.
Alcohol-related Brain Damage Removes Brain Reserve
Alcohol causes atrophy (shrinkage) of the brain, especially in the brain areas used for decision making and to control muscle movement (frontal lobes and cerebellum). The atrophy removes some of the brain’s reserve capacity. Over years, ordinary aging decreases brain function. In enough time, everyone who survives will lose enough function to be legitimately labeled as demented. Those who have lost brain reserve as the result of extensive brain atrophy will reach this point sooner, maybe ten to 20 to 30 years sooner. In this theory, alcohol-related dementia is early or premature aging.
Alcohol Damage May Cause a Chronic Excitatory State
Two brain systems work to maintain a calm but productive balance. The GABA system affects about half the brain cells and produces a calming, inhibitory effect. The GABA system is opposed by the glutamate system which tends to produce an energetic, excitatory effect.
Over time, heavy alcohol use damages the GABA system (it reduces the number of GABA receptors). This leaves the glutamate system less opposed, and leads to excess excitatory action, a state called excitotoxicity. Excitotoxicity causes oxidative damage, and injures brain cells, The damage may be cumulative, resulting, years later, in enough damage to produce dementia.
Alcohol-related Dementia Is Not Related to Thiamine (Vitamin B1) Deficiency
Another condition, Wernicke’s encephalopathy, is caused by thiamine deficiency. Alcoholics are at risk for Wernicke’s encephalopathy because they often have a poor diet and because alcohol interferes with the absorption of thiamine. With Wernicke’s encephalopathy, a person may stumble, be confused, and may have abnormal eye movements.
Untreated, many people with Wernicke’s encephalopathy progress on to Korsakoff’s psychosis. With this condition, a person usually has very poor memory, and may unintentionally tell unbelievable stories (confabulation). These are not intentionally in error – the person tries to explain something, and cannot discriminate reality from fantasy. Many people with Korsakoff’s Psychosis ultimately need institutional care.