Multiconstruct

I put together some facts on the topic for a radio interview on KFRU. It went pretty well, the hosts (simon and renee) were engaging and funny, and we talked for about 45 minutes and got out a lot of good information. The four pages of notes made me feel a lot more comfortable and i think it came across in the interview. A couple of things really struck me. One was the idea of neurogenesis. I had always read that you had all the brain cells you would ever have and alcohol kills them. In fact it says that on the info web site but i am going to edit that out because its not true. What really happens is the brain makes more brain cells all the time unless you are chronically drinking large amounts of alcohol. The good news is after a week of abstinence brain cell production booms. The fact that hit on the radio was brain shrinkage. Renee Hulshoff seemed aghast to learn your brain shrinks as you age and she referenced it on another story i caught on the drive back to the salt mines. I think I will do my next education group on the same topic, my as well learn the rap. On a practical note i will be promoting thiamine,. exercise and antidepressants for chronic alcoholics.

(lifted from NIAAA’s alcohol alert)

Equal numbers of men and women reported experiencing blackouts, despite the fact that the men drank significantly more often and more heavily than the women. This outcome suggests that regardless of the amount of alcohol consumption, females—a group infrequently studied in the literature on blackouts—are at greater risk than males for experiencing blackouts.

Using imaging with computerized tomography, two studies compared brain shrinkage, a common indicator of brain damage, in alcoholic men and women and reported that male and female alcoholics both showed significantly greater brain shrinkage than control subjects. Studies also showed that both men and women have similar learning and memory problems as a result of heavy drinking.

Wernicke–Korsakoff Syndrome

Up to 80 percent of alcoholics, however, have a deficiency in thiamine, and some of these people will go on to develop serious brain disorders such as Wernicke–Korsakoff syndrome (WKS)). WKS is a disease that consists of two separate syndromes, a short–lived and severe condition called Wernicke’s encephalopathy and a long–lasting and debilitating condition known as Korsakoff’s psychosis.

The symptoms of Wernicke’s encephalopathy include mental confusion, paralysis of the nerves that move the eyes (i.e., oculomotor disturbances), and difficulty with muscle coordination. For example, patients with Wernicke’s encephalopathy may be too confused to find their way out of a room or may not even be able to walk. Many Wernicke’s encephalopathy patients, however, do not exhibit all three of these signs and symptoms, and clinicians working with alcoholics must be aware that this disorder may be present even if the patient shows only one or two of them. In fact, studies performed after death indicate that many cases of thiamine deficiency–related encephalopathy may not be diagnosed in life because not all the “classic” signs and symptoms were present or recognized.

Approximately 80 to 90 percent of alcoholics with Wernicke’s encephalopathy also develop Korsakoff’s psychosis, a chronic and debilitating syndrome characterized by persistent learning and memory problems. Patients with Korsakoff’s psychosis are forgetful and quickly frustrated and have difficulty with walking and coordination). Although these patients have problems remembering old information (i.e., retrograde amnesia), it is their difficulty in “laying down” new information (i.e., anterograde amnesia) that is the most striking. For example, these patients can discuss in detail an event in their lives, but an hour later might not remember ever having the conversation

Prolonged liver dysfunction, such as liver cirrhosis resulting from excessive alcohol consumption, can harm the brain, leading to a serious and potentially fatal brain disorder known as hepatic encephalopathy ammonia and manganese, have a role in the development of hepatic encephalopathy. Alcohol–damaged liver cells allow excess amounts of these harmful byproducts to enter the brain, thus harming brain cells.

Hepatic encephalopathy can cause changes in sleep patterns, mood, and personality; psychiatric conditions such as anxiety and depression; severe cognitive effects such as shortened attention span; and problems with coordination such as a flapping or shaking of the hands (called asterixis). In the most serious cases, patients may slip into a coma (i.e., hepatic coma), which can be fatal.

More facts from: www.bloodalcohol.info

Alcohol can affect several parts of the brain, but in general, alcohol contracts brain tissue and depresses the central nervous system. Excessive drinking over a prolonged period of time can cause serious problems with cognition and memory.

When alcohol reaches the brain, it interferes with communication between nerve cells, by interacting with the receptors on some cells. The alcohol suppresses excitatory nerve pathway activity and increases inhibitory nerve pathway activity. Among other actions, alcohol enhances the effects of the inhibitory neurotransmitter GABA. Enhancing an inhibitor has the effect of making a person sluggish. Also, alcohol weakens the excitatory neurotransmitter glutamine, which enhances the sluggishness even farther.

The cerebral cortex processes information from your senses, processes thoughts, initiates the majority of voluntary muscle movements and has some control over lower-order brain centers. In the cerebral cortex, alcohol can:

• Affect thought processes, leading to potentially poor judgement.
• Depresses inhibition, leading one to become more talkative and more confident.
• Blunts the senses and increases the threshold for pain.

The limbic system, which consists of the hippocampus and septal area of the brain, controls memory and emotions. The affect of alcohol on this sytem is that the person may experience some memory loss and may have exaggerated states of emotion.

The cerebellum coordinates muscle movement. The cerebral cortex initiates the muscular movement by sending a signal through the medulla and spinal cord to the muscles. As the nerve signals pass through the medulla, they are influenced by nerve impulses from the cerebellum, which controls the fine movements, including those necessary for balance. When alcohol affects the cerebellum, muscle movements become uncoordinated.

The hypothalamus controls and influences many automatic functions of the brain (through the medulla), and coordinates hormonal release (through the pituitary gland). Alcohol depresses nerve centers in the hypothalamus that control sexual arousal and performance. With increased alcohol consumption, sexual desire increases – but sexual performance declines.

By inhibiting the pituitary secretion of anti-diuretic hormone (ADH), alcohol also affects urine excretion. ADH acts on the kidney to reabsorb water, so when it is inhibitted, ADH levels drop, the kidneys don’t reabsorb as much water and the kidneys produce more urine.

The medulla (brain stem) influences or controls body functions that occur automatically, such as your heart rate, temperature and breathing. When alcohol affects the medulla, a person will start to feel sleepy. Increased consumption can lead to unconscious. Needless to say, alcohol’s effect on the medulla can be fatal if it is excessive.

More stuff:

Detoxified alcoholics often have visuospatial and visuoperceptual deficits, characterized by difficulties completing tasks such as putting pieces of a puzzle together or map reading. A new study has found that, even with prolonged sobriety, alcoholics show deficits in visuoperception and frontal executive functioning of the brain.

Furthermore, alcoholics utilize a more complex higher-order cognitive system, frontal executive functions, to perform the same tasks as individuals without a history of alcoholism. Results are published in the November 2004 issue of Alcoholism: Clinical & Experimental Research.

The UNC findings, from research at UNC’s Bowles Center for Alcohol Studies, were based on an animal model of chronic alcohol dependence, in which adult rats were given alcohol over four days in amounts that produced alcohol dependency. The study is in the Nov. 3 issue of the Journal of Neuroscience.

In 2002, Dr. Fulton T. Crews, Bowles Center director, and Bowles Center research associate Dr. Kim Nixon were the first to report that alcohol, during intoxication, has a detrimental effect on the formation of new neurons in the adult rat hippocampus. This brain region is important for learning and memory – in animals and humans – and is linked to psychiatric disorders, particularly depression.

“When used in excess, alcohol damages brain structure and function. Alcoholics have impairments in the ability to reason, plan or remember,” said Crews, also professor of pharmacology and psychiatry in UNC’s School of Medicine. “A variety of psychological tests show alcoholics have a difficulty in ability to understand negative consequences.”

In the new study, senior co-author Crews and co-author Nixon found inhibition of neurogenesis, or brain cell development, during alcohol dependency, followed by a pronounced increase in new neuron formation in the hippocampus within four-to-five weeks of abstinence. This included a twofold burst in brain cell proliferation at day seven of abstinence.

“And when they stop drinking, you can show in a period of weeks, months, years, the brain grows back, there’s a return of metabolic activity, and cognitive tests show a return of function,” Crews said.

“Pharmacological agents such as antidepressants and behaviors such as running, increased physical activity and learning experiences apparently help regulate the process of neurogenesis,” he added. “Our research suggests they could be considered in the treatment of chronic alcohol dependency.”

In their report, Nixon and Crews also said that their findings for the first time provide a neuronal regeneration mechanism that may underlie the return of normal cognitive function and brain volume associated with recovery from addiction during abstinence from alcohol.

“This is really the first biological measure of a major change in neuronal structure consistent with changes that are known to occur when individuals are able to stop drinking,” said Crews.

Number of Brain Cells Not Fixed

For decades, neuroscientists believed the number of new cells, or neurons, in the adult brain was fixed early in life. Adaptive processes such as learning, memory and mood were thought tied to changes in synapses, connections between neurons.

More recently, studies have shown that the adult human brain is capable of producing new brain cells throughout life, a neurogenesis resulting in formation of hundreds of thousands of new neurons each month. “Prior to our work, everyone merely assumed that glia, the supporting cells of the brain, regenerated or that existing brain cells altered their connections,” said Nixon. “We have shown a burst in new cell birth that may be part of the brain’s recovery after the cessation of alcohol.”

Chronic alcoholism, a disease affecting more than 8 percent of the adult U.S. population, or more than 17 million Americans, produces cognitive impairments and decreased brain volumes, both of which are partially reversed during abstinence.