Alcoholism and Ataxia
Ataxia is the medical term for loss of the normal coordination required to perform voluntary body movements. There are multiple forms of this condition and, depending upon personal circumstances, any given individual can develop ataxia-related problems that alter things such as normal speech, hand-eye coordination, or the ability to perform any delicate or intricate hand motions. Long-term alcoholics frequently develop a form of ataxia called cerebellar ataxia, which alters normal function in a part of the brain called the cerebellum. Some alcoholics acquire permanent forms of this condition that continue even when drinking stops; others eventually recover significantly after an extended period of time.
People with ataxia have nerve damage that affects some portion of the central nervous system (brain and spinal cord). This system acts as the control center for nerve-related (neurological) functions throughout the body, including involuntary functions that continue without any conscious input and voluntary functions that are completely or partially under conscious control. Doctors use the term ataxia to describe distinct medical syndromes or disorders, as well as ataxic symptoms of larger syndromes or disorders. There are dozens of distinct ataxias, including disorders called ataxia telangiectasia, spinocerebellar ataxia type 5, and Friedrich’s ataxia. Some of these conditions stem from genetic inheritance, while others develop for non-hereditary reasons.
Cerebellar Ataxia Basics
Cerebellar ataxia is a symptom, not a distinct disorder. In addition to chronic alcoholism, potential underlying causes of this symptom include viral infections, multiple sclerosis, use of certain medications, pesticide exposure, strokes, and traumatic head injuries that produce bleeding in the brain. The cerebellum plays an essential role in human health by acting as the center for integration of sensory information, muscle movement, and overall body coordination. Disruption of this center can produce results that include a reduced ability to accurately gauge the passing of time, a general state of muscular looseness or floppiness, loss of the coordination that permits effective use of the muscles and joints, a reduced ability to control various aspects of movement in the extremities and eyes, and a complete loss of the ability to make rapidly shifting body movements.
Alcohol acts as a poison inside the human body and damages a wide variety of organs and structures, including the liver, pancreas, heart, bones, and brain. Since alcoholics habitually consume excessive amounts of alcohol, they commonly experience forms of this damage that get progressively worse over time. Inside the brain, alcohol directly damages the cerebellum, and long-term drinkers develop particularly severe cerebellar damage. In addition, alcohol damages connective fibers in the brain known collectively as white matter, which link the cerebellum to the rest of the brain, as well as to the rest of the central nervous system. In addition to coordination problems caused by injury to these structures, alcoholics typically experience marked decreases in their levels of a brain chemical called dopamine, which helps regulate normal function in a separate brain structure, called the striatum, which contributes to voluntary muscle control.
Drunkenness produces a loss of balance and body coordination that strongly mimics the effects of cerebellar ataxia. In alcoholics, these postural changes move from a temporary status to an ongoing status, and produce characteristic alterations in both balance and gait (which is the term used to describe the collection of coordinated limb and foot movements required for walking).
Long-Term Prospects for Improvement
A number of modern medical studies have been conducted in order to assess the long-term effects of alcoholism-related cerebellar ataxia in alcoholics who stop drinking. According to the results of a study published in 2013 in Alcoholism: Clinical and Experimental Research, abstinent alcoholics may experience relatively minor improvements in their ataxia-related symptoms within a roughly 10-week period following the onset of sobriety. However, after this 10-week period ends, there is typically no additional improvement for at least a year. The authors of a separate study, published in 2011 in Alcoholism: Clinical and Experimental Research, concluded that recovering alcoholics who abstain from drinking for at least 18 months frequently experience both balance and gait improvements that remain during periods when their eyes are open. However, in the absence of visual input, these improvements diminish significantly.
Female alcoholics commonly sustain more ataxia-related brain damage than male alcoholics. Despite this fact, the prospects for recovery from ataxia during long-term abstinence are apparently roughly equal for both genders. Even with the benefit of long-term abstinence, some recovering alcoholics experience only limited or minimal improvements in their ataxia-related symptoms.