Diseases and Disorders

Alcohol Use Disorders and Neurological Functioning

Anthony Echeverria


Abstract

One of the most prevalent medical conditions in modern society is substance abuse disorder, specifically alcohol use disorder [1]. Patients who suffer from alcoholism can potentially suffer the negative psychological and physical effects of the disorder [1]. Chronic alcohol consumption is a major underlying contributor to a variety of health issues, such as cirrhosis, vitamin deficiencies, liver disease, gastrointestinal issues, and neurological conditions such as peripheral neuropathy. Peripheral neuropathy is one of the major neurological conditions that are associated with chronic alcohol consumption as it could lead to severe nerve damage [4]. The report will cover the pathology of excessive alcohol consumption as well as its association with neurological disorders such as peripheral neuropathy.

 

Alcohol Use Disorder

Alcohol use disorder, also known as alcoholism, is a disorder where an individual develops uncontrollable drinking habits and is unable to decrease their consumption [1]. When the individual begins to consume alcohol such as beer, whiskey, etc , they begin to build tolerance against the toxicity of alcohol and it’s main ingredient, ethanol [1]. As the tolerance increases, the user is left wanting to experience the same effect causing them to drink alcohol in larger doses essentially leading to addiction. The brain chemistry also tries to adapt in order to offset the effect of alcohol, a process known as neuroadaptation [1]. The user’s brain then begins to turn on them by making the user want more alcohol rather than actually liking it, potentially strengthening the effects of withdrawal and lowering the chances of successfully detoxing [1]. Due to its addictive nature, it prompts the user to crave the drug despite being

completely aware of the consequential health effects. There are many external factors that have contributed to the cause of alcohol use disorder, such as genetic predispositions, psychological dependence, social-cultural environment, and much more [1].

 

The Composition of Alcohol

Alcohol is primarily composed of an active ingredient called ethanol, a chemical compound. Ethanol is considered to be a depressant, meaning that it is a drug that reduces and damages neuron activity and decreases the rate of bodily function [1]. It reduces the neuron’s ability to properly transmit electrical signals to communicate messages, essentially causing disinhibition and interferes with basic human functions such as speaking [1]. Alcohol also slows down sympathetic nervous system activity, which is critical in arousal and energy levels, leading to a decline in heart rate, digestion processes, liver functioning, and it also suppresses the production of epinephrine and norepinephrine [1]. 

Another significant impediment that chronic ethanol consumption causes is memory loss and cognitive decline. Ethanol is a major contributor to the decrease of the volume of the hippocampus and the increase of nerve cell death in alcoholics [2]. As alcohol, or ethanol, interferes with the hippocampus, neural activity decreases along with electrical impulses and alcohol eventually binds with neurotransmitter receptors [1].  Due to the decrease of neurons being fired and communicated, the magnitude of memory disruptions greatly increases and impedes the individual’s cognitive ability to make perceptions [1]. It may also lead to blackouts and users begin to fail to recall any information during their period of intoxication that leads up to the blackout [1]. 

 

The Correlation Between Alcohol and Certain Deficiencies

One of the crucial roles that alcohol takes on in the brain is the role of an agonist. An agonist is a molecule that greatly increases the production of neurotransmitters. In some cases, alcohol can function similarly to a certain neurotransmitter, such as gamma-aminobutyric acid, and binds to the receptors and imitates the effects of it [1]. Gamma-aminobutyric acid, also known as GABA, is a major inhibitory neurotransmitter that can potentially give individuals a rewarding feeling and lower levels of anxiety-ridden feelings [1]. However, once the alcohol wears off and the effects cease, levels of GABA drastically decrease eventually leading to a deficiency. An undersupply of GABA can lead to seizures, tremors, anxiety, and sleep disruptions [1].

Alcohol not only greatly impacts the levels of GABA, but also has an effect on thiamine levels in the brain and body systems. Individuals with alcohol use disorder tend to have a poor nutritional diet that is severely lacking in many vitamins and nutrients that are necessary for cognitive function and nerve health such as thiamine, or Vitamin B1 [3]. Alcohol also suppresses the absorption of thiamine in the digestive system. The lack of thiamine can contribute to the development of oxidative stress, which is the imbalance between free radicals and antioxidants [3]. A few health effects of chronic oxidative stress are memory loss, depression, and anxiety. Severe thiamine deficiency can cause damage to cells and nerves as it takes on an important role in the neural formation and cellular structure [3]. Thiamine deficiency can essentially cause impairments in the central nervous system which can be linked to another neurological disorder called peripheral neuropathy [3].

 

The Pathology of Neuropathy

Excessive alcohol consumption can lead to peripheral neuropathy, leaving peripheral nerves damaged and interfering with neurological and communication processes [1]. There are various classifications of peripheral neuropathy as mononeuropathy, which involves damage to a single nerve. In contrast, multiple mononeuropathy involves damage to multiple nerves in different areas, and polyneuropathy involves damage to most of the nerves [4]. 

Alcohol has the ability to reach the brain within the first five minutes of consumption [1]. It directly attacks the nervous system, specifically myelin sheaths, and starts the process of demyelination [5]. The protective covering of the nerve begins to deteriorate and eventually slows down the transmission of neural and electrical impulses [5]. Aside from the myelin sheath, alcohol also damages the branching tips of neurons, which are called dendrite fibers. This makes it difficult for dendrites to receive information and transmit impulses to the cell body, causing cognitive impairment [5].

Sensory nerves are also one of the many neurological structures that are affected greatly by alcohol consumption. The constant attacks that alcohol inflicts on sensory nerves are one of the main contributors to peripheral neuropathy [6]. The peripheral nervous system consists of two types of neurons: sensory and motor neurons [6]. Sensory neurons have the responsibility of sending out information from tissues and sensory nerve receptors to the brain and spinal cord in order for the messages to be processed [6]. Motor neurons have the responsibility of carrying information from the brain and spinal cord to muscles and glands [6]. The functioning of the peripheral nervous system ceases when ethanol enters the system [1]. As mentioned earlier, alcohol is a depressant, and once it’s consumed, it begins to inhibit neuronal processing and functioning, eventually slowing down body processes [1].

 

Symptoms

Those who are diagnosed with peripheral neuropathy experience a range of symptoms that vary by individual and gradually worsen over time. One of the most prevalent indications of neuropathy begins with numbness, tingling, and a burning sensation in the upper and lower extremities after a case of binge drinking [7]. The neurological disorder is also a cause of significant sharp, stabbing pain in many regions of the body. Others have also reported that they have gradually lost coordination of their hand movement as well. Chronic alcohol consumption also inflicts damage on motor nerves. [7]. Due to the motor nerve damage, muscle contractions, weakness, cramping, occasional periods of paralysis, and muscle atrophy have all been experienced with peripheral neuropathy [6].  

With the combination of alcohol use disorder and neuropathy, there are also a few cases that involve hair loss and thinning of the hair. Due to the decrease of neural activity caused by ethanol, it makes it harder for the brain to absorb nutrients that are vital for hair growth. Aside from the neurological effects of peripheral neuropathy, some patients have also reported an increase in incontinence, dysphagia, fainting, lightheadedness, digestion issues, arrhythmia, dyspnea, and anhidrosis [7].

 

Prognosis and Treatment

While peripheral neuropathy may not be fatal, it can carry adverse complications with the individual that cannot be cured. As the peripheral nerves are constantly being degenerated, the individual may experience a loss of sensation, body functions, and neurological dysfunctionality [4]. However, there are a few treatment options that can lessen the pain and effects of neuropathy. Since neuropathy targets muscular functions, it’s recommended that patients do physical therapy, aerobic exercise, and strength training to improve muscle health [7]. 

On a pharmacological level, there are certain medications that are prescribed to patients to accommodate certain physiological needs. Patients who have depression symptoms as a result of alcohol use disorder may be prescribed highly controlled tricyclic antidepressants, i.e. Norpramin [7]. As mentioned before, alcohol may cease levels of GABA once it wears off, potentially increasing the risk of seizures, and some patients may be prescribed anticonvulsants, i.e. Acetazolamide, gabapentin [7]. Due to the magnitude of pain that neuropathy inflicts, most patients are given over-the-counter drugs or prescribed analgesic drugs, including lidocaine, oxycodone, and morphine [7].

Besides oral medications, personal initiatives can be taken, and individuals can make significant lifestyle choices to improve their quality of life. One of the most beneficial steps that can be taken in reducing the effects of peripheral neuropathy is to sign up for a rehabilitation program that can provide the necessary support for users to quit alcohol. Individuals who suffer from alcohol use disorder and neuropathy are highly suggested that they improve their dietary plan to fill their nutritional needs such as a vitamin B1, or thiamine, deficiency [3]. In some cases, it is also beneficial to lose weight and exercise regularly as well in order for the brain and body to recuperate after the prolonged period of alcoholism.

 

Conclusion

Alcohol use disorder is an arduous journey that involves great emotional distress on the user and the family. It may lead to even more physical and mental anguish for the user if they develop neurological disorders, such as neuropathy. It is critical for all individuals to be aware of the correlation between alcoholism and peripheral nerve damage in order to prevent their family members from falling into the pit of alcohol use disorder. With scientific and therapeutic endeavors expanding each day, society is getting closer to the perfection of alcoholism treatment and the reduction of substance abuse disorders.


References


  1. Lautieri, Amanda. (16/06/2020). Short and Long Term Mental Effects of Alcohol. American Addiction Centers. https://americanaddictioncenters.org/alcoholism-treatment/mental-effects. Retrieved: 15/08/2020.

  2. Visualizing Hippocampal Damage from Alcohol. The Alcohol Pharmacology Education Partnership. https://sites.duke.edu/apep/module-3-alcohol-cell-suicide-and-the-adolescent-brain/content-visualizing-hippocampal-damage-from-alcohol/. Retrieved: 19/08/2020.

  3. Corcoran, Cait. How Vitamin B1 Helps Your Metabolism and Nerves. One Green Planet. https://www.onegreenplanet.org/natural-health/vitamin-b1-helps-metabolism-nerves/. Retrieved: 25/08/2020.

  4. Understanding Peripheral Neuropathy - The Basics. WebMD. https://www.webmd.com/brain/understanding-peripheral-neuropathy-basics#1. Retrieved: 27/08/2020.

  5. Moawad, Heidi. (1/10/2019). Demyelination: What Is It and Why Does It Happen? Healthline. https://www.healthline.com/health/multiple-sclerosis/demyelination. Retrieved: 02/09/2020.

  6. The Peripheral Nervous System. National Cancer Institute. https://training.seer.cancer.gov/anatomy/nervous/organization/pns.html. Retrieved: 11/09/2020.

  7. Peripheral Neuropathy. Columbia University Department of Neurology. https://www.columbianeurology.org/neurology/staywell/peripheral-neuropathy. Retrieved: 23/09/2020.

  8. Neuropathy. Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/14737-neuropathy. Retrieved: 24/09/2020.

Anthony Echeverria

Anthony Echeverria


Anthony Echeverria is currently a senior from Southern California. He has a profound interest in the intersection between substance-abuse disorders and neurology. In school, he is part of his school's Medical Pathway Program and participates in his school's HOSA club. He also loves volunteering with hospice care patients at local nursing homes. In his free time, Anthony enjoys going to Los Angeles and loves to visit new places, restaurants, and much more.