Alcohol Withdrawal

Briefly discuss the biological effect of alcohol on the brain; include in your answer the biological effects of intoxication.

  • Alcohol acts as an inhibitory neurotransmitter, which interferes with the flow of signals from one nerve to the other, slowing down brain activity culminating into augmentation, confusion and memory loss. Consequently, rapid mood swings as well as behavioral and emotional instability are experienced (Miller, 2006).
  • Intoxication alcohol acts on the Central Nervous system and culminates into the affecting of sensory and emotional function, learning and memory ability as well as judgment.
  • Alcohol intoxication leads to the slow deterioration of the brain through a conventional progression from intellectual functioning, motor and sensory control disturbances and finally ends with affecting heart and breathing action.
  • In essence, intoxications results to disinhibition of the typical social functioning abilities, disorientation, uncoordinated movement, slurred speech, coma, Progressive lethargy, euphoria and loss of memory and death due to the reduction of  signal flow in the brain.
  • Taste and smell are dulled while the ability for withstanding pain is increased substantially. Inherently, diverse parts of the brain are affected in accordance to different rates by alcohol, leading to alternating phases of stupor and restlessness.
  • Diverse brain parts are affected differently by alcohol, leading to alternating phases of stupor and restlessness. Consequently, memory loss culminates from temporary cutting of oxygen supply by alcohol (Jacques, & Jackson, 1999).
  • Another effect of alcohol encompasses learned behavior syndrome in which behaviors learned under the influence of alcohol, have to be re-learned again following the wearing off, of the alcohol influence. Additionally, the long-term effects of alcohol on the brain are inclusive of dependency, irreversible brain damage and tolerance.

 Describe the role of Vitamin B1 (Thiamine) in the brain and why vitamin B1 is commonly prescribed in alcohol misuse.

  • Thiamine is utilized in enhancing nerve health, therefore preventing Wernicke’s encephelopathy that leads to coordination problems and Korsakoff’s psychosis that affects memory on the short-term basis.
  • It stimulates the brain and the nervous system to absorb and control the correct amount of glucose needed to produce the right amount of energy for proper functioning.
  • Its enables the nerves cells in allowing displacement for the free crossing of the sodium membranes. Consequently, it increases carbohydrates metabolism into energy in the brain to enhance brain activity
  • It is in charge of transmitting certain nerve signals in the nervous system between the spinal cord and the brain
  • It is also in charge of maintaining positive mental attitudes, increasing brain energy, enhancement of learning abilities, prevention of memory loss and fighting stress (Paton, & Touquet, 2005).
  • The admission of thiamine works towards the reduction of the metabolic imbalances resulting from alcohol intoxication. Consequently, it is administered in cases of alcohol misuses to prevent the Korsakoff’s psychosis and Wernicke’s encephelopathy, which result from alcohol intoxication.
  • Alcohol causes the reduction of the amount of Thiamine in the body culminating into the building of pyruvic acid in the blood stream that reacts by causing difficulty in breathing, lack of mental alertness as well as heart damage. For this reason, the administration of thiamine for the alcohol abusers is essential.
  • The parasympathetic neural activity is affected substantially by alcohol misuse and to counter this effect, thiamine is recommended for boosting brain activity through the increase in carbohydrate metabolism for provision of energy.

Briefly outline the biological effects of alcohol withdrawal and why diazepam is useful for treating alcohol withdrawal; include in your answer the biological reasons why seizures may occur in alcohol withdrawal.

  • Alcohol withdrawal results from hyper-excitable state of the brain. It culminates into delirium tremens, seizures and excito-neurotoxicity.
  • The effects are in variance from placid anxiety and sleep disturbances to such life threatening effects as visual hallucinations, convulsions, delirium and death (Kalat, 2009).
  • Some effects depend on genetics, length of intake, previous detoxifications and age. These are inclusive of agitation, alcoholic hallucinosis, anorexia, panic attacks, catatonia, confusion, delirium tremens, depression, derealization and diaphoresis.
  • The other effects are inclusive of Diarrhea, Euphoria, Euphoria, Gastrointestinal upset, Hallucinations, Headaches, Hypertension, Hyperthermia, Insomnia, Irritability, Nausea and vomiting, Palpitations, Psychosis, Tachycardia, Tremors.
  • Diazepam is employed in the treatment of seizures, insomnia and anxiety, which are some of the effects culminating from alcohol withdrawal. This enhances its suitability for treating alcohol withdrawal (Jacques, & Jackson, 1999).
  • It contains anticonvulsant properties linked with the reduction of seizures in people affected by alcohol withdrawal. Consequently, it leads to a reduction of the depressive effects experienced from extreme cases of alcohol withdrawal.
  • Diazepam is not only used for alcohol withdrawal treatment due to its anticonvulsant properties, but it is utilized owing to its ability to be extracted from the body easily, therefore allowing for easy titration into a patient’s response system (Kalat, 2009).
  • Diazepam constantly produces desmethyldiazepam, a psychoactive metabolite that has a longer half-life reducing the chances for further medication in cases of constant alcohol withdrawal.
  • Seizures in alcohol withdraw occur due to the inflow of calcium ions through calcium channels into the brain cells. In this case, the altered activity of the calcium channels contributes largely to the seizures experienced in alcohol withdrawal.

Briefly discuss the pathophysiology of Wernicke’s encephalopathy and Korsakoff’s dementia and preventative measures that Jim may take to reduce this risk.

  • Wernicke encephalopathy encompasses the syndrome that causes confusion, short-memory impairment, ataxia and ophthalmoplegia, which is caused by inadequate intake of Thiamine that can be because of alcohol abuse (McCandless, 2008).
  • Is commences at an abrupt rate through disorders of eye movement, confusion, short-term memory loss, ataxia and confabulation. Consequently, the main effects of the syndrome encompass ophthalmoplegia, encephalopathy and ataxia.
  • If the syndrome remains for a long time without any form of treatment, it might culminate into coma, death and Korsakoff’s psychosis. In addition, it leads to neuron death due to the alteration experienced in glutamate uptake.
  • The recommended for of treatment for this syndrome is inclusive of thiamine administration through intramuscular and intravenous injection as well as the constant assessment of the metabolic conditions and central nervous system. Essentially overt encephalopathy can be precipitated by increased intake of large sugar doses. This should be followed by rehydration, administered for the restoration of blood volumes.
  • Korsakoff’s syndrome encompasses a syndrome that culminates from a deficiency of thiamine in the brain, which damages medial thalamus and cerebral atrophy.
  • The syndrome is ridden with six major symptoms that include anterograde amnesia, confabulation, and retrograde amnesia, lack of insight, apathy and insufficient content in conversation (Jacques, & Jackson, 1999).
  • The deficiency of thiamine that results to the syndrome mainly culminates from excessive alcohol intake or alcohol intoxication. In most cases, the syndrome is preceded by Wernicke encephalopathy.
  • The treatment encompasses supplementing the diet with thiamine, proper nutrition and finally hydration. This syndrome however requires full time care during its advanced stages.









Jacques, A., & Jackson, G. A. (1999). Understanding Dementia. Edinburgh, BE: Churchill Livingstone.

Kalat, J. W. (2009). Biological Psychology. Belmont, CA: Wadsworth, Cengage Learning.

McCandless, D. W. (2008). Metabolic Encephalopathy. New York, NY: Springer.

Miller, M. W. (2006). Brain Development: Normal Processes and the Effects of Alcohol and Nicotine. Oxford, UK: Oxford University Press.

Paton, A., & Touquet, R. (2005). ABC of Alcohol. Oxford, UK: Blackwell Publishing.








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