How Does Alcohol Consumption Affect The Central Nervous System?

How does alcohol affect the body? – Alcohol is a central nervous system depressant. This means that it is a drug that slows down brain activity. It can change your mood, behavior, and self-control. It can cause problems with memory and thinking clearly.

How does alcohol consumption affect the central nervous system quizlet?

Alcohol is a depressant which slows down all the major functions of the central nervous system. It can cause slurred speech, mental confusion, blurry vision, and poor muscle control. If enough alcohol is consumed, it severely impairs the functioning of the respiratory system, and can even casue breathing to stop.

How does alcohol depress the central nervous system?

How does alcohol affect the brain and central nervous system – Alcohol is known as a psychotropic depressant because it slows down your central nervous system. When you drink alcohol, a complex process occurs in your brain that inhibits neurons by impacting their ability to transmit impulses.

At the same time, alcohol also increases the production of neurotransmitters that make you feel good. As a review, your body’s nervous system plays an important role in communication between the brain and the rest of the body to control every day functions such as seeing, talking, walking and breathing.

The nervous system is made up of the central nervous system and the peripheral nervous system. The central nervous system contains neurons in the brain and spinal cord, while the peripheral nervous system contains neurons in the head and body. The job of the peripheral nervous system is to carry messages from the brain to other parts of the body.

Neurons use both electrical and chemical signals to communicate information – chemical signals are needed because electrical signals alone can’t transfer from one neuron to another. The chemical signals, known as neurotransmitters, help bind neuron receptors. Neurotransmitters help carry these messages to neurons.

As alcohol enters the body, it binds to certain neurotransmitters that are responsible for inhibiting communication and causes them to slow down, resulting in decreased brain activity. This lag in processing slows down your alertness, balance, movement and ability to think.

How does alcohol work as a central nervous system quizlet?

Alcohol is a drug that can become addictive. It is one of the most widely used Central Nervous System depressants. Alcohol acts as a depressant on the central nervous system ( slows it down) when it (alcohol) is absorbed into the bloodstream.

How does alcohol act as a depressant on the central nervous system quizlet?

Explain how Alcohol acts as a Depressant on the Central Nervous System (CNS)? Alcohol slows down your central nervous system, which clouds your judgment and slows down your brain activity.

What are the neurological effects of alcohol?

Abstract This article reviews the different acute and chronic neurological manifestations of excessive alcohol consumption that affect the central or peripheral nervous system. Several mechanisms can be implicated depending on the disorder, ranging from nutritional factors, alcohol-related toxicity, metabolic changes and immune-mediated mechanisms.

• Recognition and early treatment of these manifestations is essential given their association with high morbidity and significantly increased mortality.
• Eywords: Excessive alcohol consumption Neurological complications Hepatic encephalopathy Resumen En este artículo se revisan las distintas manifestaciones neurológicas del consumo excesivo de alcohol, que pueden ser agudas o crónicas y afectar al sistema nervioso central o periférico.

El mecanismo por el cual se producen varía de un grupo de trastornos a otro. Destacan factores nutricionales, efectos tóxicos del alcohol, factores metabólicos e incluso inmunológicos. Estas manifestaciones pueden conllevar una gran morbilidad y un aumento significativo de la mortalidad, por lo que es importante reconocerlas y tratarlas precozmente.

Palabras clave: Alcoholismo Complicaciones neurológicas Encefalopatía hepática Full Text Introduction Excessive or harmful alcohol consumption is defined as the consumption of 40–60 g/day of alcohol in women or 60–100 g/day in men. Although it does not meet the criteria for alcohol dependency, this level of consumption can produce clinical changes.

Alcohol use disorder appears when excessive alcohol consumption causes the deterioration of an individual’s social, work and family relationships.1 The World Health Organization’s report on excessive alcohol consumption identified more than 60 alcohol-related diseases.2 The systemic effects of alcohol include changes in the digestive tract and the liver, the heart and vascular system, the skeletal and muscular systems, nutritional status, the immune, endocrine and haematological systems, and in the central and peripheral nervous systems.

Several alcohol-related neurological complications have been described ( Table 1 ), and pathogenesis varies greatly among the different disorder groups, although one of the most frequent causes is nutritional deficiency. Alcohol can produce alcoholic liver disease that can be accompanied by a wide variety of neurological manifestations, including hepatic encephalopathy (HE).

In this article, we will examine the different neurological manifestations of excessive alcohol consumption, the neurological alterations most frequently found in alcoholic liver disease—such as HE—and the best diagnostic approach in clinical practice.

• Central nervous system involvement Acute complications Acute intoxication The symptoms of alcohol intoxication are the result of the inhibitory effect of alcohol on the nerve cells of the brain and spinal cord.
• Some of the immediate effects of acute alcohol ingestion—such as loquacity, loss of social inhibition, and aggressiveness—appear to be due to the inhibition of certain subcortical structures (perhaps the midbrain reticular formation) that modulate the activity of the cerebral cortex.3 However, as more alcohol is consumed, this inhibitory action extends to cortical and other brain stem and spinal neurons, and can cause decreased alertness and coma with respiratory failure.

Some susceptible individuals may experience amnesic lacunae and seizures after relatively mild alcohol intoxication.4 The severity of symptoms of acute alcohol intoxication are related to blood alcohol levels 5 ( Table 2 ). These levels should be taken merely as a guide, and will vary between individuals according to sex, habitual consumption, and genetic and metabolic factors.

• Acute alcohol intoxication should be treated with supportive measures and monitoring of the individual’s level of consciousness.
• Alcoholic coma, with its associated respiratory depression, is a medical emergency that requires appropriate life support measures.
• Alcohol withdrawal syndrome Alcohol withdrawal syndrome, or abstinence syndrome, is the clinical manifestation of abruptly terminating or substantially reducing intake in patients who have developed tolerance and dependence.

Alcohol acts basically through 2 specific neuronal receptors. On the one hand, it regulates the neurotransmitter gamma-aminobutyric acid type A receptor that inhibits neuronal excitability, which explains its sedative and hypnotic effects. On the other hand, alcohol increases glutamate N-methyl- d -aspartate receptor expression, which in turn increases glutamate activity and causes hyperexcitation.

Chronic alcohol consumption induces neuroadaptive changes (tolerance), increases glutamate N-methyl- d -aspartate receptor expression, and desensitises the response and the expression of gamma-aminobutyric receptors.6 The manifestations of withdrawal syndrome (a wide range of severe symptoms, ranging from distal hand tremor, anxiety, insomnia and visual hallucinations to psychomotor agitation, autonomic hyperactivity, seizures or coma) appear to be mediated by an increase in excitatory neurotransmitters at the expense of inhibitory neurotransmitters.

Symptoms typically onset 6–24 h after interruption or reduction of alcohol consumption. The most serious form, which usually appears 72 h after withdrawal, is delirium tremens, characterised by disorientation, agitation and visual hallucinations, accompanied by autonomic signs such as hyperventilation, tachycardia and diaphoresis.

It can also be accompanied by metabolic and electrolyte alterations, such as hypomagnesaemia. The mortality rate is 5–15%, mainly due to metabolic, cardiovascular and infectious complications.7 According to the European Association for the Study of the Liver, the treatment of choice in patients with acute withdrawal syndrome and alcoholic liver disease is benzodiazepines, 8 since they reduce the risk of epileptic seizures.

Long-acting benzodiazepines, such as diazepam, are used, and the dose should be tapered over time. However, in elderly patients, in patients with hepatic failure, or when excessive sedation must be avoided, the lowest possible dose of short- or intermediate-acting benzodiazepines, such as lorazepam, is recommended.

• In the case of hallucinations and agitation that do not respond to benzodiazepines, haloperidol may be added, although it should only be used in combination with benzodiazepines, because administration of antipsychotics alone may increase the risk of seizures.
• Other drugs, such as alpha-2 agonists (clonidine and dexmedetomidine) and beta-blockers, can be used as adjuvant treatments to control autonomic hyperactivity.

Studies in other drugs, such as carbamazepine, gabapentin and topiramate, have so far yielded promising results.9 Wernicke’s encephalopathy Wernicke’s encephalopathy (WE) and Korsakoff syndrome, which were originally described as separate entities, are now considered the acute and chronic stages, respectively, of Wernicke–Korsakoff syndrome.

The real prevalence of WE cannot be accurately estimated, although different studies have observed typical WE lesions in 0.2–2.8% of the autopsies performed in the general population compared with a prevalence of 12.5% in autopsies performed on alcoholics.10 WE is caused by a vitamin B1 (thiamine) deficiency, which plays a key role in carbohydrate metabolism as an essential coenzyme in the Krebs cycle and the pentose phosphate pathway (transketolase, α-ketoglutarate dehydrogenase, pyruvate dehydrogenase, etc.).

Since these enzymes regulate energy metabolism in the brain, thiamine deficiency can cause brain damage, mainly in regions with greater metabolic demand, such as the paraventricular region of the thalamus and hypothalamus, the mammillary bodies, the periaqueductal grey, the floor of the fourth ventricle, and the cerebellar vermis.

Thiamine is found in both animal and plant foods. It is absorbed by the duodenum, and bodily reserves can be depleted in 2–3 weeks. In developed countries, more than 80% of cases of WE occur in the context of malnutrition associated with alcohol consumption. However, studies have shown that WE in alcoholics can involve mechanisms other than malnutrition, such as impaired gastrointestinal absorption of thiamine and a reduced capacity to store and metabolise the vitamin in the liver.11 Other clinical situations that lead to thiamine deficiency should also be borne in mind.

These generally involve poor intestinal absorption (gastrointestinal surgery, hyperemesis gravidarum) or an increase in body requirement (systemic diseases).12 From the clinical point of view, WE is characterised by the classic triad of oculomotor disturbance, ataxia and confusion, although the complete triad occurs only in 16% of patients.13 Ocular alterations are complex, and consist mainly of a combination of alterations such as, for example, horizontal or vertical nystagmus, unilateral or bilateral oculomotor paresis, or conjugate gaze palsy.

Ataxia mainly affects the trunk by altering gait and balance; limb ataxia and dysarthria are less common. Confusion or encephalopathic symptoms, meanwhile, develop within days or weeks and are characterised by profound disorientation, inability to concentrate, apathy, indifference, inattention, drowsiness and coma.

Other signs and symptoms are hypothermia resulting from posterior hypothalamic involvement, tachycardia or postural hypotension due to autonomic nervous system dysfunction, or polyneuropathy due to multiple vitamin deficiency.12 Diagnosis is mainly clinical.

Some additional tests can help confirm or rule out other suspicions, but should never delay the start of treatment. A thiamine blood test will show thiamine serum levels and transketolase enzyme activity in peripheral blood. This test, however, usually takes time and is of little practical use since normal ranges do not rule out a diagnosis of WE.

As far as brain imaging tests are concerned, the most useful complementary test for confirming diagnosis is magnetic resonance imaging (MRI). The most distinctive lesion is reversible cytotoxic oedema, visualised in T2, FLAIR and DWI sequences in the periventricular region and diencephalon ( Fig.1 ).

Furthermore, mammalian body atrophy, which is usually present in patients with chronic lesions, can start to be detected within the first week after onset of the disease.14 WE is a medical emergency because it is potentially reversible and delayed treatment or no treatment at all can cause serious sequelae and even death.

Treatment consists of urgent thiamine replacement. Thiamine therapy has been evaluated in a single randomised double-blind study in 107 patients, in which the efficacy of different intramuscular doses (5, 20, 50, 100 and 200 mg) of thiamine daily for 2 days was compared.

• Response, defined as improved neuropsychological test score, was evaluated on the third day after treatment.
• The authors concluded that the 200 mg dose was superior to the other dosages.15 Although there is no clear consensus on the ideal thiamine dose, pharmacokinetic studies have shown the half-life of thiamine to be around 96 min, so 2 or 3 daily doses are considered appropriate.16 Given the higher incidence of adverse effects in intramuscular administration (high volume and painful administration), intravenous infusion of thiamine diluted in 100 ml of physiological saline or 5% dextrose over 30 min is recommended.

According to evidence from published series and the recommendations of the European Federation of Neurological Societies, the administration of between 100 and 200 mg of intravenous thiamine is considered adequate in non-alcoholic patients, while alcoholic patients require doses of up to 500 mg 3 times daily.10 Other recommendations are a speedy return to a normal diet and continuous treatment until clinical improvement is observed.

According to the literature, when untreated or insufficiently treated, WE-induced brain damage can lead to death in 20% of cases or to the chronic form of WE (Korsakoff syndrome) in 80% of cases.17 Chronic complications Korsakoff syndrome Korsakoff syndrome, which is mainly caused by malnutrition associated with chronic alcoholism, usually emerges in the aftermath of WE, although it can sometimes appear in patients with no history of WE, or with sub-acute, undiagnosed episodes.

However, it can also be a symptom of malnutrition due to other causes or a symptom of diseases involving ischaemic, neoplastic or other injury to the medial and inferomedial thalamic regions in the temporal lobes.18 From a clinical point of view, it is characterised by memory impairment that is out of proportion to other cognitive functions in an awake, attentive and responsive patient.

• Important manifestations are learning deficits and memory loss, affecting both anterograde and retrograde events.
• Recent memory is usually more affected than remote memory, and the creation of false memories, or confabulation, in speech that can even be induced by questions about the patient’s recent activities is characteristic of this syndrome.

Other cognitive functions, such as concentration, spatial organisation, visual or verbal abstraction, may also be affected, and patients are usually apathetic and lacking in initiative, spontaneity and self-criticism.19 Korsakoff syndrome is often thought to be untreatable; however, after thiamine administration, only 25% show no recovery, 25% experience discrete improvement, 25% significant improvement, and in 25% memory is completely recovered.20 Marchiafava–Bignami disease Marchiafava–Bignami disease was first described in 1903 in Italian alcoholic wine drinkers, and since then it has been observed in other nationalities in association with abuse of any alcoholic beverage.

1. It affects chronic alcoholics almost exclusively, although cases have occasionally been described in non-alcoholics with malnutrition.21 It is a rare entity that is characterised by progressive demyelination and necrosis of the central part of the corpus callosum.
2. On brain imaging studies, it manifests as a well defined area of demyelination in the body of the corpus callosum, which can then extend to various regions of the subcortical white matter.

The aetiology is unknown and widely debated, with some experts suggesting the existence of a toxic factor, not yet identified, which is present in some alcoholic beverages as the culprit. However, given the low prevalence of this entity in alcoholics, and the fact that it has also been described in some non-alcoholics, it probably has an unidentified nutritional, metabolic or enzymatic aetiology.22 The clinical characteristics of this disease vary, and there is no well-defined clinical syndrome.

Most patients present progressive dementia, usually subacute at onset, with predominance of apractic or aphasic disorders, oppositional hypertonia, dysarthria, frontal release reflexes and, sometimes, hemiparesis or signs of interhemispheric disconnection. Some patients also present decreased alertness and seizures.

The clinical course is variable; some patients will become comatose and die, others can survive several years with dementia, while in others partial recovery is possible.23 The diagnosis is difficult because of the wide spectrum of symptoms. Diagnosis was hitherto based on post-mortem studies, but today a history of alcoholism together with clinical manifestation and, above all, brain imaging studies, specifically MRI, are essential to confirm diagnosis.

Typical lesions seen on MRI are demyelination, swelling and necrosis of the corpus callosum, with varying degrees of subcortical white matter involvement.24 Given its uncertain aetiology, there is no specific treatment for Marchiafava–Bignami disease, although abstinence and vitamin supplements are recommended.

Good response to high doses of corticosteroids has also been reported in some studies.25 Alcohol-related dementia The term alcohol-related dementia is used to describe a form of dementia attributable to the direct effects of chronic alcohol consumption on the brain.

Studies have shown that consumption of 140 g or more of alcohol per day for a prolonged period of time can produce moderate cognitive alterations.26 However, alcohol-related dementia has never been accurately defined from a clinical or pathological perspective, and the diagnosis of this entity has sparked considerable controversy in recent years.

Furthermore, the interaction between nutritional deficiencies, consumption of other substances, psychiatric comorbidity and repeated head injuries in chronic alcoholic patients raise doubts about the existence of alcohol-related dementia per se. Some authors, therefore, prefer to use the term “alcohol-related brain damage” to describe both the aetiology and symptoms of the widely differing alcohol-related cognitive disorders presented in these patients.

Neuronal damage or depletion, from a physiopathological perspective, is believed to be related to glutamate neurotoxicity, oxidative stress and diminished neurogenesis, triggered by chronic alcohol abuse.27 Post-mortem anatomopathological studies of patients diagnosed with alcohol-related dementia often show nonspecific findings, such as predominantly frontal cerebral atrophy, typical Wernicke–Korsakoff syndrome lesions, communicating hydrocephalus, Alzheimer’s disease, or traumatic injuries of variable severity.28 From a clinical point of view, it is characterised by an insidious onset with stepwise progression of symptoms that overlap with other neurodegenerative dementias.

In the early stages, neuropsychological studies usually reveal frontal-subcortical cognitive impairment, with slowing of mental processes, attention deficit, changes in immediate or short-term memory, decline in visual spatial skills, and decline in executive functions, such as planning and organisation.29 Alcohol-related cerebellar degeneration Alcohol-related cerebellar degeneration is a common complication that affects up to 25% of alcoholics, and is one of the most frequent causes of acquired ataxia in adults.30 The pathogenesis of this entity is complex and not entirely clear, although a synergistic mechanism involving both the toxic effect of alcohol and the consequences of vitamin B1 deficiency may be involved.

Recent studies have shown the presence of anti-tissue transglutaminase 2 antibodies in chronic alcoholics, which raises the possibility of alcohol-induced hypersensitivity to gluten.31 According to the hypothesis put forward by some authors to explain this phenomenon, increased gut permeability caused by alcohol-induced intestinal mucosa lesions found in alcoholic patients could increase exposure of the immune system to pathogenic antigens (including gliadin peptides).

Then, blood–brain barrier impairment induced by chronic alcohol consumption would, by as yet unknown mechanisms, allow the passage of these antibodies to the brain, thus causing cerebellar degeneration similar to gluten-induced cerebellar ataxia.32 In fact, one study has shown a higher prevalence of anti-gliadin antibodies in patients with alcohol-induced cerebellar degeneration compared to the general population (44% vs 12%).33 From a clinical perspective, cerebellar degeneration is characterised by trunk ataxia with wide-based gait, instability and variable degrees of lower limb dysmetria.

Dysmetria in the upper limbs, dysarthria or oculomotor disturbance are less common. In most cases, cerebellar degeneration evolves over a period of several weeks or months and persists for years. Both anatomopathological and neuroimaging studies show degeneration of all the neurocellular elements of the cerebellar cortex, and particularly Purkinje cells in the anterior and superior surface of the vermis.34 Cerebellar atrophy is easily observed on CT and brain MRI scans ( Fig.2 ).

No specific treatment has been defined, although administration of vitamin supplements and abstinence from alcohol are recommended. Peripheral nervous system involvement Acute compressive neuropathy Excessive alcohol consumption is traditionally associated with ‘Saturday night palsy’, caused by compression of the radial nerve against the humerus for several hours.

• It usually occurs when the individual falls asleep with their arm hanging over the armrest of a chair, or being compressed by the weight of the body.
• Clinically, it is characterised by an inability to perform dorsiflexion of the wrist and extension of the fingers.
• Neurophysiological studies using electromyography is useful both for diagnosis and prognosis, although the condition is self-limiting and most patients recover within 3–6 months.35 Chronic alcoholic polyneuropathy Chronic polyneuropathy is the most common complication in alcoholic patients.36 Recently, strong evidence has come to light to show alcoholic polyneuropathy to be the result of a multifactorial process primarily mediated by the toxic effect of alcohol and modulated by other factors, such as genetic predisposition, thiamine deficiency, malnutrition and other systemic diseases.37 This is a predominantly axonal, sensorimotor polyneuropathy with distal, symmetric features.

The onset of symptoms is insidious and symmetric, predominantly sensory, in the form of dysesthesia, burning sensation and burning pain on the soles of the feet that later develops into cramp in the calves and the hands. Motor symptoms usually manifest later, and are characterised by muscle weakness and atrophy, especially in the distal muscles of the upper or lower limbs.

1. Vegetative vascular and skin defects (sweaty, atrophic, glossy, almost hairless skin) with associated dysautonomia are also typical.
2. The treatment consists of a balanced diet with vitamin supplements, rehabilitation and alcohol abstinence.
3. However, recovery is slow and often incomplete.
4. Patients presenting with neuropathic pain can be treated with drugs such as gabapentin or amitriptyline.

Disulfiram neuropathy Disulfiram, a drug used to facilitate alcohol abstinence, has very occasionally been associated with peripheral neuropathy. The physiopathological mechanism behind this is unknown, but it manifests as an axonal sensorimotor, dose-dependent polyneuropathy that onsets a few weeks or months after the start of disulfiram treatment.

1. Clinically, it is characterised by distal paresthesias in a stocking-glove distribution together with predominantly distal muscle weakness and distal areflexia.
2. Prognosis will depend on severity and the degree of axonal loss, although it is usually reversible after suspension of disulfiram therapy.38 Muscle involvement Acute or chronic alcoholic myopathy Alcohol can damage skeletal muscles by altering calcium channels or the integrity of the muscle fibre membrane or sarcolemma.

Clinically, alcoholic myopathy can be characterised by acute myalgia, rhabdomyolysis and elevated creatine kinase (CK). In severe cases, it can lead to acute kidney failure and myoglobinuria. The chronic form presents as muscle atrophy, usually proximal, which frequently coexists with neuroperipheral alterations, such as chronic alcoholic polyneuropathy.

1. Diagnosis is performed with neurophysiological tests (electromyography) and histopathological study of muscle biopsy.
2. In some cases, skeletal myopathy is accompanied by dilated cardiomyopathy.
3. Treatment is based on alcohol abstinence, physiotherapy and a balanced diet.
4. Prognosis is cautious, since some patients experience an improvement in clinical weakness, but others do not recover muscle strength or mass.39 Hepatic encephalopathy Hepatic encephalopathy (HE) is a common, serious complication of liver cirrhosis and an indicator of poor prognosis in these patients.

It is a complex syndrome involving neurological and psychiatric manifestations, and occurs in patients with advanced liver disease and portosystemic shunting.40 Symptoms fluctuate over time and vary greatly, ranging from tremor and dysarthria to hepatic coma, and include (a) altered level of consciousness that can progress from mild confusion to coma; (b) neuropsychiatric symptoms, such as behavioural changes, mental slowness, reversal of the sleep–wake cycle, or psychomotor agitation, and (c) neuromuscular symptoms, such as flapping.

• The West Haven criteria stratifies HE into 4 grades, from mild to most severe ( Table 3 ).
• Because the clinical manifestations of HE are non-specific and can be observed in other diseases or metabolic disorders, diagnosis is made on the basis of complementary tests that can reasonably exclude other potential causes.

Diagnosis of WE in patients with chronic alcoholism is challenging, since the differential diagnosis is extensive. Clinically, the diagnosis of WE can be difficult because, as explained previously, the classic triad is often absent. The presence of alterations in ocular motility, nystagmus and ataxia should raise suspicion of WE, while the presence of flapping or pyramidal syndrome is suggestive of HE.

Clinical findings suggestive of alcohol withdrawal are anxiety, tachycardia, visual hallucinations and postural tremor. Differential diagnosis between HE and Marchiafava–Bignami disease does not generally present any difficulty, since the latter is clinically characterised by the presence of dementia and spasticity.

Brain neuroimaging using computed tomography (CT) or MRI makes it possible to rule out structural alterations, such as space-occupying lesions, subdural haematomas or ischaemic/haemorrhagic strokes, which can be suspected when neurological focal signs are observed in the examination.

1. These imaging studies can also rule out viral or autoimmune encephalitis that can clinically overlap HE.
2. A typical MRI finding in HE is hyperintense basal ganglia on T1-weighted images, especially in the globus pallidus.
3. This is related to manganese deposits caused by portosystemic shunts, and could explain the existence of parkinsonian signs in these patients.41 An electroencephalogram, a neurophysiological test that shows the electrical activity of the brain, can rule out a non-convulsive status epilepticus or findings typical of a post-critical state.

However, HE produces alterations in brain activity that are shown on the electroencephalogram as slow frequency, high amplitude waves and three-phase waves—findings that can also be found in other metabolic comas.42 Finally, the study of cerebrospinal fluid will rule out meningitis or bacterial or viral meningoencephalitis, which should be suspected when fever and meningeal signs are present.

• Conclusions Chronic alcohol consumption can produce numerous neurological manifestations.
• The most common are polyneuropathy, cerebellar degeneration and dementia, and the most serious are WE, Korsakoff syndrome and Marchiafava–Bignami disease.
• All these are associated with significant morbidity and mortality, and therefore must be correctly diagnosed and treated in order to avoid irreversible complications.

They are caused by vitamin deficiencies, the direct toxic effects of alcohol, immune alterations and unknown mechanisms, among others. In addition, the differential diagnosis of HE can be difficult due to its similarity with alcohol-related neurological disorders.

• Conflicts of interest The authors declare that they have no conflicts of interest.
• Acknowledgements We would like to thank the Institute of Diagnostic Imaging (IDI), Magnetic Resonance Unit, Hospital Germans Trias i Pujol (Badalona, Barcelona, Spain), and particularly Fidel Núñez.
• References Diagnostic and statistical manual of mental disorders, 5th ed, DSM-5.

American Psychiatric Association, (2013), WHO Collaborative Project on Identification and Management of Alcohol-Related Problems in Primary Health Care. Report on phase IV: development of country-wide strategies for implementing early identification and brief intervention in primary health care.L.

Vonghia, L. Leggio, A. Ferruli, M. Bertini, G. Gasbarrini, G. Addolorato, Alcoholism Treatment Study Group. Acute alcohol intoxication. Eur J Intern Med, 19 (2008), pp.561-567 K. Welch. Neurological complications of alcohol and misuse of drugs. Pract Neurol, 11 (2011), pp.206-219 L. Vonghia, L. Leggio, A. Ferruli, M.

Bertini, G. Gasbarrini, G. Addolorato. Acute alcohol intoxication. Eur J Intern Med, 19 (2008), pp.561-567 H. Becker, P. Mulholland. Neurochemical mechanisms of alcohol withdrawal. Handb Clin Neurol, 125 (2014), pp.133-156 M. Schuckit. Recognition and management of withdrawal delirium (delirium tremens).

N Engl J Med, 371 (2014), pp.2109-2113 European Association for the Study of the Liver. EASL clinical practical guidelines: management of alcoholic liver disease. J Hepatol, 57 (2012), pp.399-420 A. Mirijiello, C. D’Angelo, A. Ferrulli, G. Vassallo, M. Antonelli, F. Caputo, et al, Identification and management of alcohol withdrawal syndrome.

Drugs, 75 (2015), pp.353-365 R. Galvin, G. Brathen, A. Ivashynka, M. Hillbom, R. Tanasescu, M.A. Leone. EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. Eur J Neurol, 17 (2010), pp.1408-1418 A.D. Thomson. Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of Wernicke–Korsakoff syndrome.

• Alcohol Suppl, 35 (2000), 7 G. Sechi, A. Serra.
• Wernicke’s encephalopathy: new clinical settings and recent advances in diagnosis and management.
• Lancet Neurol, 6 (2008), pp.442-455 J.
• Gascón-Bayarri.
• Encefalopatía de Wernicke en pacientes no alcohólicos: una serie de 8 casos.
• Neurología, 26 (2011), pp.540 G.

Zuccoli, M. Galluci, J. Capellades, L. Regnicolo, B. Tumiati, T. Cabada, et al, Wernicke encephalopathy: MR findings at clinical presentation in twenty-six alcoholic and nonalcoholic patients. Am J Neurorradiol, 28 (2007), pp.1328-1331 M.L. Ambrose, S.C. Bowden, G.

• Whelan. Thiamin treatment and working memory function of alcohol-dependent people: preliminary findings.
• Alcohol Clin Exp Res, 25 (2001), pp.112-116 C.
• Tallaksen, A. Sande, T.
• Bahmer, H. Bell, J. Karlsen.
• Inetics of thiamin and thiamin phosphate esters in human blood, plasma and urine after 50 mg intravenously or orally.

Eur J Clin Pharmacol, 44 (1993), pp.73-78 A.D. Thomson, E.J. Marshall. The natural history and pathophysiology of Wernicke’s encephalopathy and Korsakoff’s psychosis. Alcohol, 41 (2006), pp.151 M.D. Kopelman. The Korsakoff syndrome. Br J Psychiatry, 166 (1995), pp.154-174 M.D.

• Opelman, A.
• Thomson, I.
• Guerrini, E. Marshall.
• The Korsakoff syndrome: clinical aspects, psychology and treatment.
• Alcohol Alcoholism, 44 (2009), pp.148-154 M.
• Victor, R.D.
• Adams, G.H. Collins.
• The Wernicke–Korsakoff syndrome and related neurologic disorders due to alcoholism and malnutrition.2nd ed., FA Davis, (1989), J.

Noble, L. Weimer. Neurologic complications of alcoholism. Continuum (Minneap Minn), 20 (2014), pp.624-641 J. Navarro, S. Noriega. Enfermedad de Machiafava–Bignami. Rev Neurol, 28 (1999), pp.519-523 A. Heinrich, U. Runge, A. Khaw. Clinicoradiologic subtypes of Marchiafava–Bignami disease.

• J Neurol, 251 (2004), pp.1050-1059 M.
• Hillbom, P.
• Saloheimo, S.
• Fujioka, Z.
• Wszolek, S.
• Juleva, M. Leone.
• Diagnosis and management of Machiafava–Bignami disease: a review of CT/MRI confirmed cases.
• J Neurol Neurosurg Psychiatry, 85 (2014), pp.168-173 A.
• Gerlach, E. Oehm, J.
• Wattchow, S.
• Ziyeh, F.X.
• Glocker, T. Els.

Use of high-dose cortisone in a patient with Machiafava–Bignami disease. J Neurol, 260 (2003), pp.758-760 O.A. Parsons, S.J. Nixon. Cognitive functioning in sober social drinkers: a review of the research since 1986. J Stud Alcohol, 59 (1998), pp.180-190 R.P.

• Vetreno, J.M.
• Hall, L.M. Savage.
• Alcohol-related amnesia and dementia: animal models have revealed the contributions of different etiological factors on neuropathology, neurochemical dysfunction and cognitive impairment.
• Neurobiol Learn Mem, 96 (2011), pp.596-608 N.
• Ridley, B.
• Draper, A. Withall.
• Alcohol-related dementia: an update of the evidence.

Alzheimers Res Ther, (2013), pp.5 C.A. Munro, J. Saxton, M.A. Butters. Alcohol dementia: cortical or subcortical dementia. Arch Clin Neuropsychol, 16 (2001), pp.523-533 T. Klockgether. Sporadic ataxia with adult onset: classification and diagnostic criteria.

1. Lancet Neurol, 9 (2010), pp.94-104 H.
2. Oivisto, J.
3. Hietala, P.
4. Anttila, O. Niemela.
5. Co-occurrence of IgA antibodies against ethanol metabolites and tissue transglutaminase in alcohol consumers: correlation with proinflammatory cytokines and markers of fibrogenesis.
6. Dig Dis Sci, 53 (2008), pp.500-505 P.
7. Sianmugaraiah, N.

Hoggard, S. Currie, D. Aeschlimann, P. Aeschlimann, D. Gleeson, et al, Alcohol-related cerebellar degeneration: not all down to toxicity?. Cerebellum Ataxias, 3 (2016), pp.17 S. Currie, N. Hoggard, M. Clark, D. Sanders, I. Wilknson, P. Griffiths, et al, Alcohol induces sensitization to gluten in genetically susceptible individuals: a case control study.

PLoS One, 8 (2013), pp. e77638 O. Yokota, K. Tsuchiva, S. Terada, K. Oshima, H. Ishizu, M. Matsushita, et al, Frequency and clinicopathological characteristics of alcoholic cerebellar degeneration in Japan: a cross-sectional study of 1509 postmortems. Acta Neuropathol, 11 (2006), pp.43-51 C. McIntosh, J. Chick.

Alcohol and the nervous system. J Neurol Neurosurg Psychiatry, 75 (2004), pp. iii16-iii21 G. Vittadini, M. Buonocore, G. Colli, M. Terzi, R. Fonte, G. Biscaldi. Alcoholic polyneuropathy: a clinical and epidemiological study. Alcohol Alcohol, 36 (2001), pp.393-400 M.

1. Mellion, H.
2. Gilchrist, S.
3. De la Monte.
4. Alcohol-related peripheral neuropathy: nutritional, toxic or both.
5. Muscle Nerve, 43 (2011), pp.309-316 A. Thu, R. Rison, S. Beydoun.
6. Disulfiram neuropathy: two case reports.
7. J Med Case Rep, 19 (2016), pp.72 V.R.
8. Preedy, J.
9. Adachi, Y. Ueno, S. Ahmed, D.
10. Mantle, N.
11. Mullati, et al,

Alcoholic skeletal muscle myopathy: definitions, features, contribution of neuropathy, impact and diagnosis. Eur J Neurol, 8 (2001), pp.677-687 Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the European Association for the study of the liver and the American Association for the study of liver diseases.

• J Hepatol, 61 (2014), pp.642-659 A.
• Rovira, J.
• Alonso, J. Córdoba.
• MRI imaging findings in hepatic encephalopathy.
• Am J Neuroradiol, 39 (2008), pp.1612-1621 P.
• Amlodio, A. Gatta.
• Neurophysiological investigation of hepatic encephalopathy.
• Metab Brain Dis, 20 (2005), pp.369-379 Please cite this article as: Planas-Ballvé A, Grau-López L, Morillas RM, Planas R.

Manifestaciones neurológicas del alcoholismo. Gastroenterol Hepatol.2017;40:709–717. Copyright © 2017. Elsevier España, S.L.U. All rights reserved

What receptor does alcohol use in the CNS?

The Effects of Alcohol on the Brain – Scientists used to think of alcohol as a membrane disruptor with a generalized effect all over the brain, as the small molecule can freely diffuse across the blood–brain barrier. They now know that there are particular cells in the brain that alcohol targets by binding certain hydrophobic pockets on their surface receptors.

1. The gamma-aminobutyric acid (GABA) receptor is one of these.
2. Alcohol is an indirect GABA agonist,” says Koob.
3. GABA is the major inhibitory neurotransmitter in the brain, and GABA-like drugs are used to suppress spasms.
4. Alcohol is believed to mimic GABA’s effect in the brain, binding to GABA receptors and inhibiting neuronal signaling.

Alcohol also inhibits the major excitatory neurotransmitter, glutamate, particularly at the N-methyl-d-aspartate (NMDA) glutamate receptor. And it releases other inhibitors, such as dopamine and serotonin. Consumption of even small amounts of alcohol increases the amount of dopamine in the nucleus accumbens area of the brain—one of the so-called “reward centers.” However, it is most likely that the GABA and glutamate receptors in some of the reward centers of the basal forebrain—particularly the nucleus accumbens and the amygdala—create a system of positive reinforcement.

1. In fact, multiple neurotransmitters in various parts of the brain combine to make the consumption of small doses of alcohol enjoyable.
2. Alcohol tends to activate the whole reward system,” says Koob, who is particularly interested in the effects of alcohol in the amygdala.
3. The neurochemical effects of alcohol cause a range of short-term effects—from a mild buzz to slow reaction times, which make drunk driving so dangerous.

In the long term, these effects are also the basis for two of the defining characteristics of addiction: tolerance and dependence.

Does alcohol act on the central nervous system as a stimulant?

Alcohol As a Stimulant – While alcohol is technically a depressant, when it’s first ingested, it acts very much like a stimulant. Alcohol triggers the brain to release dopamine, a neurotransmitter that provides energy, stimulation, and good feelings. Dopamine also elevates mood, and it increases the ability to feel pleasure and motivation.

• In addition, alcohol has stimulating effects on the rest of the body in low doses.
• Heart rate and blood pressure increase, as do alertness, confidence, and energy levels.
• These stimulant effects, though, aren’t the same for everyone.
• Body chemistry, weight, age, and sex can all affect alcohol metabolism, as can the extent to which a person has built up a tolerance to alcohol.

As the blood alcohol concentration (BAC) approaches 0.05 milligrams per liter, its stimulant effects increase. However, by the time a person reaches a BAC of 0.08 mg/l (the legal level of intoxication in most regions), the depressant effects of alcohol have pushed the stimulant effects aside.

Can quitting alcohol cure anxiety?

Quitting Alcohol Cured My Anxiety – Science suggests finding alternative ways to relax and socialize away from alcohol. For example, heading out for brunch instead of dinner, an exercise class, or spending time outside. These types of activities can significantly lower symptoms and increase happy hormones in the body.

Feeling nervous or irritable Having a sense of imminent danger or panic Noticing an increase in heart rate Hyperventilating or sweating or shaking Feeling constantly tired Experiencing an erratic sleep pattern Being unable to concentrate

Also, signs of AUD include:

Experiencing a strong urge or need to drink Experiencing blackouts Drinking too to experience relaxation during highly stressful moments Alcohol interfering with work or home life Skipping activities that were enjoyable drink Being in dangerous situations under the influence Experiencing withdrawal symptoms that include anxiety

It’s true. Quitting alcohol, over time, can alleviate intense episodes of anxiety. It can also reduce the possibility of long-term anxiety disorders. Treatment options are available to address dual diagnosis care.

What are four effects alcohol has on the nervous system?

Health Effects of Alcohol Abuse – Not only can alcohol abuse cause serious problems over a period of time in the nervous system, such as memory loss, altered speech, dulled hearing, and impaired vision, but it also impacts brain and liver tissues, destroys brain cells, and depresses the nervous system in general.

Many causes of liver cancers are alcohol abuse. The effects of alcohol on the nervous system are numerous, but the main ones can be divided into three categories: acute intoxication, chronic usage, and withdrawal. Alcohol also acts as a depressant on the brain and other nerve tissue, which means that it slows down the functioning of nerve cells.

Despite this, many people think that alcohol is an anti-depressant because it has a numbing effect on the brain and is used as a “pick-me-up” experience because, initially, when people begin to drink, it causes them to become more animated and less reserved.

But the opposite occurs as they continue to drink, and more alcohol enters their brain and nervous system. The major nervous system is greatly affected by alcohol consumption and has been known to decrease control, both in gross and fine motor movements. Individuals have been known to lean on something while trying to walk, have labored breathing, and their handwriting is completely unintelligible.

They also experience changes in their brain, such as increased confusion, inability to process logic, and personality changes. Most intoxicated individuals are either extremely irritable or very maudlin, with many emotional tears. Seizures are also possible.

Potential long-term consequences of the condition include chronic pain and moderate to severe physical disabilities. Older adults are prone to the natural reduction of postural reflexes and the nerve cell degeneration that occurs with advanced age. Therefore, they may be more at risk for clinical problems associated with neuropathy, such as frequent falls and loss of balance.

In a study including more than two thousand alcohol users who have attempted to stop using it or have reported that they want to stop:

1 in 10 reported nerve damage1 in 11 reported seizures1 in 7 reported a weakened immune system

The only way to avoid the negative effects of alcohol on the nervous system is to stay sober.

What are 3 effects of alcohol on the brain and body?

ALCOHOL’S DAMAGING EFFECTS ON THE BRAIN Difficulty walking, blurred vision, slurred speech, slowed reaction times, impaired memory: Clearly, alcohol affects the brain. Some of these impairments are detectable after only one or two drinks and quickly resolve when drinking stops.

On the other hand, a person who drinks heavily over a long period of time may have brain deficits that persist well after he or she achieves sobriety. Exactly how alcohol affects the brain and the likelihood of reversing the impact of heavy drinking on the brain remain hot topics in alcohol research today.

We do know that heavy drinking may have extensive and far–reaching effects on the brain, ranging from simple “slips” in memory to permanent and debilitating conditions that require lifetime custodial care. And even moderate drinking leads to short–term impairment, as shown by extensive research on the impact of drinking on driving.

how much and how often a person drinks; the age at which he or she first began drinking, and how long he or she has been drinking; the person’s age, level of education, gender, genetic background, and family history of alcoholism; whether he or she is at risk as a result of prenatal alcohol exposure; and his or her general health status.

This Alcohol Alert reviews some common disorders associated with alcohol–related brain damage and the people at greatest risk for impairment. It looks at traditional as well as emerging therapies for the treatment and prevention of alcohol–related disorders and includes a brief look at the high–tech tools that are helping scientists to better understand the effects of alcohol on the brain.

What are 3 ways alcohol can affect your brain or body?

Image Diffusion tensor imaging (DTI) of fiber tracks in the brain of a 58-year-old man with alcohol use disorder. DTI maps white-matter pathways in a living brain. Image courtesy of Drs. Adolf Pfefferbaum and Edith V. Sullivan. Alcohol interferes with the brain’s communication pathways and can affect the way the brain looks and works.

What part of the brain does alcohol depress?

Cerebral cortex as it works with information from a person’s senses. In the cerebral cortex, alcohol can a ect thought processes, leading to potentially poor judgment. Alcohol depresses inhibition, leading one to become more talkative and more confident.

Does alcohol depress the sympathetic nervous system?

Among its many physiological effects, alcohol robustly activates the sympathetic nervous system. Our laboratory has reported that simulated binge alcohol consumption increases muscle sympathetic nerve activity (MSNA) (5), a finding consistent with several other alcohol and microneurographic studies (6–12).