ABE is an acute state of elevated bilirubin in the central nervous system. Clinically, it encompasses a wide range of symptoms. These include lethargy, decreased feeding, hypotonia or hypertonia, a high-pitched cry, spasmodic torticollis, opisthotonus, setting sun sign, fever, seizures, and even death. If the bilirubin is not rapidly reduced, ABE quickly progresses to chronic bilirubin encepalopathy.

CBE is a chronic state of severe bilirubin-induced neurological lesions. Reduction of bilirubin in this state will not reverse the sequelae. Clinically, manifestations of CBE include:

1. movement disorders - athetoid cerebral palsy and or dystonia, 60% have severe motor disability(unable to walk).

2. auditory dysfunction - auditory neuropathy (ANSD)

3. oculomotor impairments (nystagmus, strabismus, Impaired upward or downward gaze, and/or cortical visual impairment),

4. dental enamel hypoplasia/dysplasia of the deciduous teeth,

5. Gastroesophageal reflux,

6. impaired digestive function.

Intellectual disability occur in 25% of cases. But they are often look like intellectually disabled because their severe motor handicaps.

Epilepsy occur in 20% of cases.

These impairments are associated with lesions in the basal ganglia, auditory nuclei of the brain stem, and oculomotor nuclei of the brain stem. Cortex and white matter are mildly involved. Cerebellum may be involved.

Korsakoff's syndrome is an amnestic disorder caused by thiamine deficiency usually associated prolonged ingestion of alcohol. It is rare among other people but some cases have been observed after bariatric surgeries, when deficiency was not prevented by use of nutritional supplements. This neurological disorder is caused by a lack of thiamine (vitamin B) in the brain, and is also often exacerbated by the neurotoxic effects of alcohol. When Wernicke's encephalopathy accompanies Korsakoff's psychosis the combination is called the Wernicke–Korsakoff syndrome; however, a recognized episode of Wernicke's is not always obvious. The syndrome and psychosis are named after Sergei Korsakoff, a Russian neuropsychiatrist who discovered the syndrome during the late 19th century.

Different concentrations of alcohol in the human body have different effects on the subject.

The following lists the common effects of alcohol on the body, depending on the blood alcohol concentration (BAC). However, tolerance varies considerably between individuals, as does individual response to a given dosage; the effects of alcohol differ widely between people. Hence, BAC percentages are just estimates used for illustrative purposes.

- Euphoria (BAC = 0.03% to 0.12%):

- Overall improvement in mood and possible euphoria

- Increased self-confidence

- Increased sociability

- Decreased anxiety

- Shortened attention span

- Flushed appearance

- Impaired judgment

- Impaired fine muscle coordination

- Lethargy (BAC = 0.09% to 0.25%)

- Sedation

- Impaired memory and comprehension

- Delayed reactions

- Ataxia; balance difficulty; unbalanced walk

- Blurred vision; other senses may be impaired

- Confusion (BAC = 0.18% to 0.30%)

- Profound confusion

- Impaired senses

- Analgesia

- Increased ataxia; impaired speech; staggering

- Dizziness often associated with nausea ("the spins")

- Vomiting (emesis)

- Stupor (BAC = 0.25% to 0.40%)

- Severe ataxia

- Lapses in and out of consciousness

- Unconsciousness

- Anterograde amnesia

- Vomiting (death may occur due to inhalation of vomit (pulmonary aspiration) while unconscious)

- Respiratory depression (potentially life-threatening)

- Decreased heart rate (usually results in coldness and/or numbness of the limbs)

- Urinary incontinence

- Coma (BAC = 0.35% to 0.80%)

- Unconsciousness (coma)

- Depressed reflexes (i.e., pupils do not respond appropriately to changes in light)

- Marked and life-threatening respiratory depression

- Markedly decreased heart rate

- Most deaths from alcohol poisoning are caused by dosage levels in this range.

While researchers have found that moderate alcohol consumption in older adults is associated with better cognition and well-being than abstinence, excessive alcohol consumption is associated with widespread and significant brain lesions. The effects can manifest much later—mid-life Alcohol Use Disorder has been found to correlate with increased risk of severe cognitive and memory deficits in later life. Alcohol related brain damage is not only due to the direct toxic effects of alcohol; alcohol withdrawal, nutritional deficiency, electrolyte disturbances, and liver damage are also believed to contribute to alcohol-related brain damage.

There are seven major symptoms of Korsakoff's syndrome (amnestic-confabulatory syndrome):

1. anterograde amnesia, memory loss for events after the onset of the syndrome

2. retrograde amnesia, memory loss extends back for some time before the onset of the syndrome

3. amnesia of fixation, also known as fixation amnesia (loss of immediate memory, a person being unable to remember events of the past few minutes)

4. confabulation, that is, invented memories which are then taken by the patient as true due to gaps in memory, with such gaps sometimes associated with blackouts

5. minimal content in conversation

6. lack of insight

7. apathy – the patients lose interest in things quickly, and generally appear indifferent to change.

Benon R. and LeHuché R. (1920) described the characteristic signs of Korsakoff syndrome with some additional features: confabulation (false memories), fixation amnesia, paragnosia or false recognition of places, mental excitation, euphoria, etc.

Thiamine is essential for the decarboxylation of pyruvate, and deficiency during this metabolic process is thought to cause damage to the medial thalamus and mammillary bodies of the posterior hypothalamus, as well as generalized cerebral atrophy. These brain regions are all parts of the limbic system, which is heavily involved in emotion and memory.

Korsakoff's involves neuronal loss, that is, damage to neurons; gliosis, which is a result of damage to supporting cells of the central nervous system, and hemorrhage or bleeding also occurs in mammillary bodies. Damage to the dorsomedial nucleus or anterior group of the thalamus (limbic-specific nuclei) is also associated with this disorder. Cortical dysfunction may have arisen from thiamine deficiency, alcohol neurotoxicity, and/or structural damage in the diencephalon.

Originally, it was thought that a lack of initiative and a flat affect were important characteristics of emotional presentation in sufferers. Studies have questioned this, proposing that neither is necessarily a symptom of Korsakoff's. Research suggesting that Korsakoff's patients are emotionally unimpaired has made this a controversial topic. It can be argued that apathy, which usually characterizes Korsakoff's patients, reflects a deficit of emotional "expressions", without affecting the "experience" or perception of emotion.

Korsakoff's Syndrome causes deficits in declarative memory in most patients, but leaves implicit spatial, verbal, and procedural memory functioning intact. People who have Korsakoff's syndrome have deficits in the processing of contextual information. Context memories refers to the where and when of experiences, and is an essential part of recollection. The ability to store and retrieve this information, such as spatial location or temporal order information, is impaired.

Research has also suggested that Korsakoff patients have impaired executive functions, which can lead to behavioral problems and interfere with daily activities. It is unclear, however, which executive functions are affected most. Nonetheless, IQ is usually not affected by the brain damage associated with Korsakoff's syndrome.

At first it was thought that Korsakoff's patients used confabulation to fill in memory gaps. However, it has been found that confabulation and amnesia do not necessarily co-occur. Studies have shown that there is dissociation between provoked confabulation, spontaneous confabulation (which is unprovoked), and false memories. That is, patients could be led to believe certain things had happened which actually had not, but so could people without Korsakoff’s syndrome.

Alcoholic polyneuropathy usually has a gradual onset over months or even years although axonal degeneration often begins before an individual experiences any symptoms. An early warning sign (prodrome) of the possibility of developing alcoholic polyneuropathy, specially in a chronic alcoholic, would be weight loss because this usually signifies a nutritional deficiency that can lead to the development of the disease.

The disease typically involves sensory and motor loss, as well as painful physical perceptions (paresthesias), though all sensory modalities may be involved. Symptoms that affect the sensory and motor systems seem to develop symmetrically. For example, if the right foot is affected, the left foot is affected simultaneously or soon becomes affected. In most cases, the legs are affected first, followed by the arms. The hands usually become involved when the symptoms reach above the ankle. This is called a stocking-and-glove pattern of sensory disturbances.

Polyneuropathy spans a large range of severity. Some cases are seemingly asymptomatic and may only be recognized on careful examination. The most severe cases may cause profound physical disability.

Sensory symptoms are gradually followed by motor symptoms. Motor symptoms may include muscle cramps and weakness, erectile dysfunction in men, problems urinating, constipation, and diarrhea. Individuals also may experience muscle wasting and decreased or absent deep tendon reflexes. Some people may experience frequent falls and gait unsteadiness due to ataxia. This ataxia may be caused by cerebellar degeneration, sensory ataxia, or distal muscle weakness. Over time, alcoholic polyneuropathy may also cause difficulty swallowing (dysphagia), speech impairment (disarthria), muscle spasms, and muscle atrophy.

In addition to alcoholic polyneuropathy, the individual may also show other related disorders such as Wernicke-Korsakoff syndrome and cerebellar degeneration that result from alcoholism-related nutritional disorders.

The short-term effects of alcohol (also known formally as ethanol) consumption–due to drinking beer, wine, distilled spirits or other alcoholic beverages–range from a decrease in anxiety and motor skills and euphoria at lower doses to intoxication (drunkenness), stupor, unconsciousness, anterograde amnesia (memory "blackouts"), and central nervous system depression at higher doses. Cell membranes are highly permeable to alcohol, so once alcohol is in the bloodstream it can diffuse into nearly every cell in the body.

The concentration of alcohol in blood is measured via blood alcohol content (BAC). The amount and circumstances of consumption play a large part in determining the extent of intoxication; for example, eating a heavy meal before alcohol consumption causes alcohol to absorb more slowly. The amount of alcohol consumed largely determines the extent of hangovers, although hydration also plays a role. After excessive drinking, stupor and unconsciousness can occur. Extreme levels of consumption can lead to alcohol poisoning and death (a concentration in the blood stream of 0.40% will kill half of those affected). Alcohol may also cause death indirectly, by asphyxiation from vomit.

Alcohol can greatly exacerbate sleep problems. During abstinence, residual disruptions in sleep regularity and sleep patterns are the greatest predictors of relapse.

In acute poisoning, typical neurological signs are pain, muscle weakness, numbness and tingling, and, rarely, symptoms associated with inflammation of the brain. Abdominal pain, nausea, vomiting, diarrhea, and constipation are other acute symptoms. Lead's effects on the mouth include astringency and a metallic taste. Gastrointestinal problems, such as constipation, diarrhea, poor appetite, or weight loss, are common in acute poisoning. Absorption of large amounts of lead over a short time can cause shock (insufficient fluid in the circulatory system) due to loss of water from the gastrointestinal tract. Hemolysis (the rupture of red blood cells) due to acute poisoning can cause anemia and hemoglobin in the urine. Damage to kidneys can cause changes in urination such as decreased urine output. People who survive acute poisoning often go on to display symptoms of chronic poisoning.

Chronic poisoning usually presents with symptoms affecting multiple systems, but is associated with three main types of symptoms: gastrointestinal, neuromuscular, and neurological. Central nervous system and neuromuscular symptoms usually result from intense exposure, while gastrointestinal symptoms usually result from exposure over longer periods. Signs of chronic exposure include loss of short-term memory or concentration, depression, nausea, abdominal pain, loss of coordination, and numbness and tingling in the extremities. Fatigue, problems with sleep, headaches, stupor, slurred speech, and anemia are also found in chronic lead poisoning. A "lead hue" of the skin with pallor and/or lividity is another feature. A blue line along the gum with bluish black edging to the teeth, known as a Burton line, is another indication of chronic lead poisoning. Children with chronic poisoning may refuse to play or may have hyperkinetic or aggressive behavior disorders. Visual disturbance may present with gradually progressing blurred vision as a result of central scotoma, caused by toxic optic neuritis.

Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

Cholinergic syndrome occurs in acute poisonings with OP pesticides and is directly related to levels of AChE activity. Symptoms include miosis, sweating, lacrimation, gastrointestinal symptoms, respiratory difficulties, shortness of breath, slowed heart rate, cyanosis, vomiting, diarrhea, trouble sleeping, as well as other symptoms. Along with these central effects can be seen and finally seizures, convulsions, coma, respiratory failure. If the person survives the first day of poisoning personality changes can occur, aggressive events, psychotic episodes, disturbances and deficits in memory and attention, as well as other delayed effects. When death occurs, it is most commonly due to respiratory failure from the combination of central and peripheral effects, paralysis of respiratory muscles and depression of the brain respiratory center. For people afflicted with cholinergic syndrome, atropine sulfate combined with an oxime is used to combat the effects of the acute OP poisoning. Diazepam is sometimes also administered in combination with the atropine and oximes.

The intermediate syndrome (IMS) appears in the interval between the end of the cholinergic crisis and the onset of OPIDP. Symptoms associated with IMS manifest within 24–96 hours after exposure. The exact etiology, incidence, and risk factors associated with IMS are not clearly understood, but IMS is recognized as a disorder of neuromuscular junctions. IMS occurs when a person has a prolonged and severe inhibition of AChE and has been linked to specific OP pesticides such as methylparathion, dichlorvos, and parathion. Patients present with increasing weakness of facial, neck flexor and respiratory muscles.

OPIDP occurs in a small percentage of cases, roughly two weeks after exposure, where temporary paralysis occurs. This loss of function and ataxia of peripheral nerves and spinal cord is the phenomenon of OPIDP. Once the symptoms begin with shooting pains in both legs, the symptoms continue to worsen for 3–6 months. In the most severe cases quadriplegia has been observed. Treatment only affects sensory nerves, not motor neurons which may permanently lose function. The aging and phosphorylation of more than 70% of functional NTE in peripheral nerves is one of the processes involved in OPIDP. Standard treatments for OP poisoning are ineffective for OPIDP.

COPIND occurs without cholinergic symptoms and is not dependent on AChE inhibition. COPIND appears with a delay and is long lasting. Symptoms associated with COPIND include cognitive deficit, mood change, autonomic dysfunction, peripheral neuropathy, and extrapyramidal symptoms. The underlying mechanisms of COPIND have not been determined, but it is hypothesized that withdrawal of OP pesticides after chronic exposure or acute exposure could be a factor.

The symptoms of organophosphate poisoning include muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis. Other symptoms include hypertension, and hypoglycemia.

Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur.

The effects of organophosphate poisoning on muscarinic receptors are recalled using the mnemonic SLUDGEM (salivation, lacrimation, urination, defecation, gastrointestinal motility, emesis, miosis) An additional mnemonic is MUDDLES: miosis, urination, diarrhea, diaphoresis, lacrimation, excitation, and salivation.

The onset and severity of symptoms, whether acute or chronic, depends upon the specific chemical, the route of exposure (skin, lungs, or GI tract), the dose, and the individuals ability to degrade the compound, which the PON1 enzyme level will affect.

Aspirin overdose has potentially serious consequences, sometimes leading to significant morbidity and death. Patients with mild intoxication frequently have nausea and vomiting, abdominal pain, lethargy, ringing in the ears, and dizziness. More significant signs and symptoms occur in more severe poisonings and include high body temperature, fast breathing rate, respiratory alkalosis, metabolic acidosis, low blood potassium, low blood glucose, hallucinations, confusion, seizure, cerebral edema, and coma. The most common cause of death following an aspirin overdose is cardiopulmonary arrest usually due to pulmonary edema.

Alcohol-related brain damage is the damage that occurs to brain structures or function of the central nervous system as a result of the direct neurotoxic effects of alcohol intoxication or acute withdrawal. The frontal lobes are the most damaged region of the brains of alcohol abusers but other regions of the brain are also affected. The damage that occurs from heavy drinking/high blood alcohol levels causes impairments in judgement and decision making and social skills. These brain changes are linked to poor behavioural control and impulsivity, which tend to worsen the existing addiction problem.

The problems of alcoholism are well known, such as memory disorders, liver disease, high blood pressure, muscle weakness, heart problems, anaemia, low immune function, disorders of the digestive system and pancreatic problems as well as depression, unemployment and family problems including child abuse. Recently attention has been increasingly focused on binge drinking by adolescents and young adults due to neurochemical changes and brain damage which, unlike with alcoholism, can occur after a relatively short period of time; the damage is particularly evident in the corticolimbic region. This brain damage increases the risk of abnormalities in mood and cognitive abilities, increases the risk of dementia and additionally binge drinkers have an increased risk of developing chronic alcoholism.

Individuals who are impulsive are at high risk of addiction due to impaired behavioural control and increased sensation seeking behaviour. Alcohol abuse, especially during adolescence, causes a deterioration of executive functions in the frontal lobe. This brain damage from alcohol actually increases impulsivity and therefore worsens the addictive disorder.

There are five main stages of alcoholism. The first stage,occasional abuse and binge drinking, in this stage one may want to just experiment with alcohol and test their limits. These drinkers may be new to different forms of alcohol. This experimental stage is commonly seen in teens and young adults. These experimental drinkers also frequently engage in binge drinking. While they may not drink regularly, they consume exceptionally enormous amounts of alcohol at one time.

The second stage, increased drinking, in this stage one will leave the experimental stage and start drinking on a regular basis. Instead of just drinking at parties occasionally, one may find themselves drinking every weekend. Increased alcohol consumption can also lead to drinking for these reasons: as an excuse to get together with friends, to alleviate stress, out of boredom, or to combat sadness or loneliness.

The third stage, problem drinking, one will drink to get rid of their problems for them at any moment. As increased drinking continues, one becomes more dependent on alcohol and are at risk of developing alcoholism.

The fourth stage, alcohol dependence, this forms after the problem drinking stage. At this point, one has an attachment to alcohol that has taken over their regular routine. They are aware of the adverse effects, but no longer have control over their alcohol consumption. Alcohol dependence also means that one has developed a tolerance to drinking. As a result, they may have to consume larger quantities to get “buzzed” or drunk.

The fifth stage, addiction and alcoholism, this is the final and most harmful stage. One is addicted and dependent and must have alcohol all the time, if not they have withdrawals. Alcohol withdrawal is the changes the body goes through when a person suddenly stops drinking after prolonged alcohol abuse, or if one does not have alcohol for a period of time. Symptoms include trembling (shakes), insomnia, anxiety, and other physical and mental symptoms. If the alcohol is withdrawn suddenly, the brain is like an accelerated vehicle that has lost its brakes. Not surprisingly, most symptoms of withdrawal are symptoms that occur when the brain is overstimulated (Drugs.com). People with alcohol addiction physically crave the substance and are often inconsolable until they start drinking again. With prolonged abstinence neurogenesis occurs which can potentially reverse the damage from alcohol abuse.

Acute aspirin or salicylates overdose or poisoning can cause initial respiratory alkalosis though metabolic acidosis ensues thereafter. The acid-base, fluid, and electrolyte abnormalities observed in salicylate toxicity can be grouped into three broad phases:

- Phase I: Characterized by hyperventilation resulting from direct respiratory center stimulation, leading to respiratory alkalosis and compensatory alkaluria. Potassium and sodium bicarbonate are excreted in the urine. This phase may last as long as 12 hours.

- Phase II: Characterized by paradoxic aciduria in the presence of continued respiratory alkalosis occurs when sufficient potassium has been lost from the kidneys. This phase may begin within hours and may last 12–24 hours.

- Phase III: Characterized by dehydration, hypokalemia, and progressive metabolic acidosis. This phase may begin 4–6 hours after ingestion in a young infant or 24 hours or more after ingestion in an adolescent or adult.

The first symptoms of neuroleptic malignant syndrome are usually muscle cramps and tremors, fever, symptoms of autonomic nervous system instability such as unstable blood pressure, and sudden changes in mental status (agitation, delirium, or coma). Once symptoms appear, they may progress rapidly and reach peak intensity in as little as three days. These symptoms can last anywhere from eight hours to forty days.

Symptoms are sometimes misinterpreted by doctors as symptoms of mental illness which can result in delayed treatment. NMS is less likely if a person has previously been stable for a period of time on antipsychotics, especially in situations where the dose has not been changed and there are no issues of noncompliance or consumption of psychoactive substances known to worsen psychosis.

- Increased body temperature >38 °C (>100.4 °F), or

- Confused or altered consciousness

- sweating

- Rigid muscles

- Autonomic imbalance

The periods before and surrounding birth are typically normal in individuals with LNS. The most common presenting features are abnormally decreased muscle tone (hypotonia) and developmental delay, which are evident by three to six months of age. Affected individuals are late in sitting up, while most never crawl or walk. Lack of speech is also a very common trait associated with LNS.

Irritability is most often noticed along with the first signs of nervous system impairment. Within the first few years of life, extrapyramidal involvement causes abnormal involuntary muscle contractions such as loss of motor control (dystonia), writhing motions (choreoathetosis), and arching of the spine (opisthotonus). Signs of pyramidal system involvement, including spasticity, overactive reflexes (hyperreflexia) and extensor plantar reflexes, also occur. The resemblance to athetoid cerebral palsy is apparent in the neurologic aspects of LNS. As a result, most individuals are initially diagnosed as having cerebral palsy. The motor disability is so extensive that most individuals never walk, and become lifelong wheelchair users.

Signs and symptoms of alcohol withdrawal occur primarily in the central nervous system. The severity of withdrawal can vary from mild symptoms such as sleep disturbances and anxiety to severe and life-threatening symptoms such as delirium, hallucinations, and autonomic instability.

Withdrawal usually begins 6 to 24 hours after the last drink. It can last for up to one week. To be classified as alcohol withdrawal syndrome, patients must exhibit at least two of the following symptoms: increased hand tremor, insomnia, nausea or vomiting, transient hallucinations (auditory, visual or tactile), psychomotor agitation, anxiety, tonic-clonic seizures, and autonomic instability.

The severity of symptoms is dictated by a number of factors, the most important of which are degree of alcohol intake, length of time the individual has been using alcohol, and previous history of alcohol withdrawal. Symptoms are also grouped together and classified:

- Alcohol hallucinosis: patients have transient visual, auditory, or tactile hallucinations, but are otherwise clear.

- Withdrawal seizures: seizures occur within 48 hours of alcohol cessations and occur either as a single generalized tonic-clonic seizure or as a brief episode of multiple seizures.

- Delirium tremens: hyperadrenergic state, disorientation, tremors, diaphoresis, impaired attention/consciousness, and visual and auditory hallucinations. This usually occurs 24 to 72 hours after alcohol cessation. Delirium tremens is the most severe form of withdrawal and occurs in 5 to 20% of patients experiencing detoxification and 1/3 of patients experiencing withdrawal seizures.

Persons affected are cognitively impaired and have behavioral disturbances that emerge between two and three years of age. The uncontrollable self-injury associated with LNS also usually begins at three years of age. The self-injury begins with biting of the lips and tongue; as the disease progresses, affected individuals frequently develop finger biting and head banging. The self-injury can increase during times of stress. Self-harm is a distinguishing characteristic of the disease and is apparent in 85% of affected males.

The majority of individuals are cognitively impaired, which is sometimes difficult to distinguish from other symptoms because of the behavioral disturbances and motor deficits associated with the syndrome. In many ways, the behaviors may be seen as a psychological extension of the compulsion to cause self-injury, and include rejecting desired treats or travel, repaying kindness with coldness or rage, failing to answer test questions correctly despite study and a desire to succeed, provoking anger from caregivers when affection is desired.

Compulsive behaviors also occur, including aggressiveness, vomiting, spitting, and coprolalia (involuntary swearing). The development of this type of behavior is sometimes seen within the first year, or in early childhood, but others may not develop it until later in life.

Typically the severity of the symptoms experienced will depend on the amount and duration of prior alcohol consumption, as well as the number and severity of previous withdrawals. Even the most severe of these symptoms can occur in as little as 2 hours after cessation; therefore, the overall unpredictability necessitates either pre-planned hospitalization, treatment coordinated with a doctor, or at the very least rapid access to medical care, and a supporting system of friends or family should be introduced prior to addressing detoxification. In many cases, however, symptoms follow a reasonably predictable time frame as exampled below:

Six to 12 hours after the ingestion of the last drink, withdrawal symptoms such as shaking, headache, sweating, anxiety, nausea or vomiting occur. Other comparable symptoms may also exist in this period. Twelve to 24 hours after cessation, the condition may progress to such major symptoms as confusion, hallucinations (with awareness of reality), tremor, agitation, and similar ailments.

At 24 to 48 hours following the last ethanol ingestion, the possibility of seizures should be anticipated. Meanwhile, none of the earlier withdrawal symptoms will have abated. Seizures carry the risk of death for the alcoholic.

Although, most often, the patient's condition begins to improve past the 48-hour mark, it can sometimes continue to increase in severity to delirium tremens, characterized by hallucinations that are indistinguishable from reality, severe confusion, more seizures, high blood pressure and fever which can persist anywhere from 4 to 12 days.

Alcohol related brain damage causes a wide range of executive function impairments including, impaired judgment, blunted affect, poor insight, social withdrawal, depression, reduced motivation, distractibility, attentional and impulse control deficits.

Differentiating NMS from other neurological disorders can be very difficult. It requires expert judgement to separate symptoms of NMS from other diseases. Some of the most commonly mistaken diseases are encephalitis, toxic encephalopathy, status epilepticus, heat stroke, and malignant hyperthermia. Due to the comparative rarity of NMS, it is often overlooked and immediate treatment for the syndrome is delayed. Drugs such as cocaine and amphetamine may also produce similar symptoms.

The differential diagnosis is similar to that of hyperthermia, and includes serotonin syndrome. Features which distinguish NMS from serotonin syndrome include bradykinesia, muscle rigidity, and a high white blood cell count.

Drinking enough to cause a blood alcohol concentration (BAC) of 0.03–0.12% typically causes an overall improvement in mood and possible euphoria (a "happy" feeling), increased self-confidence and sociability, decreased anxiety, a flushed, red appearance in the face and impaired judgment and fine muscle coordination. A BAC of 0.09% to 0.25% causes lethargy, sedation, balance problems and blurred vision. A BAC of 0.18% to 0.30% causes profound confusion, impaired speech (e.g. slurred speech), staggering, dizziness and vomiting. A BAC from 0.25% to 0.40% causes stupor, unconsciousness, anterograde amnesia, vomiting (death may occur due to inhalation of vomit (pulmonary aspiration) while unconscious and respiratory depression (potentially life-threatening). A BAC from 0.35% to 0.80% causes a coma (unconsciousness), life-threatening respiratory depression and possibly fatal alcohol poisoning. With all alcoholic beverages, drinking while driving, operating an aircraft or heavy machinery increases the risk of an accident; many countries have penalties for drunk driving.

Neuroinflammation is inflammation of the nervous tissue. It may be initiated in response to a variety of cues, including infection, traumatic brain injury, toxic metabolites, or autoimmunity. In the central nervous system (CNS), including the brain and spinal cord, microglia are the resident innate immune cells that are activated in response to these cues. The CNS is typically an immunologically privileged site because peripheral immune cells are generally blocked by the blood–brain barrier (BBB), a specialized structure composed of astrocytes and endothelial cells. However, circulating peripheral immune cells may surpass a compromised BBB and encounter neurons and glial cells expressing major histocompatibility complex molecules, perpetuating the immune response. Although the response is initiated to protect the central nervous system from the infectious agent, the effect may be toxic and widespread inflammation as well as further migration of leukocytes through the blood–brain barrier.