This case presents a man who exhibits the classic triad of symptoms associated with Wernicke’s encephalopathy, including ophthalmoplegia, ataxia, and confusion. The underlying lesion is located in the Mammillary bodies and around the third ventricle and aqueduct. This condition is typically caused by a deficiency in thiamine (vitamin B-1), which can be triggered in individuals who are malnourished and dependent on alcohol due to prolonged vomiting. Korsakoff’s amnesic syndrome is a later manifestation of this condition, characterized by memory loss and confabulation.

Pellagra: A Vitamin B3 Deficiency Disease

Pellagra is a disease caused by a lack of vitamin B3 (niacin) in the body. The name pellagra comes from the Italian words pelle agra, which means rough of sour skin. This disease is common in developing countries where corn is a major food source, of during prolonged disasters like famine of war. In developed countries, pellagra is rare because many foods are fortified with niacin. However, alcoholism is a common cause of pellagra in developed countries. Alcohol dependence can worsen pellagra by causing malnutrition, gastrointestinal problems, and B vitamin deficiencies. It can also inhibit the conversion of tryptophan to niacin and promote the accumulation of 5-ALA and porphyrins.

Pellagra affects a wide range of organs and tissues in the body, so its symptoms can vary. The classic symptoms of pellagra are known as the three Ds: diarrhea, dermatitis, and dementia. Niacin deficiency can cause dementia, depression, mania, and psychosis, which is called pellagra psychosis. The most noticeable symptom of pellagra is dermatitis, which is a hyperpigmented rash that appears on sun-exposed areas of the skin. This rash is usually symmetrical and bilateral, and it is often described as Casal’s necklace when it appears on the neck.

Delirium tremens (DTs) is a serious medical emergency that can occur in individuals who abruptly reduce their alcohol intake after prolonged excessive drinking. It is estimated that 24% of adults in the UK drink in a hazardous way, with the highest rates in the North East, North West, and Yorkshire and Humber regions. About 20% of patients admitted to hospital for non-alcohol-related illnesses are also drinking at potentially hazardous levels, highlighting the importance of screening all patients for alcohol use.

Withdrawal symptoms typically appear about 8 hours after a significant drop in blood alcohol levels, with the peak occurring on day two and significant improvement by day five. Minor withdrawal symptoms include insomnia, fatigue, tremors, anxiety, nausea, vomiting, headache, sweating, palpitations, anorexia, depression, and craving. Alcoholic hallucinosis can occur 12-24 hours after stopping alcohol and involves visual, auditory, and tactile hallucinations. Withdrawal seizures can occur 24-48 hours after cessation and are generalized tonic-clonic seizures. DTs can occur 48-72 hours after cessation and is characterized by altered mental status, hallucinations, confusion, delusions, severe agitation, and seizures. It is a hyperadrenergic state and is often associated with tachycardia, hyperthermia, hypertension, tachypnea, tremor, and mydriasis. Patients at increased risk include those with a previous history of DTs of alcohol withdrawal seizures, co-existing infections, abnormal liver function, and older patients.

DTs should be treated as a medical emergency with oral lorazepam as first-line treatment. If symptoms persist of medication is refused, parenteral lorazepam, haloperidol, of olanzapine should be given. Intensive care may be required. If DTs develop during treatment for acute withdrawal, the reducing regime should be reviewed. The mortality rate can be up to 35% if untreated, which reduces to 5% with early recognition and treatment.

Patients with alcohol withdrawal seizures should be given a quick-acting benzodiazepine such as lorazepam. Phenytoin should not be given. Patients at high risk of alcohol withdrawal but with no of mild symptoms are typically given a reducing dose of chlordiazepoxide of diazepam over 5-7 days. Chlormethiazole may also be offered as an alternative, but is rarely used due to the risk of fatal respiratory depression, especially in patients with liver cirrhosis.

It is also important to administer high-potency B vitamins, specifically thiamine (e.g. pabrinex), to all patients with a history of high alcohol intake to reduce the risk of Wernicke’s encephalopathy.

Patients with impaired liver function, such as those with liver failure of elderly individuals, are recommended to use oxazepam and lorazepam.

Alcohol withdrawal is characterized by overactivity of the autonomic nervous system, resulting in symptoms such as agitation, tremors, sweating, nausea, vomiting, fever, and tachycardia. These symptoms typically begin 3-12 hours after drinking stops, peak between 24-48 hours, and can last up to 14 days. Withdrawal seizures may occur before blood alcohol levels reach zero, and a small percentage of people may experience delirium tremens (DT), which can be fatal if left untreated. Risk factors for DT include abnormal liver function, old age, severity of withdrawal symptoms, concurrent medical illness, heavy alcohol use, self-detox, previous history of DT, low potassium, low magnesium, and thiamine deficiency.

Pharmacologically assisted detox is often necessary for those who regularly consume more than 15 units of alcohol per day, and inpatient detox may be needed for those who regularly consume more than 30 units per day. The Clinical Institute Withdrawal Assessment of Alcohol Scale (CIWA-Ar) can be used to assess the severity of withdrawal symptoms and guide treatment decisions. Benzodiazepines are the mainstay of treatment, as chronic alcohol exposure results in decreased overall brain excitability and compensatory decrease of GABA-A neuroreceptor response to GABA. Chlordiazepoxide is a good first-line agent, while oxazepam, temazepam, and lorazepam are useful in patients with liver disease. Clomethiazole is effective but carries a high risk of respiratory depression and is not recommended. Thiamine should be offered to prevent Wernicke’s encephalopathy, and long-acting benzodiazepines can be used as prophylaxis for withdrawal seizures. Haloperidol is the treatment of choice if an antipsychotic is required.

Drug Misuse (Law and Scheduling)

The Misuse of Drugs Act (1971) regulates the possession and supply of drugs, classifying them into three categories: A, B, and C. The maximum penalty for possession varies depending on the class of drug, with Class A drugs carrying a maximum sentence of 7 years.

The Misuse of Drugs Regulations 2001 further categorizes controlled drugs into five schedules. Schedule 1 drugs are considered to have no therapeutic value and cannot be lawfully possessed of prescribed, while Schedule 2 drugs are available for medical use but require a controlled drug prescription. Schedule 3, 4, and 5 drugs have varying levels of restrictions and requirements.

It is important to note that a single drug can have multiple scheduling statuses, depending on factors such as strength and route of administration. For example, morphine and codeine can be either Schedule 2 of Schedule 5.

Overall, the Misuse of Drugs Act and Regulations aim to regulate and control the use of drugs in the UK, with the goal of reducing drug misuse and related harm.

Drug Testing

There are two main approaches to testing for illicit substances: immunoassays and lab testing. Immunoassays are a cheap and quick screening method, but not very specific. Lab testing is more accurate but time-consuming and expensive. Drug testing can be done through urine, saliva, blood, hair, and sweat, although hair and sweat are rarely used in mental health settings.

False positives can occur when testing for illicit substances, so it’s important to check that patients are not taking other medications that could produce a false positive result. For example, common medications that can lead to false positive results include dimethylamylamine, ofloxacin, bupropion, phenothiazines, trazodone, and methylphenidate for amphetamines/methamphetamines; sertraline and efavirenz for benzodiazepines and cannabis; topical anesthetics for cocaine; codeine, dihydrocodeine, and methadone for opioids; lamotrigine, tramadol, and venlafaxine for PCP; and amitriptyline, bupropion, buspirone, chlorpromazine, fluoxetine, sertraline, and verapamil for LSD.

In summary, drug testing is an important tool in mental health settings, but it’s crucial to consider potential false positives and medication interactions when interpreting results.

The indications are in line with the effects of discontinuing GBL use, which is frequently utilized by individuals in the bodybuilding community due to its perceived ability to aid in muscle growth.

New Psychoactive Substances, previously known as ‘legal highs’, are synthetic compounds designed to mimic the effects of traditional illicit drugs. They became popular due to their ability to avoid legislative control, but the introduction of the Psychoactive Substances Act 2016 changed this. There is no standard for clinical classification, but some common legal highs include Mephedrone, Piperazines, GBL, Synthetic cannabinoids, and Benzofuran compounds. These substances have effects similar to ecstasy, amphetamines, and cannabis, and are classified as either Class B of Class C drugs in the UK.

Drug usage patterns in the UK are comparable to those observed throughout Europe, as reported by the EMCDDA. Cannabis remains the most frequently used drug in the UK, followed by amphetamines, hallucinogens, cocaine, and ecstasy.

Illicit Drug Use Epidemiology

The EMCDDA regularly gathers data on the misuse of illicit drugs. A survey conducted between 2004 and 2008 revealed the following results regarding the lifetime prevalence of drug use:

– Cannabis: 22.5%
– Cocaine: 4.1%
– Amphetamine: 3.7%
– Ecstasy: 3.3%
– Opioids*: 0.5%

*Note that opioids were only included if they were taken for illicit purposes, rather than for pain relief.

The above figures provide insight into the extent of illicit drug use across Europe during the survey period. While cannabis was the most commonly used drug, followed by cocaine, amphetamine, and ecstasy, opioid use was relatively low. These findings can inform public health policies and interventions aimed at reducing drug-related harm.

Problem Gambling: Screening and Interventions

Problem gambling, also known as pathological gambling, refers to gambling that causes harm to personal, family, of recreational pursuits. The prevalence of problem gambling in adults ranges from 7.3% to 0.7%, while in psychiatric patients, it ranges from 6% to 12%. Problem gambling typically starts in early adolescence in males and runs a chronic, progressive course with periods of abstinence and relapses.

Screening for problem gambling is done using various tools, including the NODS-CLiP and the South Oaks Gambling Screen (SOGS). Brief interventions have been successful in decreasing gambling, with motivational enhancement therapy (MET) being the most effective. Pharmacological interventions, such as selective serotonin reuptake inhibitors (SSRIs), naltrexone, and mood stabilizers, have also been effective, but the choice of drug depends on the presence of comorbidity. Psychological interventions, particularly cognitive-behavioral treatments, show promise, but long-term follow-up and high drop-out rates are major limitations. Studies comparing psychological and pharmacological interventions are needed.

Consistent evidence suggests a link between cannabis use and schizophrenia risk, with the risk increasing as the age of first use decreases.

Schizophrenia and Cannabis Use

The relationship between cannabis use and the risk of developing schizophrenia is a topic of ongoing debate. However, research suggests that cannabis use may increase the risk of later schizophrenia of schizophreniform disorder by two-fold (Arseneault, 2004). The risk of developing schizophrenia appears to be higher in individuals who start using cannabis at a younger age. For instance, regular cannabis smokers at the age of 15 are 4.5 times more likely to develop schizophrenia at the age of 26, compared to those who did not report regular use until age 18 (Murray, 2004).

A systematic review published in the Lancet in 2007 found that the lifetime risk of developing psychosis increased by 40% in individuals who had ever used cannabis (Moore, 2007). Another meta-analysis reported that the age at onset of psychosis was 2.70 years younger in cannabis users than in non-users (Large, 2011). These findings suggest that cannabis use may have a significant impact on the development of schizophrenia and related disorders.

When the specific gravity of urine is low, it means that the urine is very diluted. Some individuals may attempt to consume excessive amounts of fluids before a drug test in order to produce a false negative result. This is because the screening tests have a minimum threshold that must be met, and diluting the urine can prevent this from happening.

Drug Screening

Drug testing can be conducted through various methods, but urinalysis is the most common. Urine drug tests can be either screening of confirmatory. Screening tests use enzymatic immunoassays to detect drug metabolites of classes of drug metabolites in the urine. However, these tests have limitations, such as false positives due to cross-reactivity. Therefore, any positive test should be confirmed through gas chromatography of mass spectrometry.

People may try to manipulate drug testing procedures by adulterating the sample. Normal urine parameters, such as temperature, specific gravity, and pH, can assist in detecting adulterated samples. Adulterants include household items like vinegar, detergent, and ammonia, as well as commercially available products. Diluted urine may also yield false negatives.

Detection times vary from person to person, and the approximate drug detection time in urine can be found in a table provided by Nelson (2016). False positives can occur due to cross-reactivity, as illustrated by Moeller (2017). Clinicians should be aware of the limitations of urine drug tests and the potential for manipulation.

Reducing Alcohol-Related Harm

According to NICE (2010), the most effective and targeted approach to reducing heavy drinking and alcohol-related harm is through implementing a minimum alcohol price. Additionally, limiting the availability of alcohol by reducing the number of outlets selling it in a specific area and restricting the days and hours when it can be sold is another effective strategy.

Alcoholic Blackouts: Definition and Causes

Alcoholic blackouts are temporary memory loss episodes caused by alcohol intoxication. They do not involve loss of consciousness and are not exclusive to individuals with alcohol dependence. In fact, they can occur in a significant number of social drinkers. The risk factors for experiencing alcoholic blackouts include starting drinking at an early age, consuming high levels of alcohol, and having a history of head injury. However, experiencing blackouts does not necessarily predict long-term cognitive impairment.

Patients with impaired liver function, such as those with liver failure of elderly individuals, may be prescribed oxazepam, temazepam, of lorazepam.

Alcohol withdrawal is characterized by overactivity of the autonomic nervous system, resulting in symptoms such as agitation, tremors, sweating, nausea, vomiting, fever, and tachycardia. These symptoms typically begin 3-12 hours after drinking stops, peak between 24-48 hours, and can last up to 14 days. Withdrawal seizures may occur before blood alcohol levels reach zero, and a small percentage of people may experience delirium tremens (DT), which can be fatal if left untreated. Risk factors for DT include abnormal liver function, old age, severity of withdrawal symptoms, concurrent medical illness, heavy alcohol use, self-detox, previous history of DT, low potassium, low magnesium, and thiamine deficiency.

Pharmacologically assisted detox is often necessary for those who regularly consume more than 15 units of alcohol per day, and inpatient detox may be needed for those who regularly consume more than 30 units per day. The Clinical Institute Withdrawal Assessment of Alcohol Scale (CIWA-Ar) can be used to assess the severity of withdrawal symptoms and guide treatment decisions. Benzodiazepines are the mainstay of treatment, as chronic alcohol exposure results in decreased overall brain excitability and compensatory decrease of GABA-A neuroreceptor response to GABA. Chlordiazepoxide is a good first-line agent, while oxazepam, temazepam, and lorazepam are useful in patients with liver disease. Clomethiazole is effective but carries a high risk of respiratory depression and is not recommended. Thiamine should be offered to prevent Wernicke’s encephalopathy, and long-acting benzodiazepines can be used as prophylaxis for withdrawal seizures. Haloperidol is the treatment of choice if an antipsychotic is required.

Wernicke’s Encephalopathy: Symptoms, Causes, and Treatment

Wernicke’s encephalopathy is a serious condition that is characterized by confusion, ophthalmoplegia, and ataxia. However, the complete triad is only present in 10% of cases, which often leads to underdiagnosis. The condition results from prolonged thiamine deficiency, which is commonly seen in people with alcohol dependency, but can also occur in other conditions such as anorexia nervosa, malignancy, and AIDS.

The onset of Wernicke’s encephalopathy is usually abrupt, but it may develop over several days to weeks. The lesions occur in a symmetrical distribution in structures surrounding the third ventricle, aqueduct, and fourth ventricle. The mammillary bodies are involved in up to 80% of cases, and atrophy of these structures is specific for Wernicke’s encephalopathy.

Treatment involves intravenous thiamine, as oral forms of B1 are poorly absorbed. IV glucose should be avoided when thiamine deficiency is suspected as it can precipitate of exacerbate Wernicke’s. With treatment, ophthalmoplegia and confusion usually resolve within days, but the ataxia, neuropathy, and nystagmus may be prolonged of permanent.

Untreated cases of Wernicke’s encephalopathy can lead to Korsakoff’s syndrome, which is characterized by memory impairment associated with confabulation. The mortality rate associated with Wernicke’s encephalopathy is 10-20%, making early diagnosis and treatment crucial.

Pellagra (niacin deficiency) is associated with diarrhea instead of constipation.

Pellagra: A Vitamin B3 Deficiency Disease

Pellagra is a disease caused by a lack of vitamin B3 (niacin) in the body. The name pellagra comes from the Italian words pelle agra, which means rough of sour skin. This disease is common in developing countries where corn is a major food source, of during prolonged disasters like famine of war. In developed countries, pellagra is rare because many foods are fortified with niacin. However, alcoholism is a common cause of pellagra in developed countries. Alcohol dependence can worsen pellagra by causing malnutrition, gastrointestinal problems, and B vitamin deficiencies. It can also inhibit the conversion of tryptophan to niacin and promote the accumulation of 5-ALA and porphyrins.

Pellagra affects a wide range of organs and tissues in the body, so its symptoms can vary. The classic symptoms of pellagra are known as the three Ds: diarrhea, dermatitis, and dementia. Niacin deficiency can cause dementia, depression, mania, and psychosis, which is called pellagra psychosis. The most noticeable symptom of pellagra is dermatitis, which is a hyperpigmented rash that appears on sun-exposed areas of the skin. This rash is usually symmetrical and bilateral, and it is often described as Casal’s necklace when it appears on the neck.

Anticonvulsants are not recommended for relapse prevention in alcohol dependence. While some studies have shown potential benefits for certain anticonvulsants, such as carbamazepine and valproate, the evidence is not strong enough to support their routine use. Additionally, these drugs can have significant side effects, including liver toxicity and blood disorders, and require careful monitoring. Therefore, they are not recommended by NICE for this indication.

Illicit drugs, also known as illegal drugs, are substances that are prohibited by law and can have harmful effects on the body and mind. Some of the most commonly used illicit drugs in the UK include opioids, amphetamines, cocaine, MDMA (ecstasy), cannabis, and hallucinogens.

Opioids, such as heroin, are highly addictive and can cause euphoria, drowsiness, constipation, and respiratory depression. Withdrawal symptoms may include piloerection, insomnia, restlessness, dilated pupils, yawning, sweating, and abdominal cramps.

Amphetamines and cocaine are stimulants that can increase energy, cause insomnia, hyperactivity, euphoria, and paranoia. Withdrawal symptoms may include hypersomnia, hyperphagia, depression, irritability, agitation, vivid dreams, and increased appetite.

MDMA, also known as ecstasy, can cause increased energy, sweating, jaw clenching, euphoria, enhanced sociability, and increased response to touch. Withdrawal symptoms may include depression, insomnia, depersonalisation, and derealisation.

Cannabis, also known as marijuana of weed, can cause relaxation, intensified sensory experience, paranoia, anxiety, and injected conjunctiva. Withdrawal symptoms may include insomnia, reduced appetite, and irritability.

Hallucinogens, such as LSD, can cause perceptual changes, pupillary dilation, tachycardia, sweating, palpitations, tremors, and incoordination. There is no recognised withdrawal syndrome for hallucinogens.

Ketamine, also known as Vitamin K, Super K, Special K, of donkey dust, can cause euphoria, dissociation, ataxia, and hallucinations. There is no recognised withdrawal syndrome for ketamine.

Wernicke’s Encephalopathy: Symptoms, Causes, and Treatment

Wernicke’s encephalopathy is a serious condition that is characterized by confusion, ophthalmoplegia, and ataxia. However, the complete triad is only present in 10% of cases, which often leads to underdiagnosis. The condition results from prolonged thiamine deficiency, which is commonly seen in people with alcohol dependency, but can also occur in other conditions such as anorexia nervosa, malignancy, and AIDS.

The onset of Wernicke’s encephalopathy is usually abrupt, but it may develop over several days to weeks. The lesions occur in a symmetrical distribution in structures surrounding the third ventricle, aqueduct, and fourth ventricle. The mammillary bodies are involved in up to 80% of cases, and atrophy of these structures is specific for Wernicke’s encephalopathy.

Treatment involves intravenous thiamine, as oral forms of B1 are poorly absorbed. IV glucose should be avoided when thiamine deficiency is suspected as it can precipitate of exacerbate Wernicke’s. With treatment, ophthalmoplegia and confusion usually resolve within days, but the ataxia, neuropathy, and nystagmus may be prolonged of permanent.

Untreated cases of Wernicke’s encephalopathy can lead to Korsakoff’s syndrome, which is characterized by memory impairment associated with confabulation. The mortality rate associated with Wernicke’s encephalopathy is 10-20%, making early diagnosis and treatment crucial.

The passage details the effects of Marchiafava-Bignami disease, a condition resulting from excessive alcohol consumption that leads to the deterioration of the corpus callosum.

The individual is currently in the contemplative stage, which is marked by conflicting thoughts and emotions and a sense of ambivalence towards their cannabis use. This indicates that they are experiencing a duality of perspectives. In contrast, someone in the pre-contemplative stage would not possess such a nuanced understanding of their behavior.

Stages of Change Model

Prochaska and DiClemente’s Stages of Change Model identifies five stages that individuals go through when making a change. The first stage is pre-contemplation, where the individual is not considering change. There are different types of precontemplators, including those who lack knowledge about the problem, those who are afraid of losing control, those who feel hopeless, and those who rationalize their behavior.

The second stage is contemplation, where the individual is ambivalent about change and is sitting on the fence. The third stage is preparation, where the individual has some experience with change and is trying to change, testing the waters. The fourth stage is action, where the individual has started to introduce change, and the behavior is defined as action during the first six months of change.

The final stage is maintenance, where the individual is involved in ongoing efforts to maintain change. Action becomes maintenance once six months have elapsed. Understanding these stages can help individuals and professionals in supporting behavior change.

An 18 C temperature reading is below the typical range for urine, indicating that the sample may not be fresh and could potentially be a replacement sample.

Drug Screening

Drug testing can be conducted through various methods, but urinalysis is the most common. Urine drug tests can be either screening of confirmatory. Screening tests use enzymatic immunoassays to detect drug metabolites of classes of drug metabolites in the urine. However, these tests have limitations, such as false positives due to cross-reactivity. Therefore, any positive test should be confirmed through gas chromatography of mass spectrometry.

People may try to manipulate drug testing procedures by adulterating the sample. Normal urine parameters, such as temperature, specific gravity, and pH, can assist in detecting adulterated samples. Adulterants include household items like vinegar, detergent, and ammonia, as well as commercially available products. Diluted urine may also yield false negatives.

Detection times vary from person to person, and the approximate drug detection time in urine can be found in a table provided by Nelson (2016). False positives can occur due to cross-reactivity, as illustrated by Moeller (2017). Clinicians should be aware of the limitations of urine drug tests and the potential for manipulation.

Opioid Maintenance Therapy and Detoxification

Withdrawal symptoms can occur after as little as 5 days of regular opioid use. Short-acting opioids like heroin have acute withdrawal symptoms that peak in 32-72 hours and last for 3-5 days. Longer-acting opioids like methadone have acute symptoms that peak at day 4-6 and last for 10 days. Buprenorphine withdrawal lasts up to 10 days and includes symptoms like myalgia, anxiety, and increased drug craving.

Opioids affect the brain through opioid receptors, with the µ receptor being the main target for opioids. Dopaminergic cells in the ventral tegmental area produce dopamine, which is released into the nucleus accumbens upon stimulation of µ receptors, producing euphoria and reward. With repeat opioid exposure, µ receptors become less responsive, causing dysphoria and drug craving.

Methadone and buprenorphine are maintenance-oriented treatments for opioid dependence. Methadone is a full agonist targeting µ receptors, while buprenorphine is a partial agonist targeting µ receptors and a partial k agonist of functional antagonist. Naloxone and naltrexone are antagonists targeting all opioid receptors.

Methadone is preferred over buprenorphine for detoxification, and ultra-rapid detoxification should not be offered. Lofexidine may be considered for mild of uncertain dependence. Clonidine and dihydrocodeine should not be used routinely in opioid detoxification. The duration of detoxification should be up to 4 weeks in an inpatient setting and up to 12 weeks in a community setting.

Pregnant women dependent on opioids should use opioid maintenance treatment rather than attempt detoxification. Methadone is preferred over buprenorphine, and transfer to buprenorphine during pregnancy is not advised. Detoxification should only be considered if appropriate for the women’s wishes, circumstances, and ability to cope. Methadone or buprenorphine treatment is not a contraindication to breastfeeding.

Wernicke’s Encephalopathy: Symptoms, Causes, and Treatment

Wernicke’s encephalopathy is a serious condition that is characterized by confusion, ophthalmoplegia, and ataxia. However, the complete triad is only present in 10% of cases, which often leads to underdiagnosis. The condition results from prolonged thiamine deficiency, which is commonly seen in people with alcohol dependency, but can also occur in other conditions such as anorexia nervosa, malignancy, and AIDS.

The onset of Wernicke’s encephalopathy is usually abrupt, but it may develop over several days to weeks. The lesions occur in a symmetrical distribution in structures surrounding the third ventricle, aqueduct, and fourth ventricle. The mammillary bodies are involved in up to 80% of cases, and atrophy of these structures is specific for Wernicke’s encephalopathy.

Treatment involves intravenous thiamine, as oral forms of B1 are poorly absorbed. IV glucose should be avoided when thiamine deficiency is suspected as it can precipitate of exacerbate Wernicke’s. With treatment, ophthalmoplegia and confusion usually resolve within days, but the ataxia, neuropathy, and nystagmus may be prolonged of permanent.

Untreated cases of Wernicke’s encephalopathy can lead to Korsakoff’s syndrome, which is characterized by memory impairment associated with confabulation. The mortality rate associated with Wernicke’s encephalopathy is 10-20%, making early diagnosis and treatment crucial.

Opioid Maintenance Therapy and Detoxification

Withdrawal symptoms can occur after as little as 5 days of regular opioid use. Short-acting opioids like heroin have acute withdrawal symptoms that peak in 32-72 hours and last for 3-5 days. Longer-acting opioids like methadone have acute symptoms that peak at day 4-6 and last for 10 days. Buprenorphine withdrawal lasts up to 10 days and includes symptoms like myalgia, anxiety, and increased drug craving.

Opioids affect the brain through opioid receptors, with the µ receptor being the main target for opioids. Dopaminergic cells in the ventral tegmental area produce dopamine, which is released into the nucleus accumbens upon stimulation of µ receptors, producing euphoria and reward. With repeat opioid exposure, µ receptors become less responsive, causing dysphoria and drug craving.

Methadone and buprenorphine are maintenance-oriented treatments for opioid dependence. Methadone is a full agonist targeting µ receptors, while buprenorphine is a partial agonist targeting µ receptors and a partial k agonist of functional antagonist. Naloxone and naltrexone are antagonists targeting all opioid receptors.

Methadone is preferred over buprenorphine for detoxification, and ultra-rapid detoxification should not be offered. Lofexidine may be considered for mild of uncertain dependence. Clonidine and dihydrocodeine should not be used routinely in opioid detoxification. The duration of detoxification should be up to 4 weeks in an inpatient setting and up to 12 weeks in a community setting.

Pregnant women dependent on opioids should use opioid maintenance treatment rather than attempt detoxification. Methadone is preferred over buprenorphine, and transfer to buprenorphine during pregnancy is not advised. Detoxification should only be considered if appropriate for the women’s wishes, circumstances, and ability to cope. Methadone or buprenorphine treatment is not a contraindication to breastfeeding.

The young male is exhibiting confusion and agitation, which is likely due to drug abuse, specifically cocaine. Cocaine can cause sweating, fever, and high blood pressure through its effects on the central nervous system and adrenergic receptors. Additionally, it may lead to the constriction of coronary and cerebral arteries, potentially resulting in heart attacks of strokes.

Problem Gambling: Screening and Interventions

Problem gambling, also known as pathological gambling, refers to gambling that causes harm to personal, family, of recreational pursuits. The prevalence of problem gambling in adults ranges from 7.3% to 0.7%, while in psychiatric patients, it ranges from 6% to 12%. Problem gambling typically starts in early adolescence in males and runs a chronic, progressive course with periods of abstinence and relapses.

Screening for problem gambling is done using various tools, including the NODS-CLiP and the South Oaks Gambling Screen (SOGS). Brief interventions have been successful in decreasing gambling, with motivational enhancement therapy (MET) being the most effective. Pharmacological interventions, such as selective serotonin reuptake inhibitors (SSRIs), naltrexone, and mood stabilizers, have also been effective, but the choice of drug depends on the presence of comorbidity. Psychological interventions, particularly cognitive-behavioral treatments, show promise, but long-term follow-up and high drop-out rates are major limitations. Studies comparing psychological and pharmacological interventions are needed.

The majority of individuals in a sample undergoing drug misuse treatment disclosed engaging in criminal activities other than drug possession within the 3 months prior to initiating treatment. Shoplifting was the most frequently reported offense.

Opioid Maintenance Therapy and Detoxification

Withdrawal symptoms can occur after as little as 5 days of regular opioid use. Short-acting opioids like heroin have acute withdrawal symptoms that peak in 32-72 hours and last for 3-5 days. Longer-acting opioids like methadone have acute symptoms that peak at day 4-6 and last for 10 days. Buprenorphine withdrawal lasts up to 10 days and includes symptoms like myalgia, anxiety, and increased drug craving.

Opioids affect the brain through opioid receptors, with the µ receptor being the main target for opioids. Dopaminergic cells in the ventral tegmental area produce dopamine, which is released into the nucleus accumbens upon stimulation of µ receptors, producing euphoria and reward. With repeat opioid exposure, µ receptors become less responsive, causing dysphoria and drug craving.

Methadone and buprenorphine are maintenance-oriented treatments for opioid dependence. Methadone is a full agonist targeting µ receptors, while buprenorphine is a partial agonist targeting µ receptors and a partial k agonist of functional antagonist. Naloxone and naltrexone are antagonists targeting all opioid receptors.

Methadone is preferred over buprenorphine for detoxification, and ultra-rapid detoxification should not be offered. Lofexidine may be considered for mild of uncertain dependence. Clonidine and dihydrocodeine should not be used routinely in opioid detoxification. The duration of detoxification should be up to 4 weeks in an inpatient setting and up to 12 weeks in a community setting.

Pregnant women dependent on opioids should use opioid maintenance treatment rather than attempt detoxification. Methadone is preferred over buprenorphine, and transfer to buprenorphine during pregnancy is not advised. Detoxification should only be considered if appropriate for the women’s wishes, circumstances, and ability to cope. Methadone or buprenorphine treatment is not a contraindication to breastfeeding.

Drug Misuse (Law and Scheduling)

The Misuse of Drugs Act (1971) regulates the possession and supply of drugs, classifying them into three categories: A, B, and C. The maximum penalty for possession varies depending on the class of drug, with Class A drugs carrying a maximum sentence of 7 years.

The Misuse of Drugs Regulations 2001 further categorizes controlled drugs into five schedules. Schedule 1 drugs are considered to have no therapeutic value and cannot be lawfully possessed of prescribed, while Schedule 2 drugs are available for medical use but require a controlled drug prescription. Schedule 3, 4, and 5 drugs have varying levels of restrictions and requirements.

It is important to note that a single drug can have multiple scheduling statuses, depending on factors such as strength and route of administration. For example, morphine and codeine can be either Schedule 2 of Schedule 5.

Overall, the Misuse of Drugs Act and Regulations aim to regulate and control the use of drugs in the UK, with the goal of reducing drug misuse and related harm.

Opioid Maintenance Therapy and Detoxification

Withdrawal symptoms can occur after as little as 5 days of regular opioid use. Short-acting opioids like heroin have acute withdrawal symptoms that peak in 32-72 hours and last for 3-5 days. Longer-acting opioids like methadone have acute symptoms that peak at day 4-6 and last for 10 days. Buprenorphine withdrawal lasts up to 10 days and includes symptoms like myalgia, anxiety, and increased drug craving.

Opioids affect the brain through opioid receptors, with the µ receptor being the main target for opioids. Dopaminergic cells in the ventral tegmental area produce dopamine, which is released into the nucleus accumbens upon stimulation of µ receptors, producing euphoria and reward. With repeat opioid exposure, µ receptors become less responsive, causing dysphoria and drug craving.

Methadone and buprenorphine are maintenance-oriented treatments for opioid dependence. Methadone is a full agonist targeting µ receptors, while buprenorphine is a partial agonist targeting µ receptors and a partial k agonist of functional antagonist. Naloxone and naltrexone are antagonists targeting all opioid receptors.

Methadone is preferred over buprenorphine for detoxification, and ultra-rapid detoxification should not be offered. Lofexidine may be considered for mild of uncertain dependence. Clonidine and dihydrocodeine should not be used routinely in opioid detoxification. The duration of detoxification should be up to 4 weeks in an inpatient setting and up to 12 weeks in a community setting.

Pregnant women dependent on opioids should use opioid maintenance treatment rather than attempt detoxification. Methadone is preferred over buprenorphine, and transfer to buprenorphine during pregnancy is not advised. Detoxification should only be considered if appropriate for the women’s wishes, circumstances, and ability to cope. Methadone or buprenorphine treatment is not a contraindication to breastfeeding.

Alcohol withdrawal is characterized by overactivity of the autonomic nervous system, resulting in symptoms such as agitation, tremors, sweating, nausea, vomiting, fever, and tachycardia. These symptoms typically begin 3-12 hours after drinking stops, peak between 24-48 hours, and can last up to 14 days. Withdrawal seizures may occur before blood alcohol levels reach zero, and a small percentage of people may experience delirium tremens (DT), which can be fatal if left untreated. Risk factors for DT include abnormal liver function, old age, severity of withdrawal symptoms, concurrent medical illness, heavy alcohol use, self-detox, previous history of DT, low potassium, low magnesium, and thiamine deficiency.

Pharmacologically assisted detox is often necessary for those who regularly consume more than 15 units of alcohol per day, and inpatient detox may be needed for those who regularly consume more than 30 units per day. The Clinical Institute Withdrawal Assessment of Alcohol Scale (CIWA-Ar) can be used to assess the severity of withdrawal symptoms and guide treatment decisions. Benzodiazepines are the mainstay of treatment, as chronic alcohol exposure results in decreased overall brain excitability and compensatory decrease of GABA-A neuroreceptor response to GABA. Chlordiazepoxide is a good first-line agent, while oxazepam, temazepam, and lorazepam are useful in patients with liver disease. Clomethiazole is effective but carries a high risk of respiratory depression and is not recommended. Thiamine should be offered to prevent Wernicke’s encephalopathy, and long-acting benzodiazepines can be used as prophylaxis for withdrawal seizures. Haloperidol is the treatment of choice if an antipsychotic is required.

A study has found that starting with a dose of 800 mg of Carbamazepine per day is just as effective as using Oxazepam for treating acute alcohol withdrawal. However, Phenytoin has been shown to be ineffective in treating seizures related to alcohol withdrawal. The symptoms of alcohol withdrawal are caused by a decrease in neurotransmission through type A gamma-aminobutyric pathways and an increase in neurotransmission through N-methyl-D-aspartate pathways. For more information, refer to the article Management of Drug and Alcohol Withdrawal by Kosten TR and O’Connor PG in the New England Journal of Medicine.

Illicit drugs, also known as illegal drugs, are substances that are prohibited by law and can have harmful effects on the body and mind. Some of the most commonly used illicit drugs in the UK include opioids, amphetamines, cocaine, MDMA (ecstasy), cannabis, and hallucinogens.

Opioids, such as heroin, are highly addictive and can cause euphoria, drowsiness, constipation, and respiratory depression. Withdrawal symptoms may include piloerection, insomnia, restlessness, dilated pupils, yawning, sweating, and abdominal cramps.

Amphetamines and cocaine are stimulants that can increase energy, cause insomnia, hyperactivity, euphoria, and paranoia. Withdrawal symptoms may include hypersomnia, hyperphagia, depression, irritability, agitation, vivid dreams, and increased appetite.

MDMA, also known as ecstasy, can cause increased energy, sweating, jaw clenching, euphoria, enhanced sociability, and increased response to touch. Withdrawal symptoms may include depression, insomnia, depersonalisation, and derealisation.

Cannabis, also known as marijuana of weed, can cause relaxation, intensified sensory experience, paranoia, anxiety, and injected conjunctiva. Withdrawal symptoms may include insomnia, reduced appetite, and irritability.

Hallucinogens, such as LSD, can cause perceptual changes, pupillary dilation, tachycardia, sweating, palpitations, tremors, and incoordination. There is no recognised withdrawal syndrome for hallucinogens.

Ketamine, also known as Vitamin K, Super K, Special K, of donkey dust, can cause euphoria, dissociation, ataxia, and hallucinations. There is no recognised withdrawal syndrome for ketamine.

The recommended initial treatment for opioid detoxification is methadone of buprenorphine.

Opioid Maintenance Therapy and Detoxification

Withdrawal symptoms can occur after as little as 5 days of regular opioid use. Short-acting opioids like heroin have acute withdrawal symptoms that peak in 32-72 hours and last for 3-5 days. Longer-acting opioids like methadone have acute symptoms that peak at day 4-6 and last for 10 days. Buprenorphine withdrawal lasts up to 10 days and includes symptoms like myalgia, anxiety, and increased drug craving.

Opioids affect the brain through opioid receptors, with the µ receptor being the main target for opioids. Dopaminergic cells in the ventral tegmental area produce dopamine, which is released into the nucleus accumbens upon stimulation of µ receptors, producing euphoria and reward. With repeat opioid exposure, µ receptors become less responsive, causing dysphoria and drug craving.

Methadone and buprenorphine are maintenance-oriented treatments for opioid dependence. Methadone is a full agonist targeting µ receptors, while buprenorphine is a partial agonist targeting µ receptors and a partial k agonist of functional antagonist. Naloxone and naltrexone are antagonists targeting all opioid receptors.

Methadone is preferred over buprenorphine for detoxification, and ultra-rapid detoxification should not be offered. Lofexidine may be considered for mild of uncertain dependence. Clonidine and dihydrocodeine should not be used routinely in opioid detoxification. The duration of detoxification should be up to 4 weeks in an inpatient setting and up to 12 weeks in a community setting.

Pregnant women dependent on opioids should use opioid maintenance treatment rather than attempt detoxification. Methadone is preferred over buprenorphine, and transfer to buprenorphine during pregnancy is not advised. Detoxification should only be considered if appropriate for the women’s wishes, circumstances, and ability to cope. Methadone or buprenorphine treatment is not a contraindication to breastfeeding.

Benzodiazepines and Addiction

Benzodiazepines are known to be addictive and should only be prescribed as a hypnotic or anxiolytic for a maximum of 4 weeks. Withdrawal symptoms can be physical of psychological, including stiffness, weakness, GI disturbance, paraesthesia, flu-like symptoms, visual disturbance, anxiety, insomnia, nightmares, depersonalisation, decreased memory and concentration, delusions, and hallucinations. Patients who wish to withdraw from short-acting benzodiazepines should first be converted to diazepam, which has a longer half-life and produces less severe withdrawal. The table provides approximate equivalent doses for different benzodiazepines. These guidelines are from the Maudsley Guidelines 10th Edition.

Alcohol withdrawal is characterized by overactivity of the autonomic nervous system, resulting in symptoms such as agitation, tremors, sweating, nausea, vomiting, fever, and tachycardia. These symptoms typically begin 3-12 hours after drinking stops, peak between 24-48 hours, and can last up to 14 days. Withdrawal seizures may occur before blood alcohol levels reach zero, and a small percentage of people may experience delirium tremens (DT), which can be fatal if left untreated. Risk factors for DT include abnormal liver function, old age, severity of withdrawal symptoms, concurrent medical illness, heavy alcohol use, self-detox, previous history of DT, low potassium, low magnesium, and thiamine deficiency.

Pharmacologically assisted detox is often necessary for those who regularly consume more than 15 units of alcohol per day, and inpatient detox may be needed for those who regularly consume more than 30 units per day. The Clinical Institute Withdrawal Assessment of Alcohol Scale (CIWA-Ar) can be used to assess the severity of withdrawal symptoms and guide treatment decisions. Benzodiazepines are the mainstay of treatment, as chronic alcohol exposure results in decreased overall brain excitability and compensatory decrease of GABA-A neuroreceptor response to GABA. Chlordiazepoxide is a good first-line agent, while oxazepam, temazepam, and lorazepam are useful in patients with liver disease. Clomethiazole is effective but carries a high risk of respiratory depression and is not recommended. Thiamine should be offered to prevent Wernicke’s encephalopathy, and long-acting benzodiazepines can be used as prophylaxis for withdrawal seizures. Haloperidol is the treatment of choice if an antipsychotic is required.

It is important to pay close attention to the question being asked. The question inquires about an item that was present in the original classification but not included in ICD-11. While salience is present in both classifications, the Edwards and Gross feature of ‘salience of drink seeking behaviour’ is equivalent to the ICD-11 feature of ‘Increasing precedence of alcohol use over other aspects of life’. The original classification included ‘rapid reinstatement of symptoms after a period of abstinence’, which is not present in ICD-11.

Alcohol Dependence Syndrome: ICD-11 and DSM 5 Criteria

The criteria for diagnosing alcohol dependence syndrome in the ICD-11 and DSM 5 are quite similar, as both are based on the original concept developed by Edwards and Gross in 1976. The original concept had seven elements, including narrowing of the drinking repertoire, salience of drink seeking behavior, tolerance, withdrawal symptoms, relief of withdrawal by further drinking, compulsion to drink, and rapid reinstatement of symptoms after a period of abstinence.

The DSM-5 Alcohol Use Disorder criteria include a problematic pattern of alcohol use leading to clinically significant impairment of distress, as manifested by at least two of the following occurring within a 12-month period. These include taking alcohol in larger amounts of over a longer period than intended, persistent desire of unsuccessful efforts to cut down of control alcohol use, spending a great deal of time in activities necessary to obtain alcohol, craving of a strong desire of urge to use alcohol, recurrent alcohol use resulting in a failure to fulfill major role obligations, continued alcohol use despite having persistent or recurrent social of interpersonal problems, giving up of reducing important social, occupational, of recreational activities due to alcohol use, recurrent alcohol use in physically hazardous situations, and continued alcohol use despite knowledge of having a persistent or recurrent physical or psychological problem caused or exacerbated by alcohol. Tolerance and withdrawal symptoms are also included in the criteria.

The ICD-11 Alcohol Dependence criteria include a pattern of recurrent episodic of continuous use of alcohol with evidence of impaired regulation of alcohol use, manifested by impaired control over alcohol use, increasing precedence of alcohol use over other aspects of life, and physiological features indicative of neuroadaptation to the substance, including tolerance to the effects of alcohol of a need to use increasing amounts of alcohol to achieve the same effect, withdrawal symptoms following cessation of reduction in use of alcohol, of repeated use of alcohol of pharmacologically similar substances to prevent of alleviate withdrawal symptoms. The features of dependence are usually evident over a period of at least 12 months, but the diagnosis may be made if use is continuous for at least 3 months.

Opiate withdrawal is more likely to result in diarrhoea than opiate use.

Illicit drugs, also known as illegal drugs, are substances that are prohibited by law and can have harmful effects on the body and mind. Some of the most commonly used illicit drugs in the UK include opioids, amphetamines, cocaine, MDMA (ecstasy), cannabis, and hallucinogens.

Opioids, such as heroin, are highly addictive and can cause euphoria, drowsiness, constipation, and respiratory depression. Withdrawal symptoms may include piloerection, insomnia, restlessness, dilated pupils, yawning, sweating, and abdominal cramps.

Amphetamines and cocaine are stimulants that can increase energy, cause insomnia, hyperactivity, euphoria, and paranoia. Withdrawal symptoms may include hypersomnia, hyperphagia, depression, irritability, agitation, vivid dreams, and increased appetite.

MDMA, also known as ecstasy, can cause increased energy, sweating, jaw clenching, euphoria, enhanced sociability, and increased response to touch. Withdrawal symptoms may include depression, insomnia, depersonalisation, and derealisation.

Cannabis, also known as marijuana of weed, can cause relaxation, intensified sensory experience, paranoia, anxiety, and injected conjunctiva. Withdrawal symptoms may include insomnia, reduced appetite, and irritability.

Hallucinogens, such as LSD, can cause perceptual changes, pupillary dilation, tachycardia, sweating, palpitations, tremors, and incoordination. There is no recognised withdrawal syndrome for hallucinogens.

Ketamine, also known as Vitamin K, Super K, Special K, of donkey dust, can cause euphoria, dissociation, ataxia, and hallucinations. There is no recognised withdrawal syndrome for ketamine.

Suboxone vs. Subutex: What’s the Difference?

Suboxone and Subutex are both medications used to treat opioid addiction. However, there are some key differences between the two.

Suboxone is a combination of buprenorphine and naloxone. The naloxone is added to prevent people from injecting the medication, as this was a common problem with pure buprenorphine tablets. If someone tries to inject Suboxone, the naloxone will cause intense withdrawal symptoms. However, if the tablet is swallowed as directed, the naloxone is not absorbed by the gut and does not cause any problems.

Subutex, on the other hand, contains only buprenorphine and does not include naloxone. This means that it may be more likely to be abused by injection, as there is no deterrent to prevent people from doing so.

Overall, both Suboxone and Subutex can be effective treatments for opioid addiction, but Suboxone may be a safer choice due to the addition of naloxone.

Korsakoff’s Syndrome

Korsakoff’s Syndrome, also known as amnesic syndrome, is a chronic condition that affects recent and anterograde memory in an alert and responsive patient. It is caused by prolonged thiamine (vitamin B1) deficiency and often follows Wernicke’s encephalopathy. The syndrome is characterized by a lack of insight, apathy, and confabulation. Thiamine is essential for glucose metabolism in the brain, and its deficiency leads to a toxic buildup of glucose, causing neuronal loss. The Mammillary bodies are the main areas affected in Korsakoff’s syndrome.

While intelligence on the WAIS is preserved, episodic memory is severely affected in Korsakoff’s syndrome. Semantic memory is variably affected, but implicit aspects of memory, such as response to priming and procedural memory, are preserved. Immediate memory tested with the digit span is normal, but information can only be retained for a few minutes at most. Patients with Korsakoff’s syndrome often display apathy, lack of initiative, and profound lack of insight.

Source: Kopelman M (2009) The Korsakoff Syndrome: Clinical Aspects, Psychology and Treatment. Alcohol and Alcoholism 44 (2): 148-154.

The man’s symptoms of agitation and hallucinations could be attributed to a psychotic illness, but the presence of a sustained tachycardia suggests another underlying condition. Based on the delayed presentation and the complete set of symptoms, delirium tremens is the most probable explanation. While meningitis is a possibility, it is less likely than delirium tremens, which is a common condition.

Alcohol withdrawal is characterized by overactivity of the autonomic nervous system, resulting in symptoms such as agitation, tremors, sweating, nausea, vomiting, fever, and tachycardia. These symptoms typically begin 3-12 hours after drinking stops, peak between 24-48 hours, and can last up to 14 days. Withdrawal seizures may occur before blood alcohol levels reach zero, and a small percentage of people may experience delirium tremens (DT), which can be fatal if left untreated. Risk factors for DT include abnormal liver function, old age, severity of withdrawal symptoms, concurrent medical illness, heavy alcohol use, self-detox, previous history of DT, low potassium, low magnesium, and thiamine deficiency.

Pharmacologically assisted detox is often necessary for those who regularly consume more than 15 units of alcohol per day, and inpatient detox may be needed for those who regularly consume more than 30 units per day. The Clinical Institute Withdrawal Assessment of Alcohol Scale (CIWA-Ar) can be used to assess the severity of withdrawal symptoms and guide treatment decisions. Benzodiazepines are the mainstay of treatment, as chronic alcohol exposure results in decreased overall brain excitability and compensatory decrease of GABA-A neuroreceptor response to GABA. Chlordiazepoxide is a good first-line agent, while oxazepam, temazepam, and lorazepam are useful in patients with liver disease. Clomethiazole is effective but carries a high risk of respiratory depression and is not recommended. Thiamine should be offered to prevent Wernicke’s encephalopathy, and long-acting benzodiazepines can be used as prophylaxis for withdrawal seizures. Haloperidol is the treatment of choice if an antipsychotic is required.

Individuals who smoked cannabis regularly at the age of 15 have a 4.5 times higher risk of developing schizophrenia at the age of 26, whereas those who did not report regular use until the age of 18 have a 1.65 times higher risk.

Schizophrenia and Cannabis Use

The relationship between cannabis use and the risk of developing schizophrenia is a topic of ongoing debate. However, research suggests that cannabis use may increase the risk of later schizophrenia of schizophreniform disorder by two-fold (Arseneault, 2004). The risk of developing schizophrenia appears to be higher in individuals who start using cannabis at a younger age. For instance, regular cannabis smokers at the age of 15 are 4.5 times more likely to develop schizophrenia at the age of 26, compared to those who did not report regular use until age 18 (Murray, 2004).

A systematic review published in the Lancet in 2007 found that the lifetime risk of developing psychosis increased by 40% in individuals who had ever used cannabis (Moore, 2007). Another meta-analysis reported that the age at onset of psychosis was 2.70 years younger in cannabis users than in non-users (Large, 2011). These findings suggest that cannabis use may have a significant impact on the development of schizophrenia and related disorders.

Synthetic opioids like methadone and buprenorphine are utilized as a replacement for heroin. Alpha2 adrenergic agonists such as clonidine and lofexidine are employed in detox settings to alleviate a range of opioid withdrawal symptoms.

Opioid Maintenance Therapy and Detoxification

Withdrawal symptoms can occur after as little as 5 days of regular opioid use. Short-acting opioids like heroin have acute withdrawal symptoms that peak in 32-72 hours and last for 3-5 days. Longer-acting opioids like methadone have acute symptoms that peak at day 4-6 and last for 10 days. Buprenorphine withdrawal lasts up to 10 days and includes symptoms like myalgia, anxiety, and increased drug craving.

Opioids affect the brain through opioid receptors, with the µ receptor being the main target for opioids. Dopaminergic cells in the ventral tegmental area produce dopamine, which is released into the nucleus accumbens upon stimulation of µ receptors, producing euphoria and reward. With repeat opioid exposure, µ receptors become less responsive, causing dysphoria and drug craving.

Methadone and buprenorphine are maintenance-oriented treatments for opioid dependence. Methadone is a full agonist targeting µ receptors, while buprenorphine is a partial agonist targeting µ receptors and a partial k agonist of functional antagonist. Naloxone and naltrexone are antagonists targeting all opioid receptors.

Methadone is preferred over buprenorphine for detoxification, and ultra-rapid detoxification should not be offered. Lofexidine may be considered for mild of uncertain dependence. Clonidine and dihydrocodeine should not be used routinely in opioid detoxification. The duration of detoxification should be up to 4 weeks in an inpatient setting and up to 12 weeks in a community setting.

Pregnant women dependent on opioids should use opioid maintenance treatment rather than attempt detoxification. Methadone is preferred over buprenorphine, and transfer to buprenorphine during pregnancy is not advised. Detoxification should only be considered if appropriate for the women’s wishes, circumstances, and ability to cope. Methadone or buprenorphine treatment is not a contraindication to breastfeeding.

Illicit drugs, also known as illegal drugs, are substances that are prohibited by law and can have harmful effects on the body and mind. Some of the most commonly used illicit drugs in the UK include opioids, amphetamines, cocaine, MDMA (ecstasy), cannabis, and hallucinogens.

Opioids, such as heroin, are highly addictive and can cause euphoria, drowsiness, constipation, and respiratory depression. Withdrawal symptoms may include piloerection, insomnia, restlessness, dilated pupils, yawning, sweating, and abdominal cramps.

Amphetamines and cocaine are stimulants that can increase energy, cause insomnia, hyperactivity, euphoria, and paranoia. Withdrawal symptoms may include hypersomnia, hyperphagia, depression, irritability, agitation, vivid dreams, and increased appetite.

MDMA, also known as ecstasy, can cause increased energy, sweating, jaw clenching, euphoria, enhanced sociability, and increased response to touch. Withdrawal symptoms may include depression, insomnia, depersonalisation, and derealisation.

Cannabis, also known as marijuana of weed, can cause relaxation, intensified sensory experience, paranoia, anxiety, and injected conjunctiva. Withdrawal symptoms may include insomnia, reduced appetite, and irritability.

Hallucinogens, such as LSD, can cause perceptual changes, pupillary dilation, tachycardia, sweating, palpitations, tremors, and incoordination. There is no recognised withdrawal syndrome for hallucinogens.

Ketamine, also known as Vitamin K, Super K, Special K, of donkey dust, can cause euphoria, dissociation, ataxia, and hallucinations. There is no recognised withdrawal syndrome for ketamine.

People who lack thiamine may experience Wernicke’s syndrome as a result of intravenous glucose administration.

Wernicke’s Encephalopathy: Symptoms, Causes, and Treatment

Wernicke’s encephalopathy is a serious condition that is characterized by confusion, ophthalmoplegia, and ataxia. However, the complete triad is only present in 10% of cases, which often leads to underdiagnosis. The condition results from prolonged thiamine deficiency, which is commonly seen in people with alcohol dependency, but can also occur in other conditions such as anorexia nervosa, malignancy, and AIDS.

The onset of Wernicke’s encephalopathy is usually abrupt, but it may develop over several days to weeks. The lesions occur in a symmetrical distribution in structures surrounding the third ventricle, aqueduct, and fourth ventricle. The mammillary bodies are involved in up to 80% of cases, and atrophy of these structures is specific for Wernicke’s encephalopathy.

Treatment involves intravenous thiamine, as oral forms of B1 are poorly absorbed. IV glucose should be avoided when thiamine deficiency is suspected as it can precipitate of exacerbate Wernicke’s. With treatment, ophthalmoplegia and confusion usually resolve within days, but the ataxia, neuropathy, and nystagmus may be prolonged of permanent.

Untreated cases of Wernicke’s encephalopathy can lead to Korsakoff’s syndrome, which is characterized by memory impairment associated with confabulation. The mortality rate associated with Wernicke’s encephalopathy is 10-20%, making early diagnosis and treatment crucial.

Schizophrenia and Cannabis Use

The relationship between cannabis use and the risk of developing schizophrenia is a topic of ongoing debate. However, research suggests that cannabis use may increase the risk of later schizophrenia of schizophreniform disorder by two-fold (Arseneault, 2004). The risk of developing schizophrenia appears to be higher in individuals who start using cannabis at a younger age. For instance, regular cannabis smokers at the age of 15 are 4.5 times more likely to develop schizophrenia at the age of 26, compared to those who did not report regular use until age 18 (Murray, 2004).

A systematic review published in the Lancet in 2007 found that the lifetime risk of developing psychosis increased by 40% in individuals who had ever used cannabis (Moore, 2007). Another meta-analysis reported that the age at onset of psychosis was 2.70 years younger in cannabis users than in non-users (Large, 2011). These findings suggest that cannabis use may have a significant impact on the development of schizophrenia and related disorders.

Smoking cessation can be achieved through various methods, including nicotine replacement therapy (NRT), bupropion, and varenicline. NRT is available in different forms, including patches, gum, lozenges, inhalators, and nasal spray. Combination treatment with NRT has been found to be more effective than a single product of placebo. Bupropion is a selective inhibitor of dopamine and noradrenaline reuptake and is presumed to work directly on the brain pathways involved in addiction and withdrawal. It is recommended to start bupropion while still smoking and to discontinue after 7-9 weeks. Varenicline is a partial nicotinic receptor agonist that reduces the rewarding and reinforcing effects of smoking. It is recommended to start varenicline while still smoking and to continue for 12 weeks. Nausea is the most common adverse effect of varenicline, and depression has been reported in some users. Bupropion and varenicline should be avoided in certain populations, including those with a history of bipolar disorder, epilepsy, and pregnancy of breastfeeding.

The low potential for dependence on cannabis is widely acknowledged.

Cannabis, also known as marijuana, grass, pot, weed, tea, of Mary Jane, is a plant that contains over 60 unique cannabinoids. The primary psychoactive component of cannabis is delta-9-tetrahydrocannabinol (Delta 9-THC), which is rapidly converted into 11-hydroxy-delta 9-THC, the active metabolite in the central nervous system. Specific cannabinoid receptors, including CB1 and CB2 receptors, have been identified in the body. CB1 receptors are found mainly at nerve terminals, where they inhibit transmitter release, while CB2 receptors occur mainly on immune cells and modulate cytokine release. The cannabinoid receptor is found in highest concentrations in the basal ganglia, hippocampus, and cerebellum, with lower concentrations in the cerebral cortex. Cannabis use has been associated with the amotivational syndrome, characterized by apathy, anergy, weight gain, and a lack of persistence in tasks requiring prolonged attention of tenacity.

Pregnancy and Alcohol

The advice on safe drinking levels during pregnancy varies, but the most recent recommendation is to abstain from alcohol completely. According to NICE, pregnant women of those planning a pregnancy should avoid alcohol altogether to minimize risks to the fetus. This aligns with the UK Chief Medical Officers’ Alcohol Guidelines Review from 2016. It is recommended to follow this guideline to ensure the safety of the developing baby.

Motivational Interviewing: A Model for Resolving Ambivalence and Facilitating Change

Motivational interviewing (MI) is an evidence-based method used for people with substance misuse problems. It was introduced by William Miller in 1983, based on his experience with alcoholics. MI focuses on exploring and resolving ambivalence and centres on the motivational process that facilitates change. It is based on three key elements: collaboration, evocation, and autonomy.

There are four principles of MI: expressing empathy, supporting self-efficacy, rolling with resistance, and developing discrepancy. MI involves the use of micro-counseling skills called OARS, which stands for open-ended questions, affirmations, reflections, and summaries.

Change talk is defined as statements by the client that reveal consideration of, motivation for, of commitment to change. In MI, the therapist aims to guide the client to expression of change talk. Types of change talk can be remembered by the mnemonic DARN-CAT, which stands for desire, ability, reason, need, commitment, activation, and taking steps.

Overall, MI is a model for resolving ambivalence and facilitating change that emphasizes collaboration, evocation, and autonomy. It is a useful tool for therapists working with clients with substance misuse problems.