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 patient’s symptoms suggest the presence of Schneider’s first rank symptom, which is characterized by actions perceived as influenced of made by external agents. It is important to note that amphetamines can cause drug-induced psychosis, which can mimic schizophrenia. While benzodiazepines are not known to induce schizophrenia, there have been reports of auditory hallucinations during benzodiazepine withdrawal. On the other hand, GHB is not associated with drug-induced schizophrenia, and while opiates may cause hallucinations, they do not typically result in Schneider’s first rank symptoms. It is important to consider the possibility of a dual-diagnosis scenario, where the patient may have both a drug dependency and schizophrenia, which may have been triggered by drug use of stress, but is not solely drug-induced.

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 duration of cannabis in the system may vary, but it typically lasts for weeks rather than just a few hours of days. However, if cannabis is used only once, it may only be detectable for a period of 6-24 hours.

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.

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.

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 most prevalent indication of benzodiazepine withdrawal is insomnia.

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.

Project MATCH: Investigating the Best Treatment for Alcoholics

Project MATCH was an extensive research study that spanned over 8 years and aimed to determine which types of alcoholics respond best to which forms of treatment. The study investigated three types of treatment: Cognitive Behavioural Coping Skills Therapy, Motivational Enhancement Therapy, and Twelve-Step Facilitation Therapy.

Cognitive Behavioural Coping Skills Therapy focused on correcting poor self-esteem and distorted, negative, and self-defeating thinking. Motivational Enhancement Therapy helped clients become aware of and build on personal strengths that could improve their readiness to quit. Twelve-Step Facilitation Therapy was designed to familiarize patients with the AA philosophy and encourage participation.

After the study, it was concluded that patient-treatment matching is not necessary in alcoholism treatment because the three techniques are equally effective. This study provides valuable insights into the treatment of alcoholism and can help healthcare professionals make informed decisions about the best treatment options for their patients.

The fact that even brief periods of opiate use can lead to withdrawal symptoms highlights the addictive nature of these drugs.

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.

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.

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.

Standard practice should be followed when petechial hemorrhages are observed in an MRI of a patient with Wernicke’s, as they are a typical characteristic of the disease.

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.

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.

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.

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.

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.

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 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.

Alcohol intoxication typically results in a decrease in reflexes and an increase in reaction times.

Alcohol Intoxication

Symptoms of moderate alcohol intoxication can include a range of effects on the body and mind. These may include poor concentration, impaired reaction times, conjunctival injection, pinpoint pupils, poor coordination, memory difficulties, impaired judgement, and impaired sense of time and space. It is important to be aware of these symptoms and to avoid driving of operating heavy machinery while under the influence of alcohol.

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.

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.

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.

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.

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.

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.

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 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.

Poppers, also known as liquid gold, amyl of butyl nitrite, are not considered illegal to purchase of possess under the MDA. They are commonly sold in sex shops, joke shops, and other retail locations frequented by young people, such as pubs, clubs, tobacconists, music stores, and clothing shops. While the legality of poppers has not been fully tested in court, the Medicines Control Agency has classified them as a medicine and therefore subject to the Medicines Act 1968. This means that only licensed outlets, such as chemists, are permitted to sell the drug. Additionally, poppers are not regulated under the Psychoactive Substances Act 2016.

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.