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.

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.

Testing for drugs cannot be done through nasal mucus.

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.

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.

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.

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.

The Stages of Change Model does not view relapse as a stage in the process.

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.

Heroin Nephropathy: A Study on Clinicopathology and Epidemiology

Intravenous heroin use has been linked to a rare condition called nephropathy, which affects the kidneys and is likely caused by bacterial infection. This condition is more commonly observed in African-American men, although the reasons for this are not yet understood. The American Journal of Medicine published a study in 1980 that examined the clinicopathologic and epidemiologic aspects of heroin-associated nephropathy.

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.

Individuals who have ingested PCP often exhibit difficulty with coordination and speech. The hallucinations experienced are typically intricate rather than straightforward. It is more likely for them to have excessive saliva production rather than a dry mouth.

PCP Intoxication: A Dangerous Hallucinogenic

Phencyclidine (PCP), also known as angel dust, is a hallucinogenic drug that is popular for inducing feelings of euphoria, superhuman strength, and social and sexual prowess. It is a NMDA receptor antagonist that has dissociative properties, similar to ketamine. PCP was previously used as an anesthetic and animal tranquilizer, but was soon recalled due to its adverse effects, including psychosis, agitation, and dysphoria post-operatively.

PCP is available in various forms, including white crystalline powder, tablets, crystals, and liquid. It can be snorted, smoked, ingested, of injected intravenously or subcutaneously. People who have taken PCP often present with violent behavior, nystagmus, tachycardia, hypertension, anesthesia, and analgesia. Other symptoms include impaired motor function, hallucinations, delusions, and paranoia.

PCP intoxication is best managed with benzodiazepines along with supportive measures for breathing and circulation. Antipsychotics are not recommended as they can amplify PCP-induced hyperthermia, dystonic reactions, and lower the seizure threshold. However, haloperidol may be useful for treating PCP-induced psychosis in patients who are not hyperthermic. Most deaths in PCP-intoxicated patients result from violent behavior rather than direct effects of the drug.

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.

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.

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.

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.

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.

It is not recommended to offer opioid detoxification to individuals with urgent medical conditions. However, for those in police custody of serving a short prison sentence, of those presenting in an acute of emergency setting, consideration should be given to treating opioid withdrawal symptoms with medication and referring them to further drug services as needed. If an individual seeking opioid detoxification also misuses alcohol, healthcare professionals should address their alcohol misuse, as it may worsen during opioid withdrawal of be substituted for previous opioid misuse. For those who are alcohol dependent, alcohol detoxification should be offered before starting opioid detoxification in a community of prison setting, but can be done concurrently with opioid detoxification in an inpatient setting of with stabilisation in a community setting.

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.

The vignette depicts delirium tremens (DTs), which is characterized by confusion, hallucinations, and autonomic hyperactivity. Typically, these symptoms appear 2 to 3 days after cessation of alcohol consumption and can worsen over the next few days. Mild withdrawal symptoms such as anxiety, tremors, headache, nausea, vomiting, insomnia, and sweating may occur within 6 hours of stopping drinking. Hallucinations may occur 12-24 hours after cessation, and seizures may occur within 24 to 48 hours.

Benzodiazepines, such as chlordiazepoxide, are commonly used to treat alcohol withdrawal, with a reducing regime. Lorazepam, due to its short half-life, is preferred as the first-line treatment for DTs. The Clinical Institute Withdrawal Assessment of Alcohol Scale (CIWA-Ar) can be used to assess alcohol withdrawal.

The symptom clusters mentioned are commonly associated with cannabis withdrawal, with the exception of dilation of pupils and diarrhea, which are more commonly associated with opiate withdrawal. This has led to calls for cannabis withdrawal to be recognized as a clinically significant issue and included in future diagnostic criteria.

It is uncommon for individuals experiencing alcohol withdrawal to have transient hallucinations, as they are not a typical symptom.

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.

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.

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.

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.

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.

Higher doses of naloxone are required to displace buprenorphine due to its strong affinity for opioid receptors, which can also result in a blocking effect and precipitated withdrawal if a patient is still using heroin.

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.

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.

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.

The symptoms indicate a possible case of pellagra, a condition caused by a deficiency in vitamin B3 (niacin). Pellagra can also cause ataxia. It is important to note that vitamin B1 is thiamine, and vitamin B2 is riboflavin.

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.