Asenapine exhibits affinity towards D2, 5HT2A, 5HT2C, and α1/α2 adrenergic receptors, while having relatively low affinity for H1 and ACh receptors. This makes it a second generation antipsychotic that is approved for the treatment of moderate to severe manic episodes associated with bipolar disorder. Its low affinity for H1 receptors is believed to contribute to its metabolically-neutral profile.

Projection is a coping mechanism in which one assigns their own unacceptable emotions and desires onto another person, thereby alleviating the discomfort of having conflicting feelings that do not align with their self-perception.

The Lazarus theory and the attribution theory share similarities.

Theories of Emotion

In membership exams, four main theories of emotion are commonly discussed: James-Lange theory, Cannon-Bard theory, Singer-Schachter theory, and Lazarus theory. The key to understanding the differences between these theories is to identify where the stimulus for the emotion arises.

According to the James-Lange theory, emotions occur as a result of bodily sensations. For instance, if you see a big dog, your heart races, and you feel afraid. This theory proposes that certain external stimuli stimulate specific sensory organs, leading to a particular emotion. The sequence of events suggested by this theory is as follows: event – arousal – interpretation – emotion. In other words, the stimulus for emotion arises from physical sensations.

The Cannon-Bard theory, also known as the thalami theory, proposes that when an event occurs, one experiences an emotion at the same time as physiological changes. The stimulus for emotion arises simultaneously in the body and the mind.

The Singer-Schachter theory, also known as the two-factor theory, suggests that emotions result from both physiological changes and the context. For example, if your heart is racing, and you are about to have an exam, you label yourself as afraid. However, if your heart is racing, and you are about to kiss your partner, you label your emotional state as excited. The stimulus for emotion arises via a combination of physical sensations and the mind’s appraisal of them.

Finally, the Lazarus theory proposes that a thought is required before an emotion occurs. For instance, if you see a big dog, you think it is going to bite you, and you feel afraid. The stimulus for emotion arises from the mind.

In summary, these theories offer different perspectives on the relationship between physical sensations, cognitive processes, and emotions.

Excitatory neurotransmitters include glutamate, histamine, acetylcholine, and noradrenaline, as they increase ion flow and the likelihood of action potential in neurons. However, GABA functions as an inhibitory neurotransmitter, reducing ion flow and decreasing the probability of action potential.

– A Battle’s sign is a physical indication of a basal skull fracture.
– Babinski’s sign is a clinical sign that suggests an upper motor neuron lesion.
– Kernig’s sign is a clinical sign that indicates meningeal irritation.
– Russell’s sign is characterized by scarring on the knuckles and back of the hand, and it is indicative of repeated induced vomiting.

Hoover’s Sign for Differentiating Organic and Functional Weakness

Functional weakness refers to weakness that is inconsistent with any identifiable neurological disease and may be diagnosed as conversion disorder of dissociative motor disorder. To differentiate between organic and functional weakness of pyramidal origin, Dr. Charles Franklin Hoover described Hoover’s sign over 100 years ago.

This test is typically performed on the lower limbs and is useful when the nature of hemiparesis is uncertain. When a person with organic hemiparesis is asked to flex the hip of their normal leg against resistance, they will not exert pressure on the examiner’s hand placed under the heel on the affected side. However, in hysterical weakness, the examiner will feel increased pressure on their hand. Hoover’s sign is a valuable tool for distinguishing between organic and functional weakness.

It is not recommended to combine MAOIs with SSRIs, clomipramine, of ephedrine.

MAOIs: A Guide to Mechanism of Action, Adverse Effects, and Dietary Restrictions

First introduced in the 1950s, MAOIs were the first antidepressants introduced. However, they are not the first choice in treating mental health disorders due to several dietary restrictions and safety concerns. They are only a treatment option when all other medications are unsuccessful. MAOIs may be particularly useful in atypical depression (over eating / over sleeping, mood reactivity).

MAOIs block the monoamine oxidase enzyme, which breaks down different types of neurotransmitters from the brain: norepinephrine, serotonin, dopamine, as well as tyramine. There are two types of monoamine oxidase, A and B. The MOA A are mostly distributed in the placenta, gut, and liver, but MOA B is present in the brain, liver, and platelets. Selegiline and rasagiline are irreversible and selective inhibitors of MAO type B, but safinamide is a reversible and selective MAO B inhibitor.

The most common adverse effects of MAOIs occurring early in treatment are orthostatic hypotension, daytime sleepiness, insomnia, and nausea; later common effects include weight gain, muscle pain, myoclonus, paraesthesia, and sexual dysfunction.

Pharmacodynamic interactions with MAOIs can cause two types of problem: serotonin syndrome (mainly due to SSRIs) and elevated blood pressure (caused by indirectly acting sympathomimetic amines releasers, like pseudoephedrine and phenylephrine). The combination of MAOIs and some TCAs appears safe. Only those TCAs with significant serotonin reuptake inhibition (clomipramine and imipramine) are likely to increase the risk of serotonin syndrome.

Tyramine is a monoamine found in various foods, and is an indirect sympathomimetic that can cause a hypertensive reaction in patients receiving MAOI therapy. For this reason, dietary restrictions are required for patients receiving MAOIs. These restrictions include avoiding matured/aged cheese, fermented sausage, improperly stored meat, fava of broad bean pods, and certain drinks such as on-tap beer. Allowed foods include fresh cottage cheese, processed cheese slices, fresh packaged of processed meat, and other alcohol (no more than two bottled or canned beers of two standard glasses of wine, per day).

Serotonin Syndrome and Neuroleptic Malignant Syndrome are two conditions that can be difficult to differentiate. Serotonin Syndrome is caused by excess serotonergic activity in the CNS and is characterized by neuromuscular abnormalities, altered mental state, and autonomic dysfunction. On the other hand, Neuroleptic Malignant Syndrome is a rare acute disorder of thermoregulation and neuromotor control that is almost exclusively caused by antipsychotics. The symptoms of both syndromes can overlap, but there are some distinguishing clinical features. Hyper-reflexia, ocular clonus, and tremors are more prominent in Serotonin Syndrome, while Neuroleptic Malignant Syndrome is characterized by uniform ‘lead-pipe’ rigidity and hyporeflexia. Symptoms of Serotonin Syndrome usually resolve within a few days of stopping the medication, while Neuroleptic Malignant Syndrome can take up to 14 days to remit with appropriate treatment. The following table provides a useful guide to the main differentials of Serotonin Syndrome and Neuroleptic Malignant Syndrome.

Heritability: Understanding the Concept

Heritability is a concept that is often misunderstood. It is not a measure of the extent to which genes cause a condition in an individual. Rather, it is the proportion of phenotypic variance attributable to genetic variance. In other words, it tells us how much of the variation in a condition seen in a population is due to genetic factors. Heritability is calculated using statistical techniques and can range from 0.0 to 1.0. For human behavior, most estimates of heritability fall in the moderate range of .30 to .60.

The quantity (1.0 – heritability) gives the environment ability of the trait. This is the proportion of phenotypic variance attributable to environmental variance. The following table provides estimates of heritability for major conditions:

Condition Heritability estimate (approx)
ADHD 85%
Autism 70%
Schizophrenia 55%
Bipolar 55%
Anorexia 35%
Alcohol dependence 35%
Major depression 30%
OCD 25%

It is important to note that heritability tells us nothing about individuals. It is a population-level measure that helps us understand the relative contributions of genetic and environmental factors to a particular condition.

SUDEP, of sudden unexpected death in epilepsy, is a condition where patients with epilepsy die suddenly and unexpectedly without any apparent cause. It is estimated to be responsible for 20-30% of deaths in epilepsy patients. The condition is more common in adults than in children, affecting 1 in 1,000 adults with epilepsy per year. The main risk factor for SUDEP is having active generalised tonic clonic seizures (GTCS), and better control of these seizures through improved compliance can reduce the risk of SUDEP. Other risk factors include nocturnal seizures, lamotrigine, never having been treated with an antiepileptic drug, intellectual disability, and male sex. However, the evidence for these factors is considered low. Autopsy findings in SUDEP cases do not reveal any specific cause of death, but obstruction of the airways and cardiorespiratory events such as arrhythmia are thought to be possible mechanisms.

Drug Interactions: Understanding the Different Types

Drug interactions can occur in different ways, and it is important to understand the different types to avoid potential harm. Pharmacokinetic drug interactions happen when one drug affects the metabolism, absorption, of excretion of another drug. This can be due to enzyme induction of inhibition, changes in gastrointestinal tract motility and pH, chelation, competition for renal tubular transport, of changes in protein binding. On the other hand, pharmacodynamic drug interactions occur when one drug directly alters the effect of another drug. This can happen through synergism, antagonism, of interaction at receptors, such as allosteric modulation. It is important to note that pharmacodynamic drug interactions do not involve any absorption, distribution, metabolism, of excretion processes directly. By understanding the different types of drug interactions, healthcare professionals can better manage patients’ medications and prevent potential adverse effects.

Inflammatory Cytokines and Mental Health

Research has suggested that an imbalance in the immune system, particularly the pro-inflammatory cytokines, may play a significant role in the development of common mental disorders. The strongest evidence is found in depression, where studies have shown increased levels of inflammatory markers, such as interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), and c-reactive protein (CRP), in depressed individuals compared to healthy controls (Santoft, 2020).

While most studies have focused on the differences in inflammatory markers between depressed and healthy individuals, some have also found a correlation between higher levels of inflammation and more severe depressive symptoms. The underlying cause of this chronic low-grade inflammation is not yet fully understood, but potential factors include psychosocial stress, physical inactivity, poor diet, smoking, obesity, altered gut permeability, disturbed sleep, and vitamin D deficiency.

Valproate can cause weight gain, which is particularly concerning when it is combined with other medications like clozapine.

Valproate: Forms, Doses, and Adverse Effects

Valproate comes in three forms: semi-sodium valproate, valproic acid, and sodium valproate. Semi-sodium valproate is a mix of sodium valproate and valproic acid and is licensed for acute mania associated with bipolar disorder. Valproic acid is also licensed for acute mania, but this is not consistent with the Maudsley Guidelines. Sodium valproate is licensed for epilepsy. It is important to note that doses of sodium valproate and semi-sodium valproate are not the same, with a slightly higher dose required for sodium valproate.

Valproate is associated with many adverse effects, including nausea, tremor, liver injury, vomiting/diarrhea, gingival hyperplasia, memory impairment/confusional state, somnolence, weight gain, anaemia/thrombocytopenia, alopecia (with curly regrowth), severe liver damage, and pancreatitis. Increased liver enzymes are common, particularly at the beginning of therapy, and tend to be transient. Vomiting and diarrhea tend to occur at the start of treatment and remit after a few days. Severe liver damage is most likely to occur in the first six months of therapy, with the maximum risk being between two and twelve weeks. The risk also declines with advancing age.

Valproate is a teratogen and should not be initiated in women of childbearing potential. Approximately 10% of children exposed to valproate monotherapy during pregnancy suffer from congenital malformations, with the risk being dose-dependent. The most common malformations are neural tube defects, facial dysmorphism, cleft lip and palate, craniostenosis, cardiac, renal and urogenital defects, and limb defects. There is also a dose-dependent relationship between valproate and developmental delay, with approximately 30-40% of children exposed in utero experiencing delay in their early development, such as talking and walking later, lower intellectual abilities, poor language skills, and memory problems. There is also a thought to be a 3-fold increase of autism in children exposed in utero.

Clozapine is an atypical antipsychotic drug that acts as an antagonist at various receptors, including dopamine, histamine, serotonin, adrenergic, and cholinergic receptors. It is mainly metabolized by CYP1A2, and its plasma levels can be affected by inducers and inhibitors of this enzyme. Clozapine is associated with several side effects, including drowsiness, constipation, weight gain, and hypersalivation. Hypersalivation is a paradoxical side effect, and its mechanism is not fully understood, but it may involve clozapine agonist activity at the muscarinic M4 receptor and antagonist activity at the alpha-2 adrenoceptor. Clozapine is also associated with several potentially dangerous adverse events, including agranulocytosis, myocarditis, seizures, severe orthostatic hypotension, increased mortality in elderly patients with dementia-related psychosis, colitis, pancreatitis, thrombocytopenia, thromboembolism, and insulin resistance and diabetes mellitus. The BNF advises caution in using clozapine in patients with prostatic hypertrophy, susceptibility to angle-closure glaucoma, and adults over 60 years. Valproate should be considered when using high doses of clozapine, plasma levels > 0.5 mg/l, of when the patient experiences seizures. Myocarditis is a rare but potentially fatal adverse event associated with clozapine use, and its diagnosis is based on biomarkers and clinical features. The mortality rate of clozapine-induced myocarditis is high, and subsequent use of clozapine in such cases leads to recurrence of myocarditis in most cases.

Topiramate is a medication used for epilepsy and bipolar affective disorder. It works by inhibiting voltage gated sodium channels and increasing GABA levels. Unlike most psychotropic drugs, it is associated with weight loss.

Tom Beauchamp and James Childress, American philosophers, and Raanan Gillon, a British doctor and philosopher, were the pioneers of the following fundamental principles: autonomy, which involves respecting patients’ freedom of choice and wishes; beneficence, which entails acting in the best interests of patients; non-maleficence, which requires avoiding harm (primum non nocere); and justice, which involves treating problems equally and distributing resources fairly to those in need. These four principles serve as the primary guiding principles in current practice, and most other ethical discussions relevant to clinical practice can be categorized under these topics.

Hyponatremia in Psychiatric Patients

Hyponatremia, of low serum sodium, can occur in psychiatric patients due to the disorder itself, its treatment, of other medical conditions. Symptoms include nausea, confusion, seizures, and muscular cramps. Drug-induced hyponatremia is known as the syndrome of inappropriate antidiuretic hormone hypersecretion (SIADH), which results from excessive secretion of ADH and fluid overload. Diagnosis is based on clinically euvolaemic state with low serum sodium and osmolality, raised urine sodium and osmolality. SSRIs, SNRIs, and tricyclics are the most common drugs that can cause SIADH. Risk factors for SIADH include starting a new drug, and treatment usually involves fluid restriction and sometimes demeclocycline.

In the given example, Mark is using sublimation as a defence mechanism to express his internal impulses in a socially acceptable way. It is not an example of aggression. Similarly, playing tennis cannot be considered as constructive gratifying service to others, which is a characteristic of altruism. Instead, it is an example of displacement, where Mark is transferring his emotional response to a situation that carries less emotional risk. Mark is externalizing his feelings through sublimation, rather than turning them into self-harm.

Classical Conditioning: A Learning Theory by Ivan Pavlov

Classical conditioning is a learning theory developed by Ivan Pavlov. It suggests that events that occur together are associated and acquire a similar meaning. Unlike operant conditioning, which focuses on responses to behavior, classical conditioning looks at responses to stimuli. In classical conditioning, animals behave as if they have learned to associate a stimulus with a significant event. Pavlov demonstrated that innate responses, such as a dog salivating when it sees food, can be associated with a neutral stimulus, such as ringing a bell, so that ringing the bell can cause salivation even in the absence of food.

Important terms used in classical conditioning include stimulus generalization and discrimination, higher order conditioning, spontaneous recovery, and aversive conditioning. Extinction is the laboratory analogue of exposure therapy for anxiety disorders, while Counterconditioning involves pairing a feared conditioned stimulus with a positive outcome. Incubation occurs in fear responses, and reciprocal inhibition is a technique that aims to replace an undesired response with a desired one by counterconditioning. Some stimuli are more prone to conditioning than others, which is referred to as stimulus/biological preparedness.

B.F. Skinner, a prominent figure in the field of psychology, is renowned for his contributions to the theory of reinforcement within the behaviourist perspective.

Neo-Freudians were therapists who developed their own theories while still retaining core Freudian components. Some important neo-Freudians include Alfred Adler, Carl Jung, Erik Erickson, Harry Stack Sullivan, Wilfred Bion, John Bowlby, Anna Freud, Otto Kernberg, Margaret Mahler, and Donald Winnicott. Each of these individuals contributed unique ideas to the field of psychology. For example, Carl Jung introduced the concept of the persona and differentiated between the personal and collective unconscious, while Erik Erickson is known for his stages of psychosocial development. Margaret Mahler developed theories on child development, including the three main phases of autistic, symbiotic, and separation-individuation. Donald Winnicott introduced the concept of the transitional object and the good enough mother. Overall, neo-Freudians expanded upon Freud’s ideas and helped to shape modern psychotherapy.

Antidepressants: Minimum Effective Doses

According to the Maudsley 13th, the following are the minimum effective doses for various antidepressants:

– Citalopram: 20 mg/day
– Fluoxetine: 20 mg/day
– Fluvoxamine: 50 mg/day
– Paroxetine: 20 mg/day
– Sertraline: 50 mg/day
– Mirtazapine: 30 mg/day
– Venlafaxine: 75 mg/day
– Duloxetine: 60 mg/day
– Agomelatine: 25 mg/day
– Moclobemide: 300 mg/day
– Trazodone: 150 mg/day

Note that these are minimum effective doses and may vary depending on individual factors and response to treatment. It is important to consult with a healthcare professional before starting of changing any medication regimen.

Personality Disorder Classification

A personality disorder is a persistent pattern of behavior and inner experience that deviates significantly from cultural expectations, is inflexible and pervasive, and causes distress of impairment. The DSM-5 and ICD-11 have different approaches to classifying personality disorders. DSM-5 divides them into 10 categories, grouped into clusters A, B, and C, while ICD-11 has a general category with six trait domains that can be added. To diagnose a personality disorder, the general diagnostic threshold must be met before determining the subtype(s) present. The criteria for diagnosis include inflexibility and pervasiveness of the pattern, onset in adolescence of early adulthood, stability over time, and significant distress of impairment. The disturbance must not be better explained by another mental disorder, substance misuse, of medical condition.

Course

Borderline and antisocial personality disorders tend to become less evident of remit with age, while others, particularly obsessive-compulsive and schizotypal, may persist.

Classification

The DSM-5 divides personality disorders into separate clusters A, B, and C, with additional groups for medical conditions and unspecified disorders. The ICD-11 dropped the separate categories and instead lists six trait domains that can be added to the general diagnosis.

UK Epidemiology

The prevalence of personality disorders in Great Britain, according to the British National Survey of Psychiatric Morbidity, is 4.4%, with cluster C being the most common at 2.6%, followed by cluster A at 1.6% and cluster B at 1.2%. The most prevalent specific personality disorder is obsessive-compulsive (anankastic) at 1.9%.

Alcohol screening tools are available to assist in the diagnosis of alcohol problems. One such tool is the AUDIT (Alcohol Use Disorders Identification Test), which consists of 10 questions and covers harmful use, hazardous use, and dependence. Another tool is the FAST (Fast Alcohol Screening Test), which has just 4 questions and was developed for use in a busy medical setting. The CAGE is a well-known 4 question screening tool, but recent research has questioned its value. Other tools include SASQ (Single alcohol screening questionnaire), PAT (Paddington Alcohol Test), MAST (Michigan Alcoholism Screening Test), and RAPS4 (Rapid Alcohol Problem Screen 4). These tools can help identify hazardous of harmful alcohol consumption and alcohol dependence.

Alcohol screening tools are available to assist in the diagnosis of alcohol problems. One such tool is the AUDIT (Alcohol Use Disorders Identification Test), which consists of 10 questions and covers harmful use, hazardous use, and dependence. Another tool is the FAST (Fast Alcohol Screening Test), which has just 4 questions and was developed for use in a busy medical setting. The CAGE is a well-known 4 question screening tool, but recent research has questioned its value. Other tools include SASQ (Single alcohol screening questionnaire), PAT (Paddington Alcohol Test), MAST (Michigan Alcoholism Screening Test), and RAPS4 (Rapid Alcohol Problem Screen 4). These tools can help identify hazardous of harmful alcohol consumption and alcohol dependence.

Wernicke’s aphasia is caused by a blockage in the inferior division of the middle cerebral artery, which provides blood to the temporal cortex (specifically, the posterior superior temporal gyrus of ‘Wernicke’s area’). This type of aphasia is characterized by fluent speech, but with significant comprehension difficulties. On the other hand, Broca’s aphasia is considered a non-fluent expressive aphasia, resulting from damage to Brodmann’s area in the frontal lobe.

Historical Classification of Schizophrenia

The classification of schizophrenia has evolved over time, with various individuals contributing to its development. In 1801, Phillippe Pinel used the term ‘demencé’ to describe the loss of mental abilities in chronically ill patients. Benedict Morel coined the term ‘demencé precocé’ in 1852 to describe young patients with premature dementia. Kahlbaum was the first to describe ‘paraphrenia hebetica’ in the 1860s, which was later elaborated as ‘hebephrenia’ by Hecker in 1871.

In 1893, Emil Kraepelin used the term dementia praecox to describe the condition, emphasizing the importance of delusions, hallucinations, impaired attention, thought incoherence, stereotyped movements and expressions, deterioration of emotional life, and a loss of drive as key symptoms. In 1908, Eugen Bleuler coined the term ‘schizophrenia’ to replace dementia praecox, denoting ‘a splitting of the psychic functions.’ Bleuler expanded the concept to include presentations that did not include a ‘terminal state.’

Bleuler introduced a distinction between basic and accessory symptoms and primary and secondary symptoms. Basic symptoms are necessarily present in any case of schizophrenia, while accessory symptoms may of may not occur. The fundamental features of schizophrenia were loosening of associations, disturbances of affectivity, ambivalence, and autism. The alteration of associations is the only symptom that Bleuler regarded as both basic and primary, and can thus be described as the core disturbance in the Bleulerian conception of schizophrenia.

In 1939, Langfeldt introduced the term ‘schizophreniform psychosis’ to describe patients with Bleulerian schizophrenia who did not follow a progressively deteriorating course. In the 1960s, Rado/Meehl introduced the term ‘schizotypy’ to recognize the concept of a continuum of spectrum of schizophrenia-related phenotypes. In the 1980s, Crow proposed a subclassification of schizophrenia, dividing patients into types I and II. Type I patients present with positive symptoms such as delusions and hallucinations, while type II patients present with negative symptoms such as affective flattening and poverty of speech.

Both ADHD and ASD are believed to have a strong genetic component, although only one of them is classified as a developmental disorder.

Heritability: Understanding the Concept

Heritability is a concept that is often misunderstood. It is not a measure of the extent to which genes cause a condition in an individual. Rather, it is the proportion of phenotypic variance attributable to genetic variance. In other words, it tells us how much of the variation in a condition seen in a population is due to genetic factors. Heritability is calculated using statistical techniques and can range from 0.0 to 1.0. For human behavior, most estimates of heritability fall in the moderate range of .30 to .60.

The quantity (1.0 – heritability) gives the environment ability of the trait. This is the proportion of phenotypic variance attributable to environmental variance. The following table provides estimates of heritability for major conditions:

Condition Heritability estimate (approx)
ADHD 85%
Autism 70%
Schizophrenia 55%
Bipolar 55%
Anorexia 35%
Alcohol dependence 35%
Major depression 30%
OCD 25%

It is important to note that heritability tells us nothing about individuals. It is a population-level measure that helps us understand the relative contributions of genetic and environmental factors to a particular condition.

As the concentration decreases, the half-life of a zero order reaction becomes shorter. This is because zero order kinetics involve constant elimination, meaning that the rate of elimination does not change with increasing concentration. Therefore, as the concentration decreases, there is less drug available to be eliminated at a constant rate, resulting in a shorter half-life.

The half-life of a drug is the time taken for its concentration to fall to one half of its value. Drugs with long half-lives may require a loading dose to achieve therapeutic plasma concentrations rapidly. It takes about 4.5 half-lives to reach steady state plasma levels. Most drugs follow first order kinetics, where a constant fraction of the drug in the body is eliminated per unit time. However, some drugs may follow zero order kinetics, where the plasma concentration of the drug decreases at a constant rate, despite the concentration of the drug. For drugs with nonlinear kinetics of dose-dependent kinetics, the relationship between the AUC of CSS and dose is not linear, and the kinetic parameters may vary depending on the administered dose.

Delusional Structure

Delusions can be categorized based on their logical consistency and organization. Logical delusions are consistent with logical thinking, while paralogical delusions are not. Delusions can also be organized, integrated into a formed concept, of unorganized. Highly organized, logical delusions are referred to as systematized.

The relationship between delusional beliefs and reality can also be described in different ways. Polarized delusions mix fact and delusion together, while juxtaposed delusions exist side by side with facts but do not interact. Autistic delusions completely disregard actual reality, and the patient lives in a delusional world.

The Cerebral Cortex and Neocortex

The cerebral cortex is the outermost layer of the cerebral hemispheres and is composed of three parts: the archicortex, paleocortex, and neocortex. The neocortex accounts for 90% of the cortex and is involved in higher functions such as thought and language. It is divided into 6-7 layers, with two main cell types: pyramidal cells and nonpyramidal cells. The surface of the neocortex is divided into separate areas, each given a number by Brodmann (e.g. Brodmann’s area 17 is the primary visual cortex). The surface is folded to increase surface area, with grooves called sulci and ridges called gyri. The neocortex is responsible for higher cognitive functions and is essential for human consciousness.

Wernicke’s encephalopathy is a medical emergency that requires immediate replacement of thiamine. The preferred route of administration is intravenous (IV). It is important to note that correcting hypoglycemia should not be attempted before thiamine replenishment, as a large dose of sugar, especially glucose, can worsen the encephalopathy. Rehydration to restore blood volume should follow as needed.

In the UK, Pabrinex is the usual treatment for thiamine replacement, which also contains vitamins B2, B3, B6, and C. Parenteral treatment is given for at least 5 days. The prognosis depends on the severity of the condition. Early treatment leads to rapid and complete recovery. However, established Wernicke’s encephalopathy can have serious long-term consequences, and patients may require permanent inpatient care.

Source: https://www.nice.org.uk/guidance/cg100/chapter/Recommendations#wernickes-encephalopathy
https://academic.oup.com/alcalc/article/48/4/514/533760