Temperament is the innate aspect of an individual’s personality that is believed to be influenced by genetics, while character is shaped by learned experiences. Thomas and Chess developed a classification system that assesses children’s behavior based on nine traits, including activity level, adaptability, and emotional response. They found that 65% of children fall into one of three temperament types: easy, difficult, of slow to warm up. Thomas and Chess also introduced the concept of goodness of fit, which refers to the compatibility between a child’s temperament and their environment. When there is a good fit, children are more likely to reach their potential. For example, teachers can provide active learning experiences for children with high activity levels instead of seat work.

The patient’s long-term use of a first-generation depot antipsychotic and the involuntary symptoms presented suggest a diagnosis of tardive dyskinesia. Acute anxiety is unlikely as the patient has a long standing relationship with their psychiatrist and the symptom combination does not fit. Akathisia, characterized by restlessness and leg movement, is also an unlikely diagnosis. Neuroleptic malignant syndrome (NMS) can be ruled out as the patient has had symptoms for two years. The patient is compliant with medication, has no psychotic symptoms, and is well-functioning in their job and home life, making a relapse of schizophrenia an incorrect diagnosis.

Treating akathisia is a challenging task, as there are limited options available. In many cases, the only viable solution is to decrease the use of antipsychotic medication.

Extrapyramidal side-effects (EPSE’s) are a group of side effects that affect voluntary motor control, commonly seen in patients taking antipsychotic drugs. EPSE’s include dystonias, parkinsonism, akathisia, and tardive dyskinesia. They can be frightening and uncomfortable, leading to problems with non-compliance and can even be life-threatening in the case of laryngeal dystonia. EPSE’s are thought to be due to antagonism of dopaminergic D2 receptors in the basal ganglia. Symptoms generally occur within the first few days of treatment, with dystonias appearing quickly, within a few hours of administration of the first dose. Newer antipsychotics tend to produce less EPSE’s, with clozapine carrying the lowest risk and haloperidol carrying the highest risk. Akathisia is the most resistant EPSE to treat. EPSE’s can also occur when antipsychotics are discontinued (withdrawal dystonia).

Assessment Tools:

Luria’s Test:
Luria’s test is a motor task designed by Alexander Luria, a Russian neuropsychologist. The test was developed based on his observation that individuals with significant frontal lobe damage were unable to modify their responses to a programmed motor task when the order of actions in the task was changed.

Geriatric Depression Scale:
The Geriatric Depression Scale is a screening tool used to identify depression in older adults. It is not designed to assess cognitive impairment.

Mini-Mental State Examination:
The Mini-Mental State Examination is a brief, 30-question screening tool used to assess cognitive impairment. It does not evaluate frontal lobe functions.

National Adult Reading Test:
The National Adult Reading Test is used to assess the premorbid level of intelligence in English-speaking patients.

Wechsler Adult Intelligence Scale:
The Wechsler Adult Intelligence Scale is a comprehensive assessment tool used to measure intelligence in adults and older adolescents.

The Hamilton anxiety rating scale (HAM-A) is a clinician-rated scale that measures the severity of anxiety symptoms in adults, adolescents, and children. It takes about 10-15 minutes to administer and consists of 14 items that measure both mental and physical symptoms of anxiety. Each item is scored on a scale of 0-4, with a total score range of 0-56. The impact of events scale is used to measure stress reactions after traumatic events, while the state-trait anxiety inventory (STAI) is a self-report inventory that measures both state and trait anxiety. The Zung self-rated anxiety scale is a patient-rated scale that measures anxiety levels based on cognitive, autonomic, motor, and central nervous system symptoms.

Broca’s aphasia is also known as non-fluent aphasia, while Wernicke’s aphasia is referred to as fluent aphasia.

Broca’s and Wernicke’s are two types of expressive dysphasia, which is characterized by difficulty producing speech despite intact comprehension. Dysarthria is a type of expressive dysphasia caused by damage to the speech production apparatus, while Broca’s aphasia is caused by damage to the area of the brain responsible for speech production, specifically Broca’s area located in Brodmann areas 44 and 45. On the other hand, Wernicke’s aphasia is a type of receptive of fluent aphasia caused by damage to the comprehension of speech, while the actual production of speech remains normal. Wernicke’s area is located in the posterior part of the superior temporal gyrus in the dominant hemisphere, within Brodmann area 22.

The PANSS is commonly utilized in clinical trials to assess positive and negative symptoms as well as general psychopathology (30 items in total). To measure extrapyramidal side effects, the Simpson Angus Scale, Abnormal Involuntary Movement Scale (AIMS), and Barnes Akathisia Scale are frequently employed. While the Clinical Global Impression (CGI) scale provides a general score of 1 to 5 for a patient’s overall presentation, it may not be as useful for evaluating a specific positive symptom of schizophrenia as the question suggests.

HPA Axis Dysfunction in Mood Disorders

The HPA axis, which includes regulatory neural inputs and a feedback loop involving the hypothalamus, pituitary, and adrenal glands, plays a central role in the stress response. Excessive secretion of cortisol, a glucocorticoid hormone, can lead to disruptions in cellular functioning and widespread physiologic dysfunction. Dysregulation of the HPA axis is implicated in mood disorders such as depression and bipolar affective disorder.

In depressed patients, cortisol levels often do not decrease as expected in response to the administration of dexamethasone, a synthetic corticosteroid. This abnormality in the dexamethasone suppression test is thought to be linked to genetic of acquired defects of glucocorticoid receptors. Tricyclic antidepressants have been shown to increase expression of glucocorticoid receptors, whereas this is not the case for SSRIs.

Early adverse experiences can produce long standing changes in HPA axis regulation, indicating a possible neurobiological mechanism whereby childhood trauma could be translated into increased vulnerability to mood disorder. In major depression, there is hypersecretion of cortisol, corticotropin-releasing factor (CRF), and ACTH, and associated adrenocortical enlargement. HPA abnormalities have also been found in other psychiatric disorders including Alzheimer’s and PTSD.

In bipolar disorder, dysregulation of ACTH and cortisol response after CRH stimulation have been reported. Abnormal DST results are found more often during depressive episodes in the course of bipolar disorder than in unipolar disorder. Reduced pituitary volume secondary to LHPA stimulation, resulting in pituitary hypoactivity, has been observed in bipolar patients.

Overall, HPA axis dysfunction is implicated in mood disorders, and understanding the underlying mechanisms may lead to new opportunities for treatments.

Agomelatine is a medication used to treat depression. It works by activating melatonin receptors (MT1 and MT2) and blocking serotonin 5-HT2C receptors.

Antidepressants can cause sexual dysfunction as a side-effect, although the rates vary. The impact on sexual desire, arousal, and orgasm can differ depending on the type of antidepressant. It is important to rule out other causes and consider non-pharmacological strategies such as reducing the dosage of taking drug holidays. If necessary, switching to a lower risk antidepressant of using pharmacological options such as phosphodiesterase inhibitors of mirtazapine augmentation can be considered. The Maudsley Guidelines 14th Edition provides a helpful table outlining the risk of sexual dysfunction for different antidepressants.

It is probable that this individual has experienced a traumatic injury affecting the accessory nerve.

Overview of Cranial Nerves and Their Functions

The cranial nerves are a complex system of nerves that originate from the brain and control various functions of the head and neck. There are twelve cranial nerves, each with a specific function and origin. The following table provides a simplified overview of the cranial nerves, including their origin, skull exit, modality, and functions.

The first cranial nerve, the olfactory nerve, originates from the telencephalon and exits through the cribriform plate. It is a sensory nerve that controls the sense of smell. The second cranial nerve, the optic nerve, originates from the diencephalon and exits through the optic foramen. It is a sensory nerve that controls vision.

The third cranial nerve, the oculomotor nerve, originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement, pupillary constriction, and lens accommodation. The fourth cranial nerve, the trochlear nerve, also originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement.

The fifth cranial nerve, the trigeminal nerve, originates from the pons and exits through different foramina depending on the division. It is a mixed nerve that controls chewing and sensation of the anterior 2/3 of the scalp. It also tenses the tympanic membrane to dampen loud noises.

The sixth cranial nerve, the abducens nerve, originates from the pons and exits through the superior orbital fissure. It is a motor nerve that controls eye movement. The seventh cranial nerve, the facial nerve, also originates from the pons and exits through the internal auditory canal. It is a mixed nerve that controls facial expression, taste of the anterior 2/3 of the tongue, and tension on the stapes to dampen loud noises.

The eighth cranial nerve, the vestibulocochlear nerve, originates from the pons and exits through the internal auditory canal. It is a sensory nerve that controls hearing. The ninth cranial nerve, the glossopharyngeal nerve, originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls taste of the posterior 1/3 of the tongue, elevation of the larynx and pharynx, and swallowing.

The tenth cranial nerve, the vagus nerve, also originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls swallowing, voice production, and parasympathetic supply to nearly all thoracic and abdominal viscera. The eleventh cranial nerve, the accessory nerve, originates from the medulla and exits through the jugular foramen. It is a motor nerve that controls shoulder shrugging and head turning.

The twelfth cranial nerve, the hypoglossal nerve, originates from the medulla and exits through the hypoglossal canal. It is a motor nerve that controls tongue movement. Overall, the cranial nerves play a crucial role in controlling various functions of the head and neck, and any damage of dysfunction can have significant consequences.

If there are no T wave abnormalities on the ECG, the Maudsley guidelines deem a QTc of 460 ms acceptable for women.

Amantadine and QTc Prolongation

Amantadine is a medication used to treat Parkinson’s disease and influenza. It has been associated with QTc prolongation, which can increase the risk of Torsades de points. Therefore, caution should be exercised when prescribing amantadine to patients with risk factors for QT prolongation. If a patient is already taking amantadine and develops a prolonged QTc interval, the medication should be discontinued and an alternative treatment considered. It is important to monitor the QTc interval in patients taking amantadine, especially those with risk factors for QT prolongation.

The term ‘short-term memory’ is a less advanced term compared to ‘working memory’.

Memory Forms

Memory is the ability to store, retain, and retrieve information. There are different forms of memory, including sensory memory, short-term/working memory, and long-term memory.

Sensory memory is the capacity for briefly retaining the large amounts of information that people encounter daily. It includes echoic memory (gathered through auditory stimuli), iconic memory (gathered through sight), and haptic memory (acquired through touch).

Short-term memory is the ability to keep a small amount of information available for a short period of time. Atkinson and Shiffrin’s multistore model (1968) suggests the existence of a short-term storehouse with limited capacity. Baddeley and Hitch (1974) further developed the concept of short-term memory, which eventually became known as Baddeley’s multi-storehouse model (2000). This model includes the central executive, visuospatial sketchpad, phonological buffer/loop, and episodic buffer.

Long-term memory includes declarative (of explicit) memories, which can be consciously retrieved, and nondeclarative (of implicit) memories, which cannot. Declarative memory includes episodic memory (stores personal experiences) and semantic memory (stores information about facts and concepts). Non-declarative memory includes procedural memory (recalls motor and executive skills), associative memory (storage and retrieval of information through association with other information), and non-associative memory (refers to newly learned behavior through repeated exposure to an isolated stimulus).

Overall, memory is a complex and essential cognitive function that plays a crucial role in learning, reasoning, and understanding.

Dysmegalopsia: Difficulty in Perceiving Object Size

Dysmegalopsia is a condition characterized by a reduced ability to accurately perceive the size of objects. This can manifest as either micropsia, where objects appear smaller than they actually are, of macropsia, where objects appear larger than they actually are. Dysmegalopsia can occur as a standalone symptom of as part of a group of symptoms known as the Alice in Wonderland Syndrome. In this syndrome, individuals may experience distortions in their perception of size, shape, and distance, as well as other sensory disturbances. Dysmegalopsia can be caused by various factors, including neurological conditions, migraines, and the use of certain medications.

The Heinz dilemma was a scenario used by Kohlberg to explore moral development. It goes as follows: A woman is dying from a rare cancer, and a druggist in the same town has discovered a drug that could save her. However, the druggist is charging ten times the cost of production for the drug. The women’s husband, Heinz, cannot afford the price and asks the druggist to sell it cheaper of let him pay later, but the druggist refuses. In desperation, Heinz breaks into the store to steal the drug for his wife.

The question is whether Heinz should have broken into the store to steal the drug. This dilemma raises ethical questions about the value of human life versus the right to property and profit. Some argue that Heinz was justified in stealing the drug because he was trying to save his wife’s life, and the druggist’s greed was preventing him from doing so. Others argue that stealing is always wrong, regardless of the circumstances, and that Heinz should have found another way to obtain the drug.

Kohlberg used this dilemma to study moral reasoning and development. He believed that people’s responses to moral dilemmas reveal their level of moral reasoning, which progresses through stages of increasing complexity and sophistication. According to Kohlberg, Heinz’s decision to steal the drug would be considered morally justifiable at the higher stages of moral reasoning, where individuals prioritize universal ethical principles over personal gain of social norms.

Overall, the Heinz dilemma highlights the complex nature of moral decision-making and the importance of considering multiple perspectives and ethical principles.

Kohlberg’s Six Stages of Moral Development

Kohlberg’s theory of moral development consists of six stages that can be categorized into three levels. The first level is the preconventional stage, which is characterized by obedience and punishment orientation, where the focus is on the direct consequences of actions and unquestioning deference to power. The second stage is the self-interest orientation, where right behavior is defined purely by what is in the individual’s own interest.

The second level is the conventional stage, which is characterized by interpersonal accord and conformity, where the focus is on how the individual will appear to others. The behavior should accord with a consensus view on what is good. The second stage is the authority and social order obedience driven, where what is lawful is judged to be morally right. Right behavior is dictated by societal rules, and there is a greater respect for social order and the need for laws.

The third level is the postconventional stage, which is characterized by the social contract orientation, where individual rights determine behavior. The individual views laws and rules as flexible tools for improving human purposes. The fourth stage is the universal ethical principles orientation, where the right action is the one that is consistent with abstract reasoning using universal ethical principles.

It is important to note that the age ranges for Kohlberg’s developmental stages are rough guides, and sources vary widely. Kohlberg developed his stage theory following an experiment he conducted on 72 boys aged 10-16. However, the theory is criticized as sexist as it only included boys.

Prader-Willi Syndrome: A Genetic Disorder with Unique Characteristics

Prader-Willi Syndrome is a genetic disorder that occurs when there is a deletion of genetic material from the paternal chromosome 15. This condition is a classic example of imprinting, where the expression of certain genes is dependent on whether they are inherited from the mother of father. The syndrome is characterized by several unique features, including hyperphagia (excessive eating) and obesity, short stature, delayed puberty, hypogonadism, infertility, learning difficulties, and compulsive behavior such as skin picking.

The fifth edition of the DSM-5 no longer includes subtypes of schizophrenia due to their lack of usefulness to clinicians. The previous subtypes were based on the predominant symptom at the time of evaluation, but patients often exhibited overlapping symptoms that made it difficult to distinguish between subtypes. The DSM-5 now requires individuals to exhibit at least two specified symptoms, compared to the previous threshold of one, and symptoms must have been present for six months with at least one month of active symptoms for a diagnosis to be made.

Visuomotor neurons known as mirror neurons are situated in the premotor cortex. These neurons were initially identified in a specific region of the premotor cortex in monkeys called area F5, but have since been observed in the inferior parietal lobule as well (Rizzolatti 2001).

Mirror Neurons: A Model for Imitation Learning

Mirror neurons are a unique type of visuomotor neurons that were first identified in the premotor cortex of monkeys in area F5. These neurons fire not only when the monkey performs a specific action but also when it observes another individual, whether it is a monkey of a human, performing a similar action. This discovery has led to the development of a model for understanding imitation learning.

Mirror neurons offer a fascinating insight into how humans and animals learn by imitation. They provide a neural mechanism that allows individuals to understand the actions of others and to replicate those actions themselves. This process is essential for social learning, as it enables individuals to learn from others and to adapt to their environment.

The discovery of mirror neurons has also led to new research in the field of neuroscience, as scientists seek to understand how these neurons work and how they can be used to improve our understanding of human behavior. As we continue to learn more about mirror neurons, we may be able to develop new therapies for individuals with social and communication disorders, such as autism.

Overall, mirror neurons are a fascinating area of research that has the potential to revolutionize our understanding of human behavior and learning. By studying these neurons, we may be able to unlock new insights into how we learn, communicate, and interact with others.

Lithium – Pharmacology

Pharmacokinetics:
Lithium salts are rapidly absorbed following oral administration and are almost exclusively excreted by the kidneys unchanged. Blood samples for lithium should be taken 12 hours post-dose.

Ebstein’s:
Ebstein’s anomaly is a congenital malformation consisting of a prolapse of the tricuspid valve into the right ventricle. It occurs in 1:20,000 of the general population. Initial data suggested it was more common in those using lithium but this had not held to be true.

Contraindications:
Addison’s disease, Brugada syndrome, cardiac disease associated with rhythm disorders, clinically significant renal impairment, untreated of untreatable hypothyroidism, low sodium levels.

Side-effects:
Common side effects include nausea, tremor, polyuria/polydipsia, rash/dermatitis, blurred vision, dizziness, decreased appetite, drowsiness, metallic taste, and diarrhea. Side-effects are often dose-related.

Long-term use is associated with hypothyroidism, hyperthyroidism, hypercalcemia/hyperparathyroidism, irreversible nephrogenic diabetes insipidus, and reduced GFR.

Lithium-induced diabetes insipidus:
Treatment options include stopping lithium (if feasible), keeping levels within 0.4-0.8 mmol/L, once-daily dose of the drug taken at bedtime, amiloride, thiazide diuretics, indomethacin, and desmopressin.

Toxicity:
Lithium salts have a narrow therapeutic/toxic ratio. Risk factors for lithium toxicity include drugs altering renal function, decreased circulating volume, infections, fever, decreased oral intake of water, renal insufficiency, and nephrogenic diabetes insipidus. Features of lithium toxicity include GI symptoms and neuro symptoms.

Pre-prescribing:
Before prescribing lithium, renal function, cardiac function, thyroid function, FBC, and BMI should be checked. Women of childbearing age should be advised regarding contraception, and information about toxicity should be provided.

Monitoring:
Lithium blood levels should be checked weekly until stable, and then every 3-6 months once stable. Thyroid and renal function should be checked every 6 months. Patients should be issued with an information booklet, alert card, and record book.

Agomelatine is an antidepressant that targets 5HT2C, melatonin-1, and melatonin-2 receptors and is approved for treating major depression. Bupropion is not licensed as an antidepressant in the UK but is recommended by NICE for smoking cessation. It has dopaminergic and noradrenergic effects but does not affect melatonin receptors. Escitalopram is an SSRI antidepressant that does not impact melatonin receptors. Melatonin, on the other hand, acts on melatonin receptors but is not an antidepressant; it is used to treat primary insomnia. Vortioxetine is a multimodal antidepressant that enhances serotonin and other neurotransmitter levels in the brain by targeting 5HT3, 7, 1A, and 1B receptors. It is not known to affect melatonin receptors and is not currently licensed for use in the UK.

Broca’s and Wernicke’s are two types of expressive dysphasia, which is characterized by difficulty producing speech despite intact comprehension. Dysarthria is a type of expressive dysphasia caused by damage to the speech production apparatus, while Broca’s aphasia is caused by damage to the area of the brain responsible for speech production, specifically Broca’s area located in Brodmann areas 44 and 45. On the other hand, Wernicke’s aphasia is a type of receptive of fluent aphasia caused by damage to the comprehension of speech, while the actual production of speech remains normal. Wernicke’s area is located in the posterior part of the superior temporal gyrus in the dominant hemisphere, within Brodmann area 22.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Antipsychotics and Sexual Dysfunction: Causes, Risks, and Management

Sexual dysfunction is a common side effect of antipsychotic medication, with the highest risk associated with risperidone and haloperidol due to their effect on prolactin levels. Clozapine, olanzapine, quetiapine, aripiprazole, asenapine, and lurasidone are associated with lower rates of sexual dysfunction. The Arizona Sexual Experiences Scale (ASEX) can be used to measure sexual dysfunction before and during treatment. Management options include excluding other causes, watchful waiting, dose reduction, switching to a lower risk agent, adding aripiprazole, considering an antidote medication, of using sildenafil for erectile dysfunction. It is important to address sexual dysfunction to improve quality of life and medication adherence.

Types of Delusions

Delusions come in many different forms. It is important to familiarize oneself with these types as they may be tested in an exam. Some of the most common types of delusions include:

– Folie a deux: a shared delusion between two or more people
– Grandiose: belief that one has special powers, beliefs, of purpose
– Hypochondriacal: belief that something is physically wrong with the patient
– Ekbom’s syndrome: belief that one has been infested with insects
– Othello syndrome: belief that a sexual partner is cheating on them
– Capgras delusion: belief that a person close to them has been replaced by a double
– Fregoli delusion: patient identifies a familiar person (usually suspected to be a persecutor) in other people they meet
– Syndrome of subjective doubles: belief that doubles of him/her exist
– Lycanthropy: belief that one has been transformed into an animal
– De Clérambault’s syndrome: false belief that a person is in love with them
– Cotard’s syndrome/nihilistic delusions: belief that they are dead of do not exist
– Referential: belief that others/TV/radio are speaking directly to of about the patient
– Delusional perception: belief that a normal percept (product of perception) has a special meaning
– Pseudocyesis: a condition whereby a woman believes herself to be pregnant when she is not. Objective signs accompany the belief such as abdominal enlargement, menstrual disturbance, apparent foetal movements, nausea, breast changes, and labour pains.

Remembering these types of delusions can be helpful in understanding and diagnosing patients with delusional disorders.

The observation that haloperidol, which has a high D2 occupancy, has a greater likelihood of causing EPSE, while clozapine, which has a lower D2 occupancy, has a lower risk, is in line with the research.

Extrapyramidal side-effects (EPSE’s) are a group of side effects that affect voluntary motor control, commonly seen in patients taking antipsychotic drugs. EPSE’s include dystonias, parkinsonism, akathisia, and tardive dyskinesia. They can be frightening and uncomfortable, leading to problems with non-compliance and can even be life-threatening in the case of laryngeal dystonia. EPSE’s are thought to be due to antagonism of dopaminergic D2 receptors in the basal ganglia. Symptoms generally occur within the first few days of treatment, with dystonias appearing quickly, within a few hours of administration of the first dose. Newer antipsychotics tend to produce less EPSE’s, with clozapine carrying the lowest risk and haloperidol carrying the highest risk. Akathisia is the most resistant EPSE to treat. EPSE’s can also occur when antipsychotics are discontinued (withdrawal dystonia).

NMS can be identified by three primary symptoms: hyperthermia, rigidity, and elevated creatine phosphokinase concentration. If these symptoms are not present, the diagnosis of NMS should be reconsidered as other symptoms may be present in patients taking neuroleptics without having NMS. This information was reported by P Adnet in the British Journal of Anaesthesia in 2000.

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.

Linguistic Development and Risk Factors for Delayed Speech and Language

The development of language skills is an important aspect of a child’s growth. The prelinguistic period, from birth to 12 months, is marked by crying, babbling, and echolalia. From 6 to 12 months, a child responds to their name and can differentiate between angry and friendly tones. By 18 to 24 months, a child can use up to 40-50 words, mainly nouns, and starts to combine words in short phrases. By 36 to 48 months, a child has a vocabulary of 900-1000 words, can use plurals and past tense, and can handle three-word sentences easily.

However, there are risk factors associated with delayed speech and language development. These include a positive family history, male gender, twins, lower maternal education, childhood illness, being born late in the family order, young mother at birth, and low socioeconomic status. of these, a positive family history is considered the most reliable risk factor. It is important to monitor a child’s language development and seek professional help if there are concerns about delayed speech and language.

Schizotypal PD is classified differently in DSM-IV and ICD-10, with the latter listing it under psychotic disorders. It is genetically linked to schizophrenia and often found in first-degree relatives of those with the disorder. In this case, there is no evidence of schizophrenia or schizoaffective disorder, but the individual’s beliefs are outside of cultural norms. The DSM-IV criteria for schizotypal PD include social and interpersonal deficits, cognitive of perceptual distortions, and eccentric behavior. The individual must exhibit at least five of the listed criteria, such as odd beliefs of magical thinking, unusual perceptual experiences, and suspiciousness of paranoid ideation. The disorder cannot be exclusively attributed to another mental health condition.

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).

While antipsychotics, tricyclic antidepressants, and citalopram are known to cause QTc prolongation and require ECG monitoring, they are not the only drugs that can cause this condition. However, in psychiatric practice, they are the most commonly prescribed drugs associated with QTc prolongation. It is important to note that clarithromycin is a high-risk drug for QTc prolongation, unlike the other drugs listed, which are considered low risk.

Immunologic Adverse Drug Reactions

Immunologic adverse drug reactions account for a small percentage of all adverse drug reactions, ranging from 5 to 10%. These reactions are classified using the Gell and Coombs system, which categorizes them into four groups: Type I, Type II, Type III, and Type IV reactions.

Type I reactions occur when a drug-IgE complex binds to mast cells, leading to the release of histamine and other inflammatory mediators. These reactions typically cause anaphylaxis, urticaria, and bronchospasm and occur within minutes to hours after exposure.

Type II reactions occur when an IgG of IgM antibody binds to a cell that has been altered by a drug-hapten. These reactions often manifest as blood abnormalities, such as thrombocytopenia and neutropenia, and their timing is variable.

Type III reactions occur when drug-antibody complexes activate the complement system, leading to fever, rash, urticaria, and vasculitis. These reactions occur 1 to 3 weeks after exposure.

Type IV reactions arise when the MHC system presents drug molecules to T cells, resulting in allergic contact dermatitis and rashes. These reactions occur 2 to 7 days after cutaneous exposure.