Hyperkinesia is a defining feature of tics.

Movement Disorders: Key Features

Movement disorders refer to a range of conditions that affect voluntary muscle movements. These disorders can be caused by various factors, including neurological conditions, medication side effects, and metabolic imbalances. The following table outlines some of the key features of common movement disorders:

Akinesia: Absence of loss of control of voluntary muscle movements, often seen in severe Parkinson’s disease.

Bradykinesia: Slowness of voluntary movement, a core symptom of Parkinson’s disease.

Akathisia: Subjective feeling of inner restlessness, often caused by antipsychotic medication use.

Athetosis: Continuous stream of slow, flowing, writhing involuntary movements, often seen in cerebral palsy, stroke, and Huntington’s disease.

Chorea: Brief, quasi-purposeful, irregular contractions that appear to flow from one muscle to the next, often seen in Huntington’s disease and Wilson’s disease.

Dystonia: Involuntary sustained of intermittent muscle contractions that cause twisting and repetitive movements, abnormal postures, of both.

Dyskinesia: General term referring to problems with voluntary movements and the presence of involuntary movements, often drug-induced.

Myoclonus: A sequence of repeated, often non-rhythmic, brief shock-like jerks due to sudden involuntary contraction of relaxation of one of more muscles.

Parkinsonism: Syndrome characterized by tremor, rigidity, and bradykinesia.

Tic: Sudden, repetitive, non-rhythmic, stereotyped motor movement of vocalization involving discrete muscle groups, often seen in Tourette’s syndrome.

Tremor: Involuntary, rhythmic, alternating movement of one of more body parts, often seen in essential tremor, Parkinson’s disease, and alcohol withdrawal.

Hemiballismus: Repetitive, but constantly varying, large amplitude involuntary movements of the proximal parts of the limbs, often seen in stroke and traumatic brain injury.

Stereotypies: Repetitive, simple movements that can be voluntarily suppressed, often seen in autism and intellectual disability.

It is important to consider the underlying conditions and factors that may contribute to movement disorders in order to properly diagnose and treat these conditions.

Huntington’s Disease: Genetics and Pathology

Huntington’s disease is a genetic disorder that follows an autosomal dominant pattern of inheritance. It is caused by a mutation in the Huntington gene, which is located on chromosome 4. The mutation involves an abnormal expansion of a trinucleotide repeat sequence (CAG), which leads to the production of a toxic protein that damages brain cells.

The severity of the disease and the age of onset are related to the number of CAG repeats. Normally, the CAG sequence is repeated less than 27 times, but in Huntington’s disease, it is repeated many more times. The disease shows anticipation, meaning that it tends to worsen with each successive generation.

The symptoms of Huntington’s disease typically begin in the third of fourth decade of life, but in rare cases, they can appear in childhood of adolescence. The most common symptoms include involuntary movements (chorea), cognitive decline, and psychiatric disturbances.

The pathological hallmark of Huntington’s disease is the gross bilateral atrophy of the head of the caudate and putamen, which are regions of the brain involved in movement control. The EEG of patients with Huntington’s disease shows a flattened trace, indicating a loss of brain activity.

Macroscopic pathological findings include frontal atrophy, marked atrophy of the caudate and putamen, and enlarged ventricles. Microscopic findings include neuronal loss and gliosis in the cortex, neuronal loss in the striatum, and the presence of inclusion bodies in the neurons of the cortex and striatum.

In conclusion, Huntington’s disease is a devastating genetic disorder that affects the brain and causes a range of motor, cognitive, and psychiatric symptoms. The disease is caused by a mutation in the Huntington gene, which leads to the production of a toxic protein that damages brain cells. The pathological changes in the brain include atrophy of the caudate and putamen, neuronal loss, and the presence of inclusion bodies.

In order for splitting to be present, the patient must demonstrate an inability to recognize others as multifaceted individuals with both positive and negative qualities, and instead resort to idealizing of devaluing them. Additionally, the patient may project their emotions onto an object they deem less significant.

Intermediate Mechanism: Rationalisation

Rationalisation is a defense mechanism commonly used by individuals to create false but credible justifications for their behavior of actions. It involves the use of logical reasoning to explain away of justify unacceptable behavior of feelings. The individual may not be aware that they are using this mechanism, and it can be difficult to identify in oneself.

Rationalisation is considered an intermediate mechanism, as it is common in healthy individuals from ages three to ninety, as well as in neurotic disorders and in mastering acute adult stress. It can be dramatically changed by conventional psychotherapeutic interpretation.

Examples of rationalisation include a student who fails an exam and blames the teacher for not teaching the material well enough, of a person who cheats on their partner and justifies it by saying their partner was neglectful of unaffectionate. It allows the individual to avoid taking responsibility for their actions and to maintain a positive self-image.

Overall, rationalisation can be a useful defense mechanism in certain situations, but it can also be harmful if it leads to a lack of accountability and an inability to learn from mistakes.

Headache, nausea, vomiting, papilledema, and ocular palsies are symptoms of increased intracranial pressure, which are not typically present in cases of normal pressure hydrocephalus.

Normal Pressure Hydrocephalus

Normal pressure hydrocephalus is a type of chronic communicating hydrocephalus, which occurs due to the impaired reabsorption of cerebrospinal fluid (CSF) by the arachnoid villi. Although the CSF pressure is typically high, it remains within the normal range, and therefore, it does not cause symptoms of high intracranial pressure (ICP) such as headache and nausea. Instead, patients with normal pressure hydrocephalus usually present with a classic triad of symptoms, including incontinence, gait ataxia, and dementia, which is often referred to as wet, wobbly, and wacky. Unfortunately, this condition is often misdiagnosed as Parkinson’s of Alzheimer’s disease.

The classic triad of normal pressure hydrocephalus, also known as Hakim’s triad, includes gait instability, urinary incontinence, and dementia. On the other hand, non-communicating hydrocephalus results from the obstruction of CSF flow in the third of fourth ventricle, which causes symptoms of raised intracranial pressure, such as headache, vomiting, hypertension, bradycardia, altered consciousness, and papilledema.

Functions of the Hypothalamus

The hypothalamus is a vital part of the brain that plays a crucial role in regulating various bodily functions. It receives and integrates sensory information about the internal environment and directs actions to control internal homeostasis. The hypothalamus contains several nuclei and fiber tracts, each with specific functions.

The suprachiasmatic nucleus (SCN) is responsible for regulating circadian rhythms. Neurons in the SCN have an intrinsic rhythm of discharge activity and receive input from the retina. The SCN is considered the body’s master clock, but it has multiple connections with other hypothalamic nuclei.

Body temperature control is mainly under the control of the preoptic, anterior, and posterior nuclei, which have temperature-sensitive neurons. As the temperature goes above 37ºC, warm-sensitive neurons are activated, triggering parasympathetic activity to promote heat loss. As the temperature goes below 37ºC, cold-sensitive neurons are activated, triggering sympathetic activity to promote conservation of heat.

The hypothalamus also plays a role in regulating prolactin secretion. Dopamine is tonically secreted by dopaminergic neurons that project from the arcuate nucleus of the hypothalamus into the anterior pituitary gland via the tuberoinfundibular pathway. The dopamine that is released acts on lactotrophic cells through D2-receptors, inhibiting prolactin synthesis. In the absence of pregnancy of lactation, prolactin is constitutively inhibited by dopamine. Dopamine antagonists result in hyperprolactinemia, while dopamine agonists inhibit prolactin secretion.

In summary, the hypothalamus is a complex structure that regulates various bodily functions, including circadian rhythms, body temperature, and prolactin secretion. Dysfunction of the hypothalamus can lead to various disorders, such as sleep-rhythm disorder, diabetes insipidus, hyperprolactinemia, and obesity.

Assessing Executive Function with the Hayling and Brixton Tests

The Hayling and Brixton tests are two assessments designed to evaluate executive function. The Hayling Sentence Completion Test consists of two sets of 15 sentences, with the last word missing. In the first section, participants complete the sentences, providing a measure of response initiation speed. The second part, the Hayling, requires participants to complete a sentence with a nonsense ending word, suppressing a sensible one. This provides measures of response suppression ability and thinking time. Performance on such tests has been linked to frontal lobe dysfunction and dysexecutive symptoms in everyday life.

The Brixton Test is a rule detection and rule following task. Impairments on such tasks are commonly demonstrated in individuals with dysexecutive problems. Overall, these tests provide valuable insights into executive function and can help identify areas of weakness that may require intervention.

Serotonin: Synthesis and Breakdown

Serotonin, also known as 5-Hydroxytryptamine (5-HT), is synthesized in the central nervous system (CNS) in the raphe nuclei located in the brainstem, as well as in the gastrointestinal (GI) tract in enterochromaffin cells. The amino acid L-tryptophan, obtained from the diet, is used to synthesize serotonin. L-tryptophan can cross the blood-brain barrier, but serotonin cannot.

The transformation of L-tryptophan into serotonin involves two steps. First, hydroxylation to 5-hydroxytryptophan is catalyzed by tryptophan hydroxylase. Second, decarboxylation of 5-hydroxytryptophan to serotonin (5-hydroxytryptamine) is catalyzed by L-aromatic amino acid decarboxylase.

Serotonin is taken up from the synapse by a monoamine transporter (SERT). Substances that block this transporter include MDMA, amphetamine, cocaine, TCAs, and SSRIs. Serotonin is broken down by monoamine oxidase (MAO) and then by aldehyde dehydrogenase to 5-Hydroxyindoleacetic acid (5-HIAA).

The superego encompasses the ‘ego ideal’, which embodies exemplary attitudes and conduct. One can liken the Superego to a moral compass of conscience.

Freud’s Structural Theory: Understanding the Three Areas of the Mind

According to Freud’s structural model, the human mind is divided into three distinct areas: the Id, the Ego, and the Superego. The Id is the part of the mind that contains instinctive drives and operates on the ‘pleasure principle’. It functions without a sense of time and is governed by ‘primary process thinking’. The Ego, on the other hand, attempts to modify the drives from the Id with external reality. It operates on the ‘reality principle’ and has conscious, preconscious, and unconscious aspects. It is also home to the defense mechanisms. Finally, the Superego acts as a critical agency, constantly observing a person’s behavior. Freud believed that it developed from the internalized values of a child’s main caregivers. The Superego contains the ‘ego ideal’, which represents ideal attitudes and behavior. It is often referred to as the conscience. Understanding these three areas of the mind is crucial to understanding Freud’s structural theory.

Aphasia is a language impairment that affects the production of comprehension of speech, as well as the ability to read of write. The areas involved in language are situated around the Sylvian fissure, referred to as the ‘perisylvian language area’. For repetition, the primary auditory cortex, Wernicke, Broca via the Arcuate fasciculus (AF), Broca recodes into articulatory plan, primary motor cortex, and pyramidal system to cranial nerves are involved. For oral reading, the visual cortex to Wernicke and the same processes as for repetition follows. For writing, Wernicke via AF to premotor cortex for arm and hand, movement planned, sent to motor cortex. The classification of aphasia is complex and imprecise, with the Boston Group classification and Luria’s aphasia interpretation being the most influential. The important subtypes of aphasia include global aphasia, Broca’s aphasia, Wernicke’s aphasia, conduction aphasia, anomic aphasia, transcortical motor aphasia, and transcortical sensory aphasia. Additional syndromes include alexia without agraphia, alexia with agraphia, and pure word deafness.

ADHD and Genetics

Decades of research have shown that genetics play a crucial role in the development of attention deficit hyperactivity disorder (ADHD) and its comorbidity with other disorders. However, twin estimates of heritability being less than 100% suggest that environmental factors also play a role. Parents and siblings of a child with ADHD are more likely to have ADHD themselves, but the way ADHD is inherited is complex and not related to a single genetic fault. The heritability of ADHD is around 74%, and longitudinal studies show that two-thirds of ADHD youth will continue to have impairing symptoms of ADHD in adulthood. Adoption studies suggest that the familial factors of ADHD are attributable to genetic factors rather than shared environmental factors. The heritability is similar in males and females, and studies suggest that the diagnosis of ADHD is the extreme of a continuous distribution of ADHD symptoms in the population. Several candidate genes, including DAT1, DRD4, DRD5, 5 HTT, HTR1B, and SNAP25, have been identified as significantly associated with ADHD.

Source: Faraone (2019) Genetics of attention deficit hyperactivity disorder. Molecular Psychiatry volume 24, pages 562–575 (2019).

In 1913, Ebbinghaus found that short-term memory had a limit of seven (+/- two) ‘chunks’ of information, which was later supported by George Miller in 1956 and is now known as Miller’s law. Atkinson and Shiffrin proposed a two-part memory store, one for current information and one for long-term storage. Baddely and Hitch suggested replacing short-term memory with working memory, which includes central executive, articulatory (phonological) loop, and visuospatial scratch pad functions. According to Lloyd, less than one hundredth of the information sensed by humans reaches the short-term memory store. Solso proposed passive decay theory to explain the forgetting of long-term memory.

A drug in depot form is released slowly.

Depot antipsychotics (long-term injectables) are available for both first-generation and second-generation antipsychotics. The efficacy of first-generation antipsychotic depots is considered to be broadly similar, with zuclopenthixol potentially being more effective in preventing relapses but with an increased burden of adverse effects. Second-generation antipsychotic depots have a lower propensity for extrapyramidal symptoms compared to first-generation antipsychotic depots. Test doses should be administered for first-generation antipsychotic depots, and only gluteal injection is licensed for olanzapine depots. Post-injection syndrome is a potential adverse effect of olanzapine depots, which can cause significant weight gain. Patients may be most at risk of deterioration immediately after a depot rather than just before, and relapse seems to occur 3-6 months after withdrawing a depot.

The steady state for this scenario is 337.5 hours, which is equivalent to 14 days. This calculation was obtained by multiplying the half-life of 75 hours by a factor of 4.5, as per the given formula.

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.

Gestalt Psychology and the Laws of Perceptual Organization

Gestalt psychology emerged as a response to structuralism, which aimed to break down thoughts into their basic components. Instead, Gestalt psychologists recognized that individual items must be examined together, as they interact and add complexity to the overall picture. Max Wertheimer, Kurt Koffka, and Wolfgang Köhler are important names associated with Gestalt psychology. Wertheimer discovered the phi phenomenon, which explains how rapid sequences of perceptual events create the illusion of motion. The Gestalt laws of perceptual organization explain how we tend to organize parts into wholes. These laws include symmetry and order, similarity, proximity, continuity, closure, and common fate. These laws help us understand how the mind groups similar elements into collective entities of totalities, and how spatial or temporal grouping of elements may induce the mind to perceive a collective of totality. Additionally, the laws explain how points that are connected by straight of curving lines are seen in a way that follows the smoothest path, and how things are grouped together if they seem to complete a picture. Finally, elements with the same moving direction are perceived as a collective of unit.

Methylphenidate commonly causes a decrease in appetite, while the other listed side-effects are considered rare of uncommon.

ADHD medications can be classified into stimulant and non-stimulant drugs. The therapeutic effects of these drugs are believed to be mediated through the action of noradrenaline in the prefrontal cortex. Common side effects of these drugs include decreased appetite, insomnia, nervousness, headache, and nausea. Stimulant drugs like dexamphetamine, methylphenidate, and lisdexamfetamine inhibit the reuptake of dopamine and noradrenaline. Non-stimulant drugs like atomoxetine, guanfacine, and clonidine work by increasing noradrenaline levels in the synaptic cleft through different mechanisms. The most common side effects of these drugs are decreased appetite, somnolence, headache, and abdominal pain.

Night terrors are a type of sleep disorder that typically occur during the first few hours of sleep. They are characterized by sudden and intense feelings of fear, panic, of terror that can cause the person to scream, thrash around, of even try to escape from their bed. Unlike nightmares, which occur during REM sleep and are often remembered upon waking, night terrors occur during non-REM sleep and are usually not remembered. Night terrors are most common in children, but can also occur in adults. They are thought to be caused by a combination of genetic and environmental factors, and may be triggered by stress, anxiety, of sleep deprivation. Treatment for night terrors may include improving sleep hygiene, reducing stress, and in some cases, medication.

Functions of the Hypothalamus

The hypothalamus is a vital part of the brain that plays a crucial role in regulating various bodily functions. It receives and integrates sensory information about the internal environment and directs actions to control internal homeostasis. The hypothalamus contains several nuclei and fiber tracts, each with specific functions.

The suprachiasmatic nucleus (SCN) is responsible for regulating circadian rhythms. Neurons in the SCN have an intrinsic rhythm of discharge activity and receive input from the retina. The SCN is considered the body’s master clock, but it has multiple connections with other hypothalamic nuclei.

Body temperature control is mainly under the control of the preoptic, anterior, and posterior nuclei, which have temperature-sensitive neurons. As the temperature goes above 37ºC, warm-sensitive neurons are activated, triggering parasympathetic activity to promote heat loss. As the temperature goes below 37ºC, cold-sensitive neurons are activated, triggering sympathetic activity to promote conservation of heat.

The hypothalamus also plays a role in regulating prolactin secretion. Dopamine is tonically secreted by dopaminergic neurons that project from the arcuate nucleus of the hypothalamus into the anterior pituitary gland via the tuberoinfundibular pathway. The dopamine that is released acts on lactotrophic cells through D2-receptors, inhibiting prolactin synthesis. In the absence of pregnancy of lactation, prolactin is constitutively inhibited by dopamine. Dopamine antagonists result in hyperprolactinemia, while dopamine agonists inhibit prolactin secretion.

In summary, the hypothalamus is a complex structure that regulates various bodily functions, including circadian rhythms, body temperature, and prolactin secretion. Dysfunction of the hypothalamus can lead to various disorders, such as sleep-rhythm disorder, diabetes insipidus, hyperprolactinemia, and obesity.

ADRs only occur when medications are used at ABNORMAL doses. (FALSE)

Adverse Drug Reactions (ADRs) refer to the harmful effects associated with the use of a medication at a normal dose. These reactions are classified into two types: Type A and Type B. Type A reactions can be predicted from the pharmacology of the drug and are dose-dependent, meaning they can be reversed by withdrawing the drug. On the other hand, Type B reactions cannot be predicted from the known pharmacology of the drug and include allergic reactions.

Type A reactions account for up to 80% of all ADRs, while Type B reactions are less common. Allergic reactions are a type of Type B reaction and are further subdivided by Gell and Coombs into four types: Type I (IgE-mediated) reactions, Type II (cytotoxic) reactions, Type III (immune complex) reactions, and Type IV (cell-mediated) reactions. Proper identification and management of ADRs are crucial in ensuring patient safety and optimizing treatment outcomes.

The First Pass Effect in Psychiatric Drugs

The first-pass effect is a process in drug metabolism that significantly reduces the concentration of a drug before it reaches the systemic circulation. This phenomenon is related to the liver and gut wall, which absorb and metabolize the drug before it can enter the bloodstream. Psychiatric drugs are not exempt from this effect, and some undergo a significant reduction in concentration before reaching their target site. Examples of psychiatric drugs that undergo a significant first-pass effect include imipramine, fluphenazine, morphine, diazepam, and buprenorphine. On the other hand, some drugs undergo little to no first-pass effect, such as lithium and pregabalin.

Orally administered drugs are the most affected by the first-pass effect. However, there are other routes of administration that can avoid of partly avoid this effect. These include sublingual, rectal (partly avoids first pass), intravenous, intramuscular, transdermal, and inhalation. Understanding the first-pass effect is crucial in drug development and administration, especially in psychiatric drugs, where the concentration of the drug can significantly affect its efficacy and safety.

Speech disturbances can be caused by organic of psychogenic disorders. In this case, the patient is experiencing dissociative aphonia, which is a conversion disorder where psychological stress is converted into physical symptoms. Aphonia is the loss of ability to vocalize, resulting in whispered speech, and can also occur in organic disorders. Dysphonia is a speech impairment characterized by hoarseness but without complete loss of function. Echolalia is the automatic repetition of words of parts of sentences spoken in the presence of the person. Logoclonia is a condition where the patient may get stuck on a particular word, resulting in spasmodic repetition of syllables of words. Stuttering is a speech disorder characterized by involuntary repetitions, prolongations, of blocks in speech flow, resulting in silent pauses of difficulty producing sounds.

Modes of Inheritance

Genetic disorders can be passed down from one generation to the next in various ways. There are four main modes of inheritance: autosomal dominant, autosomal recessive, X-linked (sex-linked), and multifactorial.

Autosomal Dominant Inheritance

Autosomal dominant inheritance occurs when one faulty gene causes a problem despite the presence of a normal one. This type of inheritance shows vertical transmission, meaning it is based on the appearance of the family pedigree. If only one parent is affected, there is a 50% chance of each child expressing the condition. Autosomal dominant conditions often show pleiotropy, where a single gene influences several characteristics.

Autosomal Recessive Inheritance

In autosomal recessive conditions, a person requires two faulty copies of a gene to manifest a disease. A person with one healthy and one faulty gene will generally not manifest a disease and is labelled a carrier. Autosomal recessive conditions demonstrate horizontal transmission.

X-linked (Sex-linked) Inheritance

In X-linked conditions, the problem gene lies on the X chromosome. This means that all males are affected. Like autosomal conditions, they can be dominant of recessive. Affected males are unable to pass the condition on to their sons. In X-linked recessive conditions, the inheritance pattern is characterised by transmission from affected males to male grandchildren via affected carrier daughters.

Multifactorial Inheritance

Multifactorial conditions result from the interaction between genes from both parents and the environment.

Olanzapine belongs to the thienobenzodiazepine class.

Antipsychotics can be classified in different ways, with the most common being typical (first generation) and atypical (second generation) types. Typical antipsychotics block dopamine (D2) receptors and have varying degrees of M1, Alpha-1, and H1 receptor blockade. Atypical antipsychotics have a lower propensity for extrapyramidal side-effects and are attributed to the combination of relatively lower D2 antagonism with 5HT2A antagonism. They are also classified by structure, with examples including phenothiazines, butyrophenones, thioxanthenes, diphenylbutylpiperidine, dibenzodiazepines, benzoxazoles, thienobenzodiazepine, substituted benzamides, and arylpiperidylindole (quinolone). Studies have found little evidence to support the superiority of atypicals over typicals in terms of efficacy, discontinuation rates, of adherence, with the main difference being the side-effect profile. The Royal College also favors classification by structure.

While alpha (α) and beta (β) activity are typical in adults who are awake and at rest, delta activity (δ) may suggest the presence of a brain tumor. Mu (μ) activity is linked to movement, and theta activity (θ) is uncommon in the waking adult population, occurring briefly in only 15% of individuals.

Paraschemazia is a type of body image distortion that involves a feeling that certain body parts are twisted, distorted, of separated from the rest of the body. This can be caused by various factors, including hallucinogenic drug use, epileptic aura, and migraine. Body image distortions can be caused by both organic and psychiatric conditions. Organic causes may include Brown-Séquard paralysis, epileptic aura, and migraine, while psychiatric causes may include anorexia nervosa, hypochondriasis, depersonalization, and conversion disorders. Hemiasomatognosia is a specific type of body image distortion where the person feels that one half of their body is missing, and it can occur in epileptic aura and migraine. Other types of body image distortions include hyperschemazia, where parts of the body feel magnified in size, and hyposchemazia, where parts of the body feel diminished in size.

Principles of Therapeutic Communities

Therapeutic communities are based on four main principles that guide their operations. The first principle is communalism, which emphasizes that staff and service users should not be separated by uniforms of behaviours. This means that everyone in the community is treated equally and with respect. The second principle is democratisation, which involves shared decision-making and unit management. This means that everyone in the community has a say in how things are run and decisions are made collectively. The third principle is permissiveness, which involves accepting and tolerating occasional unpredictable behaviour. This means that members of the community are encouraged to be themselves and express their emotions freely. The fourth principle is reality confrontation, which involves group members challenging self-deception among others. This means that members of the community are encouraged to be honest with themselves and others.

Group cohesion is another important aspect of therapeutic communities. It refers to the sense of belonging and acceptance that members of the community feel. This sense of belonging is fostered by the shared goal that the community is working towards. Members of the community understand that they are all in this together and that they need to support each other to achieve their goals. The sense of belonging and acceptance that comes with group cohesion is essential for the success of therapeutic communities.

The symptoms reported by the patient are likely caused by the side-effects of lithium. Increased thirst is a common occurrence when starting lithium treatment. Patients with psoriasis may not be suitable candidates for lithium use. Although the mechanism behind pedal edema is not fully understood, it is a well-known side-effect of lithium treatment, as reported in a case study by Paravathypriya (2016) in the International Journal of Pharmacy and Pharmaceutical Sciences.

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.

The Brief Psychiatric Rating Scale assesses the level of cooperation with the interview, utilizing a combination of self-report and clinical observation. Due to its reliance on these methods, it cannot be conducted via telephone.

Brief Psychiatric Rating Scale: An Instrument for Evaluating Psychopathology in Psychiatric Patients

The Brief Psychiatric Rating Scale (BPRS) is a widely used tool for assessing psychopathology in psychiatric patients. It was developed in the 1960s by Overall and Gorham, using factor analysis, to evaluate the severity of schizophrenic states and provide clinicians with a quick way to assess patient change. Initially, the BPRS consisted of 16 items, but two more items were added to create the standard 18-item version. Later, an expanded 24-item version was introduced to measure additional aspects of schizophrenia, such as bizarre behavior, self-neglect, suicidality, elevated mood, motor hyperactivity, and distractibility.

The BPRS is rated by a clinician, who assesses each item on a 7-point scale of severity. Higher scores indicate greater severity of symptoms. The assessment relies on a combination of self-report and observation. Several variables are rated based on observation, while the rest are assessed through a short interview. The total score severity, using the 18-item version, has been estimated as mildly ill (31), moderately ill (41), and markedly ill (53). The administration of the BPRS can take 10-40 minutes, and versions have been validated for use in both children and older adults. As it is clinician-administered, the BPRS does not require patients to be able to read of write.

Erik Erikson and Daniel Levinson expanded the understanding of adult development. Erikson proposed a life-span model of human development consisting of eight successive psychosocial stages, each associated with an inherent conflict of crisis that the individual must encounter and successfully resolve to proceed with development. Levinson proposed a developmental theory consisting of universal stages of phases that extend from the infancy state to the elderly state, based on biographical interviews of 40 men in America. Both theorists maintained that personality develops in a predetermined order and builds upon each previous stage, and that failure to successfully negotiate a stage can result in a reduced ability to complete further stages and therefore a more unhealthy personality and sense of self. However, Levinson’s theory is age-based rather than event-based, and his model proposed a ‘life sequence’ consisting of a series of alternating stable (structure-building) periods and cross-era transitional (structure-changing) periods, with transitional periods typically lasting 5 years.

Serotonin: Synthesis and Breakdown

Serotonin, also known as 5-Hydroxytryptamine (5-HT), is synthesized in the central nervous system (CNS) in the raphe nuclei located in the brainstem, as well as in the gastrointestinal (GI) tract in enterochromaffin cells. The amino acid L-tryptophan, obtained from the diet, is used to synthesize serotonin. L-tryptophan can cross the blood-brain barrier, but serotonin cannot.

The transformation of L-tryptophan into serotonin involves two steps. First, hydroxylation to 5-hydroxytryptophan is catalyzed by tryptophan hydroxylase. Second, decarboxylation of 5-hydroxytryptophan to serotonin (5-hydroxytryptamine) is catalyzed by L-aromatic amino acid decarboxylase.

Serotonin is taken up from the synapse by a monoamine transporter (SERT). Substances that block this transporter include MDMA, amphetamine, cocaine, TCAs, and SSRIs. Serotonin is broken down by monoamine oxidase (MAO) and then by aldehyde dehydrogenase to 5-Hydroxyindoleacetic acid (5-HIAA).

Choline, which is essential for the synthesis of the neurotransmitter acetylcholine, can be obtained in significant quantities from vegetables, seeds, egg yolk, and liver. However, it is only present in small amounts in most fruits, egg whites, and many beverages.