A Historical Note on the Development of Zimelidine, the First Selective Serotonin Reuptake Inhibitor

In 1960s, evidence began to emerge suggesting a significant role of serotonin in depression. This led to the development of zimelidine, the first selective serotonin reuptake inhibitor (SSRI). Zimelidine was derived from pheniramine and was marketed in Europe in 1982. However, it was removed from the market in 1983 due to severe side effects such as hypersensitivity reactions and Guillain-Barre syndrome.

Despite its short-lived availability, zimelidine paved the way for the development of other SSRIs such as fluoxetine, which was approved by the FDA in 1987 and launched in the US market in 1988 under the trade name Prozac. The development of SSRIs revolutionized the treatment of depression and other mood disorders, providing a safer and more effective alternative to earlier antidepressants such as the tricyclics and MAO inhibitors.

The effectiveness of minocycline, a tetracycline antibiotic, in providing neuroprotection has been observed in vitro. This study aimed to evaluate the impact of minocycline on negative symptoms in individuals diagnosed with schizophrenia at the beginning of the trial and after one year of follow-up. Minocycline is recognized for its ability to be well-tolerated in acne treatment and its capacity to cross the blood-brain barrier. Preliminary findings have indicated that it may be effective in preventing the onset of negative symptoms in schizophrenia. There have been no clinical trials conducted on the other antibiotics.

Declarations

The World Medical Association has established global ethical standards through various declarations. These include:

Declaration of Geneva: This declaration was created as a revision of the Hippocratic Oath after the atrocities committed in Nazi Germany.

Declaration of Helsinki: This statement outlines ethical principles for medical research involving human subjects.

Declaration of Tokyo: This declaration states that doctors should not participate in, condone, of allow torture, degradation, of cruel treatment of prisoners of detainees.

Declaration of Malta: This declaration provides guidance to doctors treating individuals on hunger strike.

Declaration of Lisbon: This international statement outlines the rights of patients.

Declaration of Ottawa: This declaration sets out the principles necessary for optimal child health.

Each of these declarations serves as a guide for medical professionals to uphold ethical standards in their practice.

Understanding Grief: Normal and Abnormal Phases

Grief is a natural response to loss, and it is a complex process that can take different forms and durations. John Bowlby and Kubler-Ross have proposed models to describe the typical phases of grief, which can vary in intensity and duration for each individual. Bowlby’s model includes shock-numbness, yearning-searching, disorganization-despair, and reorganization, while Kubler-Ross’s model includes denial-dissociation-isolation, anger, bargaining, depression, and acceptance.

However, some people may experience abnormal grief, which can be categorized as inhibited, delayed, of chronic/prolonged. Inhibited grief refers to the absence of expected grief symptoms at any stage, while delayed grief involves avoiding painful symptoms within two weeks of loss. Chronic/prolonged grief is characterized by continued significant grief-related symptoms six months after loss.

It is important to distinguish between normal grief and major depression, as a high proportion of people may meet the criteria for major depression in the first year following bereavement. Some features that can help differentiate between the two include generalized guilt, thoughts of death unrelated to the deceased, feelings of worthlessness, psychomotor retardation, and prolonged functional impairment.

Overall, understanding the phases and types of grief can help individuals and their loved ones navigate the grieving process and seek appropriate support and resources.

Mannerisms are deliberate movements that convey a specific meaning, while tics are involuntary muscle contractions that disrupt normal activities and are often preceded by a strong urge. Hemiballismus refers to uncontrolled flinging movements of one arm and leg, while chorea involves irregular, jerky, and unpredictable movements that can occur anywhere in the body. Athetosis describes writhing movements, particularly in the arms and hands, and is often associated with cerebral palsy resulting from perinatal anoxia of kernicterus. Infants with athetosis may exhibit delayed motor milestones and floppy movements before developing athetoid movements before the age of 5.

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.

Tricyclic Antidepressants: Uses, Types, and Side-Effects

Tricyclic antidepressants (TCAs) are a type of medication used for depression and neuropathic pain. However, due to their side-effects and toxicity in overdose, they are not commonly used for depression anymore. TCAs can be divided into two types: first generation (tertiary amines) and second generation (secondary amines). The secondary amines have a lower side effect profile and act primarily on noradrenaline, while the tertiary amines boost serotonin and noradrenaline.

Some examples of secondary amines include desipramine, nortriptyline, protriptyline, and amoxapine. Examples of tertiary amines include amitriptyline, lofepramine, imipramine, clomipramine, dosulepin (dothiepin), doxepin, trimipramine, and butriptyline. Common side-effects of TCAs include drowsiness, dry mouth, blurred vision, constipation, and urinary retention.

Low-dose amitriptyline is commonly used for neuropathic pain and prophylaxis of headache. Lofepramine has a lower incidence of toxicity in overdose. However, amitriptyline and dosulepin (dothiepin) are considered the most dangerous in overdose. It is important to consult with a healthcare provider before taking any medication and to follow their instructions carefully.

The psychosocial theory of development, as described by Erikson, involves eight stages that continue into adulthood and require the resolution of a crisis at each stage. Bowlby is known for attachment theory and maternal deprivation, while Freud focused on psychosexual development. Kohlberg studied moral development, and Piaget developed the cognitive model of development.

It is crucial to recognize that SIADH can have various physical origins that could be the primary cause in a patient who has been given psychotropic medication and develops the condition. The hypothalamus can be affected by brain-related conditions such as stroke, leading to the development of SIADH. Additionally, it is important to remain vigilant for any underlying cancer.

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.

Abnormal movements known as athetoid movements are commonly associated with issues in the basal ganglia.

Cerebellar Dysfunction: Symptoms and Signs

Cerebellar dysfunction is a condition that affects the cerebellum, a part of the brain responsible for coordinating movement and balance. The symptoms and signs of cerebellar dysfunction include ataxia, intention tremor, nystagmus, broad-based gait, slurred speech, dysdiadochokinesis, and dysmetria (lack of finger-nose coordination).

Ataxia refers to the lack of coordination of voluntary movements, resulting in unsteady gait, difficulty with balance, and clumsiness. Intention tremor is a type of tremor that occurs during voluntary movements, such as reaching for an object. Nystagmus is an involuntary movement of the eyes, characterized by rapid, jerky movements.

Broad-based gait refers to a wide stance while walking, which is often seen in individuals with cerebellar dysfunction. Slurred speech, also known as dysarthria, is a common symptom of cerebellar dysfunction, which affects the ability to articulate words clearly. Dysdiadochokinesis is the inability to perform rapid alternating movements, such as tapping the fingers on the palm of the hand.

Dysmetria refers to the inability to accurately judge the distance and direction of movements, resulting in errors in reaching for objects of touching the nose with the finger. These symptoms and signs of cerebellar dysfunction can be caused by a variety of conditions, including stroke, multiple sclerosis, and alcoholism. Treatment depends on the underlying cause and may include medications, physical therapy, and surgery.

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).

When transaminase levels are elevated, it is important to conduct further investigations into liver function. While albumin levels may eventually decrease in cases of liver failure, it is a slow process. Therefore, the prothrombin time / INR is a better investigation to consider. Although ultrasound can be useful in investigating abnormal liver function, it is not urgent in this case. Instead, a prothrombin time test would be the preferred investigation.

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.

The hormone ADH (also known as vasopressin) is released from the posterior pituitary gland and promotes water retention and increased blood pressure by constricting arterioles. Conversely, the hormones ACTH, growth hormone, luteinizing hormone, and thyroid stimulating hormone are all released from the anterior pituitary gland and have various effects on the body, such as stimulating hormone production in the adrenal glands, promoting bone and muscle growth, regulating sex gland function, and stimulating the release of thyroxine.

Parkinson plus syndromes, including multisystem atrophy, exhibit a limited efficacy towards Parkinson’s treatment, such as levodopa.

Multisystem Atrophy: A Parkinson Plus Syndrome

Multisystem atrophy is a type of Parkinson plus syndrome that is characterized by three main features: Parkinsonism, autonomic failure, and cerebellar ataxia. It can present in three different ways, including Shy-Drager Syndrome, Striatonigral degeneration, and Olivopontocerebellar atrophy, each with varying degrees of the three main features.

Macroscopic features of multisystem atrophy include pallor of the substantia nigra, greenish discoloration and atrophy of the putamen, and cerebellar atrophy. Microscopic features include the presence of Papp-Lantos bodies, which are alpha-synuclein inclusions found in oligodendrocytes in the substantia nigra, cerebellum, and basal ganglia.

Overall, multisystem atrophy is a complex and debilitating condition that affects multiple systems in the body, leading to a range of symptoms and challenges for patients and their caregivers.

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.

Given that olanzapine is a once daily medication, it is reasonable to estimate its half-life to fall within the range of 20-30 hours. As it happens, the actual half-life of olanzapine is 30 hours.

Antipsychotic Half-life and Time to Steady State

Antipsychotic medications are commonly used to treat various mental health conditions, including schizophrenia and bipolar disorder. Understanding the half-life and time to steady state of these medications is important for determining dosing and monitoring their effectiveness.

Aripiprazole has a half-life of 75 hours and takes approximately 2 weeks to reach steady state. Olanzapine has a half-life of 30 hours and takes about 1 week to reach steady state. Risperidone has a half-life of 20 hours when taken orally and takes 2-3 days to reach steady state. Clozapine and Amisulpride both have a half-life of 12 hours and take 2-3 days to reach steady state. Ziprasidone has a shorter half-life of 7 hours and takes 2-3 days to reach steady state. Quetiapine has the shortest half-life of 6 hours and also takes 2-3 days to reach steady state.

Knowing the half-life and time to steady state of antipsychotic medications can help healthcare providers determine the appropriate dosing and frequency of administration. It can also aid in monitoring the effectiveness of the medication and adjusting the treatment plan as needed.

Nitric Oxide and Depression

Recent research has indicated that nitric oxide (NO) may play a role in the development of depression. Inhibitors of NO synthase have been found to exhibit antidepressant-like effects in preclinical studies, suggesting that NO may be involved in the pathogenesis of depression. These findings suggest that targeting NO signaling pathways may be a potential therapeutic approach for treating depression. Further research is needed to fully understand the role of NO in depression and to develop effective treatments based on this knowledge.

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.

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.

The absence of a halo distinguishes the Lewy bodies found in the brainstem from those found in the cortex. These bodies consist of alpha-synuclein protein, along with other proteins like ubiquitin, neurofilament protein, and alpha B crystallin. Additionally, they may contain tau proteins and are sometimes encircled by neurofibrillary tangles.

Lewy body dementia is a neurodegenerative disorder that is characterized by both macroscopic and microscopic changes in the brain. Macroscopically, there is cerebral atrophy, but it is less marked than in Alzheimer’s disease, and the brain weight is usually in the normal range. There is also pallor of the substantia nigra and the locus coeruleus, which are regions of the brain that produce dopamine and norepinephrine, respectively.

Microscopically, Lewy body dementia is characterized by the presence of intracellular protein accumulations called Lewy bodies. The major component of a Lewy body is alpha synuclein, and as they grow, they start to draw in other proteins such as ubiquitin. Lewy bodies are also found in Alzheimer’s disease, but they tend to be in the amygdala. They can also be found in healthy individuals, although it has been suggested that these may be pre-clinical cases of dementia with Lewy bodies. Lewy bodies are also found in other neurodegenerative disorders such as progressive supranuclear palsy, corticobasal degeneration, and multiple system atrophy.

In Lewy body dementia, Lewy bodies are mainly found within the brainstem, but they are also found in non-brainstem regions such as the amygdaloid nucleus, parahippocampal gyrus, cingulate cortex, and cerebral neocortex. Classic brainstem Lewy bodies are spherical intraneuronal cytoplasmic inclusions, characterized by hyaline eosinophilic cores, concentric lamellar bands, narrow pale halos, and immunoreactivity for alpha synuclein and ubiquitin. In contrast, cortical Lewy bodies typically lack a halo.

Most brains with Lewy body dementia also show some plaques and tangles, although in most instances, the lesions are not nearly as severe as in Alzheimer’s disease. Neuronal loss and gliosis are usually restricted to brainstem regions, particularly the substantia nigra and locus ceruleus.

Alcohol Dependence Treatment Options

Nalmefene has recently been approved for reducing alcohol consumption in alcohol-dependent patients who have a high risk of drinking but do not experience physical withdrawal symptoms and do not require immediate detoxification.

Acamprosate, when used in conjunction with counseling, may help maintain abstinence in alcohol-dependent patients who experience strong cravings.

Bupropion hydrochloride, which has been used as an antidepressant, has been found to be effective in maintaining smoking cessation.

Disulfiram, when consumed with alcohol, causes an extremely unpleasant systemic reaction due to the accumulation of acetaldehyde.

Naltrexone, an opioid-receptor antagonist, may be used to treat alcohol dependence after successful withdrawal.

Psychiatric Syndromes

Couvade syndrome, also known as sympathetic pregnancy, is a conversion disorder that affects expectant fathers. It is characterized by the experience of physical symptoms of pregnancy. This is not a delusion, as the individual does not believe they are pregnant. Epidemiology, such as prevalence rates, may be useful in understanding this syndrome.

Capgras syndrome is a delusional misidentification syndrome in which an individual believes that a familiar person has been replaced by an imposter.

Cotard’s syndrome is a condition characterized by nihilistic delusions, such as the belief that one is dead.

Frégoli syndrome is a delusional misidentification syndrome in which the patient falsely identifies familiar people in strangers.

Koro is a culture-specific syndrome in which the patient believes that their penis is retracting into their abdomen and that they will die as a result.

Torsades de pointes may not be present on an ECG even if the patient experiences recurring episodes, as it has a tendency to appear and disappear.

QTc Prolongation: Risks and Identification

The QT interval is a measure of the time it takes for the ventricles to repolarize and is calculated from the beginning of the QRS complex to the end of the T wave. However, the QT interval varies with the heart rate, making it difficult to use a single number as a cut-off for a prolonged QT. Instead, a corrected QT interval (QTc) is calculated for each heart rate using various formulas. A QTc over the 99th percentile is considered abnormally prolonged, with approximate values of 470 ms for males and 480 ms for females.

Prolonged QT intervals can lead to torsade de pointes (TdP), a polymorphic ventricular tachycardia that can be fatal if it degenerates into ventricular fibrillation. TdP is characterized by a twisting of the QRS complexes around an isoelectric line and is often asymptomatic but can also be associated with syncope and death. An accurate diagnosis requires an ECG to be recorded during the event. It is important to note that an increase in the QT interval due to a new conduction block should not be considered indicative of acquired LQTS and risk for TdP.

Catecholamines are a group of chemical compounds that have a distinct structure consisting of a benzene ring with two hydroxyl groups, an intermediate ethyl chain, and a terminal amine group. These compounds play an important role in the body and are involved in various physiological processes. The three main catecholamines found in the body are dopamine, adrenaline, and noradrenaline. All of these compounds are derived from the amino acid tyrosine. Overall, catecholamines are essential for maintaining proper bodily functions and are involved in a wide range of physiological processes.

Genomic Imprinting and its Role in Psychiatric Disorders

Genomic imprinting is a phenomenon where a piece of DNA behaves differently depending on whether it is inherited from the mother of the father. This is because DNA sequences are marked of imprinted in the ovaries and testes, which affects their expression. In psychiatry, two classic examples of genomic imprinting disorders are Prader-Willi and Angelman syndrome.

Prader-Willi syndrome is caused by a deletion of chromosome 15q when inherited from the father. This disorder is characterized by hypotonia, short stature, polyphagia, obesity, small gonads, and mild mental retardation. On the other hand, Angelman syndrome, also known as Happy Puppet syndrome, is caused by a deletion of 15q when inherited from the mother. This disorder is characterized by an unusually happy demeanor, developmental delay, seizures, sleep disturbance, and jerky hand movements.

Overall, genomic imprinting plays a crucial role in the development of psychiatric disorders. Understanding the mechanisms behind genomic imprinting can help in the diagnosis and treatment of these disorders.

The concept of ‘peek a boo’ is based on the idea that young children have not yet fully grasped the concept of object permanence.

Piaget’s Stages of Development and Key Concepts

Piaget developed four stages of development that describe how children think and acquire knowledge. The first stage is the Sensorimotor stage, which occurs from birth to 18-24 months. In this stage, infants learn through sensory observation and gain control of their motor functions through activity, exploration, and manipulation of the environment.

The second stage is the Preoperational stage, which occurs from 2 to 7 years. During this stage, children use symbols and language more extensively, but they are unable to think logically of deductively. They also use a type of magical thinking and animistic thinking.

The third stage is the Concrete Operational stage, which occurs from 7 to 11 years. In this stage, egocentric thought is replaced by operational thought, which involves dealing with a wide array of information outside the child. Children in this stage begin to use limited logical thought and can serialise, order, and group things into classes on the basis of common characteristics.

The fourth and final stage is the Formal Operations stage, which occurs from 11 through the end of adolescence. This stage is characterized by the ability to think abstractly, to reason deductively, to define concepts, and also by the emergence of skills for dealing with permutations and combinations.

Piaget also developed key concepts, including schema, assimilation, and accommodation. A schema is a category of knowledge and the process of obtaining that knowledge. Assimilation is the process of taking new information into an existing schema, while accommodation involves altering a schema in view of additional information.

Overall, Piaget’s stages of development and key concepts provide a framework for understanding how children learn and acquire knowledge.

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.

Electroencephalography

Electroencephalography (EEG) is a clinical test that records the brain’s spontaneous electrical activity over a short period of time using multiple electrodes placed on the scalp. It is mainly used to rule out organic conditions and can help differentiate dementia from other disorders such as metabolic encephalopathies, CJD, herpes encephalitis, and non-convulsive status epilepticus. EEG can also distinguish possible psychotic episodes and acute confusional states from non-convulsive status epilepticus.

Not all abnormal EEGs represent an underlying condition, and psychotropic medications can affect EEG findings. EEG abnormalities can also be triggered purposely by activation procedures such as hyperventilation, photic stimulation, certain drugs, and sleep deprivation.

Specific waveforms are seen in an EEG, including delta, theta, alpha, sigma, beta, and gamma waves. Delta waves are found frontally in adults and posteriorly in children during slow wave sleep, and excessive amounts when awake may indicate pathology. Theta waves are generally seen in young children, drowsy and sleeping adults, and during meditation. Alpha waves are seen posteriorly when relaxed and when the eyes are closed, and are also seen in meditation. Sigma waves are bursts of oscillatory activity that occur in stage 2 sleep. Beta waves are seen frontally when busy of concentrating, and gamma waves are seen in advanced/very experienced meditators.

Certain conditions are associated with specific EEG changes, such as nonspecific slowing in early CJD, low voltage EEG in Huntington’s, diffuse slowing in encephalopathy, and reduced alpha and beta with increased delta and theta in Alzheimer’s.

Common epileptiform patterns include spikes, spike/sharp waves, and spike-waves. Medications can have important effects on EEG findings, with clozapine decreasing alpha and increasing delta and theta, lithium increasing all waveforms, lamotrigine decreasing all waveforms, and valproate having inconclusive effects on delta and theta and increasing beta.

Overall, EEG is a useful tool in clinical contexts for ruling out organic conditions and differentiating between various disorders.

History of Psychiatric Terms

In the exams, it is important to be familiar with the individuals associated with certain psychiatric terms. For example, Kraepelin is associated with dementia praecox and manic depression, while Bleuler is associated with schizophrenia. Other terms and their associated individuals include Hebephrenia (Hecker), Catatonia (Kahlbaum), Schizoaffective (Kasanin), Neurasthenia (Beard), Unipolar and bipolar (Kleist), Hypnosis (Braid), Group dynamics (Lewin), Group psychotherapy (Moreno), Psychopathic inferiority (Koch), Psychiatry (Reil), and Institutional Neurosis (Barton).

It should be noted that there is some debate over the origins of certain terms. While Kraepelin is often credited with coining the term dementia praecox, some sources suggest that it was first used in its Latin form by Arnold Pick in 1891. The original term demence precoce was first used by Morel in 1852. Despite this, the College appears to favor the Kraepelin attribution.

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).