Lost Key Syndrome

The official designation of the Lost Key Syndrome is Dysexecutive Syndrome. It consists cf a group of symptoms, usually resulting from brain damage to the frontal lobe. The syndrome describes a common pattern of dysfunction in functions, such as planning, abstract thinking, flexibility and behavioural control. Although many of the symptoms regularly co-occur, it is common to encounter patients who have several, but not all symptoms.
Patients are left wondering whether these symptoms are the result of their brain injury, whether they are just a result of the patient is getting older, or whether they simply lost their keys for the umpteenth time.

These symptoms that fall into cognitive, behavioural and emotional categories and tend to occur together. Many of the symptoms can be seen as a direct result of impairment to the central executive component of working memory, which is responsible for attentional control and inhibition.

The Lost Key Syndrome often seems to occur with other disorders, such as schizophrenia, dementia, Alzheimer's disease, meningitis and chronic alcoholism[1].

Assessment of patients with the Lost Key Syndrome can be difficult because traditional tests generally focus on one specific problem for a short period of time. People with Lost Key Syndrome can do fairly well on these tests because their problems are related to integrating individual skills into everyday tasks. The lack of everyday application of traditional tests is known as low ecological validity.

There is no cure for individuals with the Lost Key Syndrome, but there are several therapies to help them cope with their symptoms in everyday life.

[1] Abbruzzese et al: Persistent dysexecutive syndrome after pneumococcal meningitis complicated by recurrent ischemic strokes: A case report in World Journal of Clinical Diseases - 2023

Female Inconsistency Syndrome

The Female Inconsistency Syndrome describes a very specific type of character, known as Mary Sue.

A Mary Sue is a character archetype in fiction, usually a young woman, who is often portrayed as inexplicably competent across all domains, gifted with unique talents or powers, liked or respected by most other characters, unrealistically free of weaknesses, extremely attractive, innately virtuous, and/or generally lacking meaningful character flaws[1].
[Batgirl and the actress who played her]

Mostly, she is a slim and beautiful young woman. If a Mary Sue hits a grown man weighing about 100 kilograms, he will fall down like he's been hit by a 10-ton truck.

As a literary trope, the Mary Sue archetype is broadly associated with poor-quality writing, and stories featuring a Mary Sue character are often considered weaker for it. Though the term is mostly used negatively, it is occasionally used positively.

Always female and almost always the main character, a Mary Sue is often an author's idealized self-insertion and may serve as a form of wish fulfillment. Mary Sue stories are often written by adolescent authors or adults who didn't grow out of their adolescence[2].

There's a syndrome lurking beneath that childish writing. Why would a grown man write about a fictional and idealized woman who has no flaws? In this divisive world where 'woke' is equivalent to 'broke', such a unnatural depiction of women will drive away the public that simply wants to watch a movie to be entertained. 

[1] Framke: What is a Mary Sue, and does Star Wars: The Force Awakens have one? in Vox - 2015. See here.
[2] Whatsawhizzer: The Mary Sue and Female Inconsistency Syndrome in wattpad. See here.

Hypochondria Paradox

Once called hypochondriasis, it has now a new designation: illness anxiety disorder. It was added as a separate disorder in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) in 2013. It is a rare condition with symptoms that go beyond average health worries.
Symptoms include a ersistent anxiety or fear of developing or having a serious medical illness that adversely affects their daily life. This fear persists despite normal physical examination and laboratory testing results. Patients pay excessive attention to normal bodily sensations (such as functions of digestion or sweating) and misinterpret these sensations as indicators of severe disease[1]. Some may change doctors repeatedly. Others may avoid medical care.

Many of us are mild hypochondriacs. But there are also people on the other extreme of the spectrum who live in a perpetual state of worry and suffering and rumination about having a serious illness.

A large Swedish study has uncovered a paradox about people diagnosed with an excessive fear of serious illness: They tend to die earlier than people who aren’t hypervigilant about health concerns[2].

Older research had suggested the risk of suicide might be lower for people with the condition, but according to data in the new study, the risk of suicide was in fact four times higher for the people with the diagnosis.

Researchers looked at 4,100 people diagnosed with hypochondriasis and matched them with 41,000 people similar in age, sex and county of residence. They used a measurement called person years, which accounts for the number of people and how long they were tracked.

The researchers found that people with the diagnosis have an increased risk of death from both natural and unnatural causes, particularly suicide. Chronic stress and its impact on the body could explain some of the difference, the authors wrote.

The Hypochondria Paradox is therefore: The more you worry about dying early, the earlier you die.


[1] French, Hameed: Illness Anxiety Disorder in StatPearls – 2023. See here.
[2] David Mataix-Cols et al: All-Cause and Cause-Specific Mortality Among Individuals With Hypochondriasis in JAMA Psychiatry – 2023. See here.

Newyorkitis

Newyorkitis is an affliction generally seen in people living in New York, and especially in Manhattan. It was first described by surgeon John H. Girdner describing "a condition of mind, body, and soul" that he had observed among patients living in the New York City borough of Manhattan[1].
John H. Girdner (1856-1933) was a prominent New York surgeon. He taught at medical schools and was the author of numerous satirical and philosophical articles for magazines.

Girdner ascribed a variety of physical symptoms to living in Manhattan, including nearsightedness (caused by the presence of buildings in all directions), irritated hearing (irritated by constant noise), and a "rapidity and nervousness and lack of deliberation in all muscular movements." Other symptoms included "haste, rudeness, restlessness, arrogance, contemptuousness, excitability, anxiety, pursuit of novelty and of grandeur, pretensions of omniscience, and therefore prescience, which of course undermines any pleasure taken in novelty."

Yes, Newyorkitis was described as "satirical" in obituaries at the time of Girdner's death, and in reviews at the time of publication of his book 'Newyorkitis' in 1901, but time has been kind to Girdner.

A 2020 article observed that at the time, the press "saw evidence of Girdner’s syndrome everywhere."[2] A New York Tribune article on Newyorkitis reported in 1905 that “there were three thousand cases of men falling dead or dying suddenly, an increase of five hundred over any previous year. The pace of the average New Yorker,” the article concluded, “is not only too fast, it is deadly.” In 1908, the Tribune reported that treatment for the condition was being offered at a New York YMCA. It was described as "straight psychology applied directly to the abnormal conditions of urban business and social life."

The stressor was already seen in the Victorian Age in Britain. The advent of steam powered machines added an urgency to everyday life that was previously unknown. Add to this the poverty, pollution, and disease that pervaded the crowded cities, and you will understand the effect it all had on the Victorian minds[3].

[1] Girdner: Newyorkitis – 1901
[2] Charlee Dyroff: An Inflammation of Place: On the symptoms and spread of Newyorkitis in Lapham's Quarterly – 2020. See here.
[3] Fred de Vries: The fear of cats in Victorian times – 2017. See here.

Parental Alienation Syndrome

Getting divorced is never a happy occasion, but responsible parents always want to make sure that their children suffer as little as possible. Using your children as a weapon to get back at your ex-spouse is the vilest thing a parent can do.
Enter the Parental Alienation Syndrome, a term introduced by child psychiatrist Richard Gardner in 1985 to describe signs and symptoms he believed to be exhibited by children who have been alienated from one parent through manipulation by the other parent, usually in the context of child custody disputes[1].

Gardner describes the syndrome as follows: A childhood disorder that arises almost exclusively in the context of disputes over child custody. Its primary manifestation is the child's campaign of denigration against a parent, a campaign without justification. This results from the combination of programming (brainwashing) due to parental indoctrination and the child's own contributions to the vilification of the target parent. When physical or sexual abuse is present, animosity may be justified, and so the explanation of the child's hostility as parental alienation syndrome is inapplicable.

Gardner believed that a set of behaviours that he observed in some families involved in child custody litigation could be used to diagnose psychological manipulation or undue influence of a child by a parent, typically by the other parent who may be attempting to prevent an ongoing relationship between a child and other family members after family separation or divorce.

Proposed symptoms included extreme but unwarranted fear, and disrespect or hostility towards a parent.

The perpetrator may - deliberately or unconsciously - use a variety of tactics to indoctrinate: one parent could tell a child that the other parent hates him and never wants to speak to them, when in reality that parent calls (or tries to call) to speak to the child virtually every day but is refused to do so. A mother might try to convince her daughter to believe and to report to the authorities that the father verbally, physically or sexually abused her. Offenders may blame the other parent for the collapse of the marriage, punish the child for wanting to pursue a relationship with the parent, or move far away so that maintaining a relationship is extremely difficult[2].

Use of the term 'Syndrome' has not generally been accepted by either the medical or legal communities and research has been broadly criticized for lacking scientific validity and reliability. Still, it is a vile abuse of children with potential long lasting effects.

[1] Gardner: Recent trends in divorce and custody litigation in Academy Forum - 1985
[2] Clemente, Padilla-Racero: Are children susceptible to manipulation? The best interest of children and their testimony in Children and Youth Services Review – 2015.

Autumn Sneezing Syndrome

Hay fever is a seasonal type of allergic rhinitis. It is a type of inflammation in the nose that occurs when the immune system overreacts to environmental allergens in the air, such as pollen.
Signs and symptoms include a runny or stuffy nose, sneezing, red, itchy, and watery eyes, and swelling around the eyes.

Until recently, hay fever was limited to spring, summer, and early fall. That's logical, because those are the periods in which plants release their pollen for the purpose of sexual reproduction.

But nowadays, autumn allergies are becoming more common. This phenomenon, called Autumn Sneezing Syndrome, is said to be caused by changing pollen patterns as well as an invasive family of plants called ragweeds (Ambrosia). A single plant may produce about a billion grains of pollen per season. Ragweed pollen can remain airborne for days and travel great distances, and can even be carried over 500 kilometers.

Ragweeds, native to the Americas, have been introduced to Europe in the nineteenth century and especially during World War I, and have spread rapidly since the 1950s.

'Usually you get hay fever starting with the tree pollen in March and April and then grass pollen from May to August, then that was the end of it for most people,' said Dr Adrian Morris, principal allergist at Surrey Allergy Clinic (UK).

Dr Morris said the number of people affected was increasing, in part, due to allergic reactions caused by ragweed, which sheds its pollen later in the year than most plants.

The major allergenic compound in the pollen has been identified as Amb a 1, a 38 kDa nonglycosylated protein composed of two subunits. It also contains other allergenic components, such as profilin and calcium-binding proteins[1].

However, Dr Morris said the main reason why such a large amount of people were continuing to experience allergies long after the summer months was still unclear, emphasising it was a 'reasonably new phenomenon'.

[1] Wopfner et al: The spectrum of allergens in ragweed and mugwort pollen in International Archives of Allergy and Immunology – 2005

Fish Odour Syndrome

If your doctor decides you are afflicted with Fish Odour Syndrome, he might soften the blow by claiming you have a condition called Trimethylaminuria.
The symptoms of Fish Odour Syndrome can be present from birth, but they may not start until later in life, often around puberty. That smell may be constant or may come and go.

The only symptom is that you emit an unpleasant smell, typically of rotting fish – although some might describe it as smelling like other smelly things – that can affect your breath, sweat, urine, and vaginal fluids.

In the Fish Odour Syndrome, the body is unable to turn a strong-smelling chemical called trimethylamine – produced in the gut when bacteria break down certain foods – into a different chemical that doesn't smell. This means trimethylamine builds up in the body and gets into bodily fluids like sweat. That particular sweaty condition is also called Bromhidrosis.

The problem lies in a faulty gene, the FMO3 gene. It provides instructions for making an enzyme that is part of a larger enzyme family called flavin-containing dimethylaniline monooxygenases (FMOs). These enzymes break down compounds that contain nitrogen, sulfur, or phosphorus. The FMO3 enzyme, which is made chiefly in the liver, is responsible for breaking down nitrogen-containing compounds derived from the diet.

Things that can make it worse include sweating, stress, periods and certain foods – such as fish, eggs, and beans.

The Fish Odour Syndrome is probably caused by one or more faulty genes that a person inherits from their parents, but this isn't always the case.

There's currently no cure. Patients are advised to avoid choline-rich foods and take hygienic measures[1].

[1] Kloster, Erichsen: Trimethylaminuria in Tidsskrift for den Norske lægeforening - 2021

Olfactory Reference Syndrome

Olfactory Reference Syndrome is characterized by a distressing or impairing belief by a person that they emit a foul or offensive body odour. The odour is imagined, slight or imperceptible to others[1].
Patients with Olfactory Reference Syndrome are preoccupied, usually for many hours a day, with a distressing or impairing belief that they emit one or more foul or offensive body odours, which are not perceived by others or are actually only slight. They may believe, for example, that they have very bad breath or emit foul-smelling sweat from their armpits or other areas of their skin. Other worries include emitting a smell of urine, flatulence, or unpleasant odours from the genital area. Occasionally, patients believe that they emit odours like old cheese, garbage or rotten food.

The preoccupation with body odour is usually accompanied by repetitive bahaviours, such as smelling themselves, excessive showering, changing clothes and/or reassurance seeking. These behaviours attempt to alleviate the substantial distress caused by the preoccupation with body odour. Most people with Olfactory Reference Syndrome also make efforts to camouflage the perceived odour, for instance with perfume, deodorant, mouthwash and/or bubblegum.

This disorder often results in shame, embarrassment, significant distress, avoidance behaviour, social phobia, and social isolation.

Insight is usually poor or absent. Very few recognize that their belief about the body odour is inaccurate. Thus many patients hope to find treatment to aleviate their problems, such as tonsillectomy for perceived halitosis, proctectomy (anus removal) for perceived anal/flatulence odour.

Cases have been reported from around the world. It is difficult to estimate the prevalence of this condition because data is limited and unreliable. Males appear to be affected twice as commonly as females.

Olfactory Reference Syndrome shares clinical features of both Obsessive-Compulsive Disorder and Social Anxiety Disorder[2]. This suggests that the comorbidity of Obsessive-Compulsive Disorder and Social Anxiety Disorder most likely explains the development of Olfactory Reference Syndrome.

There is no agreed treatment for Olfactory Reference Syndrome. Treatment often includes antidepressants, followed by antipsychotics, and various psychotherapies. Antidepressants seem to be more helpful than antipsychotics.

[1] Phillips, Menard W: Olfactory reference syndrome: Demographic and clinical features of imagined body odour in General Hospital Psychiatry - 2011
[2] Tada: Olfactory Reference Syndrome: Its Relationship to Comorbidity of Social Anxiety Disorder and Obsessive-Compulsive Disorder in Journal of Nervous and Mental Disease - 2023

Neuroleptic Malignant Syndrome

Suppose you need to be prescribed antipsychotic drugs. You (or your loved ones) obviously hope that these drugs will have the desired effect. But for some, an even worse fate than a psychosis lies dormant.
Neuroleptic malignant syndrome is a potentially life-threatening idiosyncratic reaction to antipsychotic drugs characterized by fever, altered mental status, muscle rigidity, and autonomic dysfunction[1]. ‌The fever might result in hyperpyrexia, a condition where the body temperature goes above 41.5o Celsius due to changes in the hypothalamus, the organ in the brain that regulates temperature.‌

The syndrome has been associated with virtually all neuroleptic drugs, including newer atypical antipsychotics, as well as a variety of other medications that affect central dopaminergic neurotransmission.

The first reported case of Neuroleptic Malignant Syndrome appeared in 1956, shortly after the introduction of the antipsychotic drug chlorpromazine (thorazine), which is primarily used to treat psychiatric disorders such as schizophrenia[2]. In the 60s, the medical world became increasingly worried and case studies started to appear regularly in journals[3].

Although uncommon, Neuroleptic Malignant Syndrome remains a critical consideration in the differential diagnosis of patients presenting with fever and mental status changes because it requires prompt recognition to prevent significant morbidity and death.

Treatment includes immediately stopping the offending drug and implementing supportive measures, as well as pharmacological interventions in more severe cases. Maintaining vigilant awareness of the clinical features of Neuroleptic Malignant Syndrome to diagnose and treat the disorder early, however, remains the most important strategy.

[1] Berman: Neuroleptic Malignant Syndrome in The Neurohospitalist – 2011
[2] Ayd: Fatal hyperpyrexia during chlorpromazine therapy in Journal of Clinical and Experimental Psychopathology – 1956
[3] Delay et al: Neuroleptique majeur non phénothiazine et non réserpine, l'halopéridol, dans le traitement des psychoses in Annales Médico-Psychologiques (Paris) - 1960

Great Sheep Panics

The Great Sheep Panic is also known as the 'Great Sheep Panic of 1888' or the 'Mysterious Oxfordshire Sheep Panic of 1888'. It was an event that occurred on 3 November 1888 across southern England, when tens of thousands of sheep fled from various fields across some 520 square kilometers of Oxfordshire.
On the evening of 3 November 1888, at around eight o'clock, thousands of sheep had, supposedly by a simultaneous impulse, burst from their bonds, fields, and dwellings. They had been found the next morning, widely scattered, some of them still panting with terror under hedges, and many crowded into corners of fields, some miles from the fields they had been left in the previous evening.

The Times reported on 20 November 1888 that "malicious mischief was out of the question because a thousand men could not have frightened and released all these sheep." Interestingly, another panic occurred in 1889, in Berkshire (southern England), not far from Reading. Again, on the night of December 4, 1893, another very remarkable panic among sheep occurred in the northern and middle parts of Oxfordshire, extending into adjoining parts of the counties of Warwickshire, Gloucestershire, and Berkshire.

The heavy, oppressive atmosphere accompanying the thick darkness, the susceptibility of sheep to atmospheric disturbances, and their nervous and timid dispositions would all tend to increase the fright the sheep experienced. The cause of the panic being a cloud rolling along so low down as (apparently) to touch the ground, the tops of the hills and the highlying ground would naturally be most affected; and this is observed to be the case, although locally the usual direction followed by thunderstorms has indicated a line along which sheep stampeded on nearly every farm[1].

[1] Author unknown: Sheep panic in Nature - 1921

Galileo Syndrome

The Galileo Syndrome is also called the Galileo Fallacy, and is best known for its use by conspiracy theorists and anti-vax adherents.
The Galileo Syndrome is a logical fallacy that asserts that if your ideas provoke the establishment to supposedly vilify or threaten you, then you must be right — "everyone says I am wrong, therefore I am right."

It is not known if Galileo Galileo (1564-1642) actually expressed those words in Latin (Omnes, inquit, Fallor, ergo recte). Better known is his E pur si muove ('and yet it moves') uttered in 1633 after being forced to recant his claims that the Earth moves around the Sun, rather than the opposite.

Stupid people use this argument too often in response to serious criticisms on their views on a subject that they simply don't understand. What proponents of this fallacy fail to understand is that not all people who challenge the mainstream scientific consensus are martyrs or revolutionaries: in most cases, they are just simply idiots.

Another, closely related quote is 'First They Ignore You, Then They Ridicule You, Then They Fight You, Then You Win'.

This quote is invariably misattributed to Mahatma Gandhi (1869-1948) and proudly repeated like a mantra by complete idiots who think that their idea of science must be more true than that of a scientist who spent his entire working life to understand his chosen field.

Delving deep into history we find the first version of this misattributed quote in 1914 in a speech by the American labour union leader Nicholas Klein when he says 'And, my friends, in this story you have a history of this entire movement. First they ignore you. Then they ridicule you. And then they attack you and want to burn you. And then they build monuments to you. And that, is what is going to happen to the Amalgamated Clothing Workers of America'.

Selective Sound Sensitivity Syndrome

Selective Sound Sensitivity Syndrome is also known as misophonia or sound-rage. It is a disorder of decreased tolerance to specific sounds or their associated stimuli, or cues. These cues, known as "triggers", are experienced as unpleasant or distressing and tend to evoke strong negative emotional, physiological, and behavioral responses that are not seen in most other people.
Negative reactions to these trigger sounds range from annoyance to anger, with possible activation of the fight-or-flight response. The responses do not seem to be elicited by the loudness of the sound, but rather by its specific pattern or meaning to the hearer. Triggers are commonly repetitive stimuli and are primarily, but not exclusively, related to the human body, such as chewing, eating, smacking lips, slurping, coughing, throat clearing, sniffing, and swallowing.

Once a trigger stimulus is detected, people with Selective Sound Sensitivity Syndrome may have difficulty distracting themselves from the stimulus, and may experience suffering, distress, and/or impairment in social, occupational, or academic functioning.

The expression of symptoms varies, as does the severity, which ranges from mild (anxiety, discomfort, and/or disgust) to severe (rage, anger, hatred, panic, fear, and/or emotional distress). Some people with Selective Sound Sensitivity Syndrome are aware that their reactions triggers are disproportionate to the circumstances.

Symptoms are typically first observed in childhood or early adolescence. Selective Sound Sensitivity Syndrome is probably a symptomatic manifestation of an underlying (other) psychiatric disorder, including mood disorders, anxiety disorders, ADHD, OCD, depressive disorders, and autism[1][2]. Its mechanism is also not yet fully understood, but it appears that it may be caused by a dysfunction of the central nervous system in the brain.

In 2022, clinical and scientific leaders convened to create a consensus definition of Selective Sound Sensitivity Syndrome agreeing that it is a disorder of decreased tolerance to specific sounds and their associated stimuli[3].

Health care providers generally try to help people cope with misophonia by recognizing what the person is experiencing and working on coping strategies.

[1] Cavanna, Seri: Misophonia: current perspectives in Neuropsychiatric Disease and Treatment – 2015. See here.
[2] Guzick et al: Clinical characteristics, impairment, and psychiatric morbidity in 102 youth with misophonia in Journal of Affective Disorders – 2023. See here.
[3] Swedo et al: Consensus Definition of Misophonia: A Delphi Study in Frontiers in Neuroscience – 2022. See here.

E-cigarette or Vaping-use Associated Lung Injury (EVALI)

EVALI is the acronym of E-cigarette or Vaping-use Associated Lung Injury. It is a serious inflammatory condition that damages your lungs. It develops as a result of vaping, the use an electronic cigarette (e-cigarette) that heats a liquid into an aerosol that is inhaled (breathed in) into the lungs. You inhale liquid nicotine, propylene glycol, vegetable glycerine, and flavouring.
EVALI is a relatively new condition with the first reported case in 2019. As a result, healthcare providers and medical researchers aren’t sure of EVALI’s long-term effects or outlook. EVALI can develop suddenly and last only a little while (acute) or progress gradually and steadily over a longer period (subacute). Severe cases can be fatal. The symptoms can affect people who’ve used vaping products up to 90 days before symptoms started.

Yes, EVALI is serious. About 90% of reported EVALI cases require hospitalization. As of early 2020, EVALI was responsible for nearly 3,000 hospitalizations and almost 70 deaths.

EVALI symptoms include chest pain, cough, shortness of breath (dyspnea), accelerated heartbeat (tachycardia), abdominal pain, nausea and vomiting, diarrhea, fever, chills, unexplained weight loss, irriversable lung damage, and death. Some chemicals in vaping products can also cause cardiovascular disease and biological changes that are associated with cancer development.

There may be a link between EVALI and vitamin E acetate[1]. Vitamin E acetate is a synthetic form of vitamin E. While vitamin E acetate is safe to ingest, but it may cause lung damage when you heat it and inhale it as a vapour. Other components, propylene glycol and glycerol significantly damage human small airway epithelial cells (SAECs)[2].

Because EVALI shares many of the same symptoms as lung infections, your doctor may initially treat you with antibiotics or antivirals to rule out an infection. Your treatment may also include corticosteroids, drugs that help reduce inflammation.

[1] Boudi et al: Vitamin E Acetate as a Plausible Cause of Acute Vaping-related Illness in Cureus – 2019. See here.
[2] Kumura et al: Propylene glycol, a component of electronic cigarette liquid, damages epithelial cells in human small airways in Respiratory Research – 2022. See here.

Green Flash Phenomenon

Most of you have heard of the Green Flash Phenomenon via the movie 'Pirates of the Caribbean: At World's End' (2007).
Green Flash (and Green Ray) is the term given to rare meteorological optical phenomena that occur transiently around the moment of sunset or sunrise, when a green spot is visible for a short period of time above the sun, or a green ray shoots up from the sunset point. According to Pirate Lore, it was a flash that shoots up into the sky at the last glimpse of sunset, signaling the return of a soul from the world of the dead, or trying to get back from Davy Jones' Locker.

These phenomena usually are seen at an unobstructed horizon, such as over the ocean, but are possible over cloud tops and mountain tops as well. The green appearance usually lasts for no more than two seconds. Rarely, the green flash can resemble a green ray shooting up from the sunset or sunrise point.

Green flash occurs because the atmosphere causes the light from the Sun to separate, or refract, into different frequencies. Green flashes are enhanced by mirages, which increase refraction. A green flash is more likely to be seen in stable, clear air, when more of the light from the setting sun reaches the observer without being scattered. One might expect to see a blue flash, since blue light is refracted most of all and the blue component of the sun's light is therefore the last to disappear below the horizon, but the blue is preferentially scattered out of the line of sight, and the remaining light ends up appearing green.
In addition to atmospheric refraction and lensing, another primary cause of the Green Flash Phenomenon may be due to a phenomenon discovered by American researchers in 2014. They found that when two photons of infrared light collide with a human retina cell, they cause what the researchers call 'a double hit'. It creates the perception of bright neon green[1]. The researchers discovered this inadvertently while working with powerful infrared lasers - which should have been invisible to them - yet the researchers consistently kept seeing bright green flashes from the source of the laser. Because the Green Flash Phenomenon occurs exactly where we would expect the bulk of refracted infrared sunlight: just beyond red but not by much. The most likely hypothesis is that the Green Flash Phenomenon is refracted and magnified infrared light that 'double-hits' the retina or camera lens, creating the effect of bright green.

[1] Palczewska et al: Human infrared vision is triggered by two-photon chromophore isomerization in PNAS - 2014

Solipsism Syndrome

Well, that's an interesting syndrome, you might think. If only I knew that 'Solipsism' meant. Soplipsism is a word that is coined from Latin, where sōlus means 'alone' (think 'solitaire') and ipse means 'himself' or 'herself'. Taken together, it means something like 'alone with himself (or herself)'.
Solipsism Syndrome refers to a psychological state in which a person feels that reality is not external to their mind. Periods of extended isolation may predispose people to this condition. In particular, the syndrome has been identified as a potential concern for individuals living in outer space for extended periods of time.

Individuals experiencing Solipsism Syndrome feel that reality is not 'real' in the sense of being external to their own minds. The syndrome is characterized by feelings of loneliness, detachment and indifference to the outside world.

Solipsism Syndrome is not currently recognized as a psychiatric disorder by the American Psychiatric Association, though it shares some similarities with Depersonalization Disorder, which ís recognized and therefore ís included in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR) uit 2022.

Solipsism Syndrome is distinct from solipsism, which is merely a philosophical position that nothing exists or can be known to exist outside of one's own mind rather than a psychological state. Advocates of this philosophy do not necessarily suffer from solipsism syndrome, and sufferers do not necessarily subscribe to solipsism as a school of intellectual thought.

Periods of extended isolation may predispose people to solipsism syndrome. In particular, the syndrome has been identified as a potential challenge for American astronauts, Russian cosmonauts and Chinese taikonauts on long-term missions. Also, prisoners and psychiatric patient who can endure long periods of solitary confinement may be in danger of suffering from the solipsism syndrome.

Lost Penis Syndrome

The Lost Penis Syndrome is a term often used in non-clinical settings to describe the subjective perception of the loss of cutaneous and proprioceptive feelings of the male organ during vaginal penetration. In other words: you don't feel that your penis feels anything that it should be feeling. Your penis feels lost.
Although deserving clinical attention, this syndrome did not receive any consideration in the medical literature. Notwithstanding, it represents a relatively unexceptional condition, and it is often reported together with other sexual dysfunctions, especially delayed ejaculation, anejaculation, male anorgasmia and inability to maintain a full erection.

Time for researchers to closely look at the problem[1].

Efficient penile erection and sensitivity, optimal vaginal lubrication and trophism (vaginal pH) contribute to penovaginal friction. Whenever one of these processes does not occur, loss of penile sensation defined as Lost Penis Syndrome can occur.

Sociocultural, psychopathological and age-related factors are also implicated in the etiology.

The researcher unearthed four types of Lost Penis Syndrome from the literature review: anatomical and/or functional, behavioral, psychopathological and iatrogenic.

According to the subtype, a wide variety of treatments can be employed, including the vasodilating drug PDE5i, testosterone replacement therapy and vaginal cosmetic surgery, as well as targeted therapy for concomitant sexual comorbidity.

[1] Elena Colonnello et al: The Lost Penis Syndrome: A New Clinical Entity in Sexual Medicine in Sexual Medicine Reviews – 2022. See here.

Pomperipossa Effect

Astrid Lindgren (1907-2002) was a very successful Swedish writer of fiction and screenplays. She is best known for several children's book series, featuring Pippi Longstocking. Her books sold massively worldwide and that meant royalties for Astrid Lindgren.
In 1975 the Swedish Social Democrat Government introduced a new tax regime that meant self-employed individuals like Astrid Lindgren had to pay both regular income tax and employer’s fees. In Lindgren’s case this meant a marginal tax rate of 102%. Which meant that she had to pay more in tax than she actually earned.

As a reaction, Astrid Lindgren wrote 'Pomperipossa in Monismania’ (English: ‘Pomperipossa in the World of Money’), a satirical allegory about a writer of children's books in a distant country. The story was published in Stockholm’s leading evening tabloid newspaper, Expressen, on 3 March 1976.

Publicly, Lindgren continued to support the party for all her life, but private letters reveal that she supported the opposition in the 1976 election and that she feared that the Social Democratic Party after 44 years of consecutive rule was turning Sweden into a socialist dictatorship.

This idiocy has subsequently been dubbed the ‘Pomperipossa Effect’ by economists[1]. Even the Swedes, who are normally fairly passive over high levels of tax, were so incensed that the next year the Social Democrats were thrown out of government. The Pomperipossa Effect is thus a way to commit political suicide.

The English translation of 'Pomperipossa in Monismania' can be read here.

[1] Professor Ian Angell (Department of Management, London School of Economics): The Pomperipossa Effect - 2014

Bullshit Asymmetry Principle

The Bullshit Asymmetry Principle is also known as Brandolini's Law, first publicly formulated in 2013 by Alberto Brandolini, an Italian programmer.
The principle emphasizes the effort of debunking misinformation, in comparison to the relative ease of creating it in the first place. The law states the following: The amount of energy needed to refute bullshit is an order of magnitude bigger than that needed to produce it.

The Bullshit Asymmetry Principle has gained huge importance in the age of social media, where any idiot can publish misinformation he or she believes is true. Misinformation, such as anti-vaccine claims or conspiracy theories, are easily published on social media and any other idiot will readily believe it. Real scientists, who have studied the subject almost for their etire working life, will not be believed because they are 'funded by...' and must therefore be distrusted. An idiot watches a few videos on YouTube and then thinks he or she knows more than the scientists.

The persistent claim that vaccines cause autism is a prime example of Brandolini's law. These false claims were first published in 1998 by (now discredited) former physician Andrew Wakefield and are still ventilated by Robert F. Kennedy Jr to feed his narcissism. Despite extensive investigation showing no relationship between vaccines and autism, the false and nefarious claims had a disastrous effect on public health[1]. Decades of research and attempts to educate the public have failed to eradicate the misinformation.

Already in 1845, the economist and writer Claude-Frédéric Bastiat (1801-1850) stumbled on an early notion of the Bullshit Asymmetry Principle when he obserevd that 'We must confess that our adversaries have a marked advantage over us in the discussion. In very few words they can announce a half-truth; and in order to demonstrate that it is incomplete, we are obliged to have recourse to long and dry dissertations'.

As the philosopher Terry Pratchett wrote in his 'Hogfather': The truth may be out there, but the lies are inside your head.

[1] Signorini et al: Vaccine Efficacy Denial: A Growing Concern Affecting Modern Science, and Impacting Public Health in Endocrine, Metabolic & Immune Disorders - Drug Targets - 2022.

Abilene Paradox

In 1974, Jerry B. Harvey, professor of management science at the George Washington University in Washington, D.C , introduced an interesting quirk of group agreement. He called it the Abilene Paradox and explains it as a “failure to manage agreement”[1].
He described it as the tendency of people to go along with what they think the group wants to do — even when they themselves don’t want to do it. If more and more members of the group go along with the idea, it gets more and more difficult to become the spoilsport.

The Abilene Paradox describes a group dynamic where the collective agrees on a path of action that none of the individual members want to do.

To illustrate this phenomenon, Harvey recalls the following story: On a hot afternoon visiting in Coleman, Texas, the family is comfortably playing dominoes on a porch, until the father-in-law suggests that they take a 53 mile (85 kilometers) trip to Abilene for dinner. The wife says, "Sounds like a great idea." The husband, despite having reservations because the drive is long and hot, thinks that his preferences must be out-of-step with the group and says, "Sounds good to me. I just hope your mother wants to go." The mother-in-law then says, "Of course I want to go. I haven't been to Abilene in a long time."

As expected, the drive is hot, dusty, and long. When they arrive at the cafeteria, the food is as bad as the drive. They arrive back home four hours later, exhausted.

One of them dishonestly says, "It was a great trip, wasn't it?" The mother-in-law says that, actually, she would rather have stayed home, but went along since the other three were so enthusiastic. The husband says, "I wasn't delighted to be doing what we were doing. I only went to satisfy the rest of you." The wife says, "I just went along to keep you happy. I would have had to be crazy to want to go out in the heat like that." The father-in-law then says that he only suggested it because he thought the others might be bored.

The group sits back, perplexed that they together decided to take a trip that none of them wanted. They each would have preferred to sit comfortably but did not admit to it when they still had time to enjoy the afternoon.

The Abilene Paradox results from a kind of false cognitive dissonance. Cognitive dissonance is the psychological discomfort that arises when we do something out of sync with what we believe to be true. In this case, we want to be in alignment with others, but we also feel that what we think the group wants to do is a bad idea. This results in a difficult choice: deal with the discomfort of speaking up or the discomfort of being dishonest about your true feelings.

[1] Jerry B. Harvey: The Abilene Paradox: The Management of Agreement in Organizational Dynamics – 1988. See here.

Hogwarts Headache

A Hogwarts headache is a generalized headache as a result from spending many hours reading an unusually long (or heavy) volume such as one of J.K. Rowling's Harry Potter books. The pain resolved in one to two days after the patient finished the book.
The term Hogwarts headache was coined by Dr. Howard J. Bennett in a Letter to the Editor of The New England Journal of Medicine on October 30, 2003. Dr. Bennett's letter was entitled "Hogwarts Headaches - Misery for Muggles"[1]

Bennet had to evaluate three children between 8 and 10 years of age who presented with a two-to-three-day history of generalized headaches. In each case, the headache was dull and the pain fluctuated throughout the day. One patient also reported neck and wrist pain. All the patients were afebrile and free of any symptoms suggesting an underlying infectious or neurologic cause. On further questioning, it was determined that each child had spent many hours reading J.K. Rowling's latest book in the Harry Potter series. Two patients read the book lying prone, and the third propped the book on her legs and rested her head on a pillow.

The presumed diagnosis for each child was a tension headache brought on by the effort required to plow through a more than 700-page book. The obvious cure for this malady — that is, taking a break from reading — was rejected by two of the patients, who instead preferred paracetamol, a painkiller called acetaminophen in the US, Canada, Japan, and South Korea. In all cases, the pain resolved one to two days after the patient had finished the book.
You wonder why parents take their children to see a doctor with a bit of a headache after reading for hours on end, something they've never done before. Parents are strange creatures.

[1] Bennett: Hogwarts Headaches — Misery for Muggles in The New England Journal of Medicine – 2003. See here.

Black Urine Disease

Black Urine Disease is also known as Alkaptonuria, as scientists never waste a a good opportunity to make something sound more interesting.
Black Urine Disease is rare (one in 250,000 people) inherited recessive genetic disease that results in a build-up of a substance in the blood called homogentisic acid, staining the tissues dark. In addition, the condition prevents the body from entirely breaking down two amino acids called tyrosine and phenylalanine that are responsible for body pigmentation. Homogentisic acid and its oxidized form alkapton are excreted in the urine, giving it an unusually dark color.

The accumulating homogentisic becomes overt in form of severe spondylosis, peripheral arthropathy, tendon rupture, bone osteoporosis as well as aortic valve stenosis and skin pigmentation, as well as precipitating as kidney stones and stones in other organs[1].

Symptoms of Black Urine Disease usually develop in people over 30 years old, although the dark discoloration of the urine is present from birth. Black Urine Disease seems more common in Slovakia and the Dominican Republic.

Apart from treatment of the complications (such as pain relief and joint replacement for the cartilage damage), the drug (read: herbicide) nitisinone has been found to suppress the production of homogentisic acid, and research is ongoing as to whether it can improve symptoms[2].

[1] Grosicka, Kucharz: Alkaptonuria in Wiadomości Lekarskie (Medical News) – 2009
[2] Häberle: Suitability of nitisinone for alkaptonuria in Lancet - 2020

Aspirin-Exacerbated Respiratory Disease (AERD)

Aspirin-exacerbated respiratory disease (AERD), also known as Samter’s Triad, is a chronic medical condition that has three clinical features: [I] asthma, [II] sinusitis with recurrent nasal polyps, and [II] sensitivity to aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) that inhibit an enzyme called cyclooxygenase-1 (or COX-1).
This sensitivity usually manifests as respiratory reactions that occur upon taking an aspirin or related drug, though the exact cause of the reactions is not known. Approximately 9% of all adults with asthma and 30% of patients with asthma and nasal polyps have Aspirin-Exacerbated Respiratory Disease. Other, less common symptoms may include a loss of smell, skin flushing, rashes, abdominal pain, occasionally vomiting.

Usually, Aspirin-Exacerbated Respiratory Disease develops quite suddenly in adulthood, usually between the ages of 20 and 50, and there is no clearly understood trigger that triggers the disease.

About 75% of all patients with Aspirin-Exacerbated Respiratory Disease develop mild-to-moderate respiratory reactions when they drink alcohol[1]. These reactions are not always specific to just one type of alcohol and often occur after consuming less than one glass of alcohol.

There is no one specific test or blood result that alone can be used to diagnose the disease. The triple symptoms of asthma plus nasal polyps plus respiratory reactions to NSAIDs is all that is needed for the diagnosis.

Most patients with Aspirin-Exacerbated Respiratory Disease will need to use daily medications to control their symptoms and often need to use daily inhaled corticosteroids for asthma. Intranasal steroid sprays or steroid sinus rinses can help to control the nasal symptoms, and nasal polyps can also be treated with occasional courses of oral steroids. Several non-steroid medications are also available, specifically medications that inhibit the production of leukotrienes (zileuton) or block the function of leukotrienes (montelukast and zafirlukast). Despite intensive medical therapy, the need for surgical removal of nasal polyps in Aspirin-Exacerbated Respiratory Disease is very common, though unfortunately the rate of recurrence of nasal polyps after surgery is high.

Aspirin desensitization in patients with Aspirin-Exacerbated Respiratory Disease can be performed by administering gradually increasing doses of aspirin in a hospital setting. The goal of aspirin desensitization is to have the patient begin long-term daily aspirin therapy, which in some patients can decrease the regrowth of nasal polyps.

[1] Candelo et al: Relationship Between Alcohol Intolerance and Aspirin-Exacerbated Respiratory Disease (AERD): Systematic Review in Otolaryngology: Head and Neck Surgery - 2023

Mean Girl Phenomenon

Mean Girl Phenomenon, also known as relational aggression, is a survival tactic for people who are insecure, immature, jealous, egotistical, and yes, narcissistic. It can be described as covert or indirect aggression or bullying in which harm is caused through damage to relationships or social status within a group, rather than through physical violence[1].
Mean Girl Phenomenon often goes unnoticed by parents, educators, and even society in general. One of the problems is, the people you least expect it from, fall into this category.

Tweens, teens and young adults that participate in relational aggression are often able to manipulate others and it go undetected by society. In fact, some are so cunning, that no one would ever suspect them of hurting others and sometimes very shocked by it. You know that person, the one that smiles, is overly nice to you, listens to all your problems and then stabs you in the back by using it against you. It's gossiping or emotional bullying with a negative intent.

Research shows that one of the top reasons’ girls engage in relational aggression is to establish or maintain their social status. Girls will use relational aggression to socially isolate someone while increasing their own social status. They also do this to protect their reputation or get the jump on someone else. They collect the data they need and use it when it most fits their needs.

As you would expect, relational aggression is associated with cognitive aspects of social intelligence, whereas overt aggression by lack of social skills[2].

[1] Doyle, McLoughlin: Do Science and Common Wisdom Collide or Coincide in their Understanding of Relational Aggression? in Frontiers in Psychology – 2010. See here.
[2] Andreou et al: Social Preference, Perceived Popularity and Social Intelligence: Relations to Overt and Relational Aggression in School Psychology International - 2016

Sluggish schizophrenia

Sluggish schizophrenia (or slow progressive schizophrenia) was a fictional diagnosis used (or rather misused) in the former Soviet Union in the decades following the Second World War[1]. It was a political tool that the government employed to oppress anti-Soviet dissenters. The Western psychiatric institutions never recognized the diagnosis.
Doctors used it to describe a supposed form of schizophrenia with a slow, progressive course. However, people could receive a diagnosis even if they showed no symptoms of schizophrenia or psychosis, as doctors would allege that symptoms could appear at any time.

The Institute of Psychiatry of the Academy of Medical Sciences of the USSR defined three forms of schizophrenia depending on whether the condition was continuous, recurrent, or mixed.

According to dubious Soviet research from that era, people with sluggish schizophrenia experienced psychopathy, hypochondria, depersonalization or anxiety. Symptoms included pessimism, poor social adaptation, and conflict with authorities. These were themselves sufficient for a formal diagnosis of 'sluggish schizophrenia with few symptoms'. Patients with sluggish schizophrenia could present as seemingly sane but manifest minimal (and clinically relevant) personality changes which could remain unnoticed by the untrained eye. As recent as 2012, delusion of reformism was mentioned as a symptom of mental disorder in the Russian version of the 'Diagnostic and Statistical Manual of Mental Disorders' (DSM): the 'Психиатрия: Национальное руководство' ('Psychiatry: National Manual').

The term 'sluggish schizophrenia' was introduced in the 1930s by Dr. Grunya Sukhareva (1891-1981), who used the term in a 1933 article in which she described a type of schizophrenia that developed slowly in children beginning before puberty[2]. Next, Andrei Snezhnevsky (1904-1987) 'developed' the diagnostic criteria for sluggish schizophrenia in the 1960s. Psychiatrists and doctors in the USSR and some other Eastern Bloc countries used it until 1989, when the Soviet Union collapsed.

Many experts in the West believe that Snezhnevsky developed the concept of sluggish schizophrenia under instructions from the KGB and the Communist Party. The theory was that anyone who opposed the Soviet regime must be mentally ill, because there was no other reason for their antisocial behaviour. Furthermore, diagnosing individuals with sluggish schizophrenia quickly became a tool for handling political dissent.

The Soviet Union’s approach to mental illness, in general, was quite different from that of the Western world. In the USSR, systemic political abuse of psychiatry took place, and authorities used false psychiatric diagnoses as a tool to suppress political dissent.

Especially individuals, involved in the publication or distribution of anti-state literature (samizdat) or political activism, were targets. Psychiatrists would incarcerate these individuals in maximum security mental institutions or in the Soviet forced labour camp system, better known as the Gulag Archipellago.

Once doctors discharged someone with sluggish schizophrenia, they would have lost their civil rights and would be unable to find employment.

Today, the misuse of psychiatry is making a comeback in Russia. Nothing ever changes, especially in Russia. The same misuse of psychiatry to 're-educate' dissenters is now common practice in China and North Korea.

[1] Zajicek et al: Soviet psychiatry and the origins of the sluggish schizophrenia concept, 1912–1936 in History of the Human Sciences - 2018. See here.
[2] Sukhareva: К проблеме дефектности при мягких формах шизофрении [On the problem of defectiveness in mild forms of schizophrenia] in Nevropatol Psikhiatriia Psikhogigiena - 1933

Blue Angel Syndrome

Der blaue Engel ('The Blue Angel') is a classic movie (1930) starring Marlene Dietrich and Emil Jannings.
Professor Immanuel Rath (Emil Jannings) is a respected teacher at the local Gymnasium, in the waning days of the Weimar Republic. Demanding of his students, and filled with a sense of responsibility for their well-being, Rath is scandalized to learn that they have been secretly passing around pictures of Lola Lola (Marlene Dietrich), a performer at the nearby cabaret, called 'Der blaue Engel'.

Rath visits the nightclub in the hope of catching his pupils, but also to confront Lola Lola for corrupting them. Instead, Rath instead falls prey to the singer. Charmed and intoxicated by her sultry act, symbolized by her song, 'Ich bin von Kopf bis Fuß auf Liebe eingestellt', Lola Lola becomes his all-consuming passion, and Rath tries to have an illicit romance with her. When he succeeds, he experiences a fleeting sense of liberation, but soon he realizes the dire consequences of his actions.

His students and employer discover the affair, making his position as a teacher and moral instructor untenable, and he is forced to resign. But that is only the beginning of his miseries. While Lola agrees to marry Rath, she shows little affection for him and takes delight in humiliating him with menial tasks while expressing interest in other men.

Rath’s progressive realization of what is happening to him leads, inexorably, to the film’s tragic ending. He begins to wallow in his predicament, until the psychic pain overwhelms him, and he turns insane.
This type of pathological infatuation has been termed the Blue Angel Syndrome[1].

It is described as a form of psychological masochism. Masochism itself can be defined as any behavior that is repetitively self-destructive. Thus, there is a clear difference between a normal pattern of falling in love normally and a masochistic pattern.

[1] Camille Bruno: Pathological infatuation or the Blue Angel syndrome in Archives of Psychiatric Nursing – 1992. See here.

Brooklyn Syndrome

The term Brooklyn Syndrome was coined during WWII by Navy psychiatrists who were tasked with examining recruits to establish if a recruit is neuropsychiatrically unfit to join the armed services[1].
Sometimes they would encounter recruits who seemed to be truculent and would have a sort of chip-on-the-shoulder attitude.

Initially regarded as a psychopathology, it occurred so frequently the physicians subsequently recognized it as a pattern of behavior characteristic of men from cities where men are seemingly overly argumentative or personally combative.

The Navy psychiatrists have learned by experience that such a recruit is not necessarily a psychiatric personality unfit for service; he may be a perfectly normal guy from Brooklyn.

The psychiatrists have christened this rather harmless, but irritating 'social pattern' the 'Brooklyn syndrome'.

[1] Wittson, Harris, and Hunt: An Evaluation of the Brief Psychiatric Interview in Journal of Psychology - 1943

Whisker Fatigue Syndrome

Cat's whiskers are sensing hairs that give them extra signals about their environment. The sensory organs at the base of the whiskers, called proprioceptors, tell cats a lot about their world. They provide your cat with information regarding her own orientation in space and the what and where of her environment
While cats can voluntarily 'turn on' the sensory focus of their whiskers exactly where they want, whisker receptors mostly respond to a cat’s autonomic system — the sympathetic and parasympathetic nerves that respond to the internal and external environment without conscious control.

The Whisker Fatigue Syndrome is a sort of information overload that stresses out your cat. Because whisker hairs are so sensitive, every time your cat comes into contact with an object or detects movement, even a small change in air current or a slight brush against her face, messages are transmitted from those sensory organs at the base of her whiskers to her brain

Not all vets believe that whisker fatigue is a real condition or cause for concern.

Whisker fatigue is not a disease and appears to manifest primarily with the repeated daily contact with food and water bowls. However, a cat who is stressed is not happy, and if she avoids eating and drinking, she might become malnourished and/or dehydrated.

Preventing or stopping Whisker Fatigue Syndrome means reducing stress. That can be achieved by simple means, like replacing your cat’s food and water bowls with wider bowls so that her whiskers don't touch the sides of the bowl while eating and drinking.

La Mancha Negra

La Mancha Negra means 'The Black Stain' in Spanish. It denotes a mysterious black substance that has oozed from (or on) roads in Caracas (Venezuela), first appearing in 1986. Since its first appearance, La Mancha Negra has caused more than 1,800 deaths in the five years before 1992. La Mancha Negra has been described as an inch-thick, slippery, greasy, black, thick substance that has the consistency of chewed bubble gum.
In 1986, a smudge some 50 meters long was noticed by workers as they patched the 30-year-old asphalt on a highway between Caracas and its airport. Initially, concerns for La Mancha Negra – as it was soon called - were low, but it soon spread. As much as 13 kilometers of highway were soon covered with the unknown bituminous material that contracted and expanded with the weather. It was found to grow when conditions were humid but to shrink when it was cold and dry. It seemed to prefer tunnels and the uphill slopes outside the airport. By 1992 the stain had spread throughout the city of Caracas.

La Mancha Negra made roads slippery, causing vehicles to crash into one another or run off the road. Experts have tried to pinpoint the chemical composition, but were unable to reach a conclusion in 1994.

In 1991, a group of experts consulted President Carlos Andrés Pérez about the problem but could not pinpoint the cause of the substance.[3] 1,800 deaths were then attributed to La Mancha Negra in the five years before
Finally, the government poured tons of pulverized limestone over the La Mancha Negra to 'dry it up'. This seemed to work for a while, but created a different problem; the roads then became so dusty that drivers and local residents complained that the air was unbreathable.

Early 1996, the roads became slick with the substance once more, due to the lack of maintenance, low rainfall and the generally poor condition of vehicles in Caracas. Special cleaning equipment was brought in from Germany, and the phenomenon seemed to have abated for several years thereafter. However, La Mancha Negra reappeared in 2001 on several roads in Caracas.

The most accepted theory is that La Mancha Negra is the result of countless old cars leaking their fluids, such as cheap petrol, motoroil and brake fluid, over the roads[1]. Researchers now think that La Mancha Negra is just an accumulation of those fluids with dust on the roads that over time formed a paste. The roads literally shine with the oil drippings of thousands of cars that labor up an incline into the city each day.

[1] Regina Garcia Cano: On Venezuelan roads, old cars prevail, break down everywhere in AP News - 2022. See here.

Pupula Duplex Anomaly

Pupula duplex anomaly, also known as polycoria, is a condition of the eye characterized by more than one pupillary opening in the iris. It may be congenital or result from a disease affecting the iris. It results in decreased function of iris and pupil, affecting the physical eye and visualization.
In the early history of China, double pupils were seen as a sign that a child would become a great king or sage.

Pupula duplex anomaly is extremely rare. It is often congenital, however not diagnosed until adulthood. The general cause of pupula duplex anomaly is unknown, but there are some other eye conditions that are in association with pupula duplex anomaly. These include (although not often) polar cataracts, glaucoma, abnormally long eyelashes, abnormal eye development, and poor vision.

There have been cases diagnosed from age three to adulthood. The prevalence of true pupula duplex anomaly is minimal. The two kinds of pupula duplex anomaly are true polycoria and false or pseudopolycoria[1].

In cases of true polycoria, there is an extra pupil that tends to be reactive to light and medication.To be considered true polycoria the extra pupil and the principal pupil must dilate and contract simultaneously with triggers such as light and administered drugs. The extraneous pupil is circa 2.5 millimeters away from the principal pupil. In cases of true polycoria there is an intact sphincter muscle, which contracts and dilates the pupils. In an eye without polycoria, the sphincter muscle is a part of the iris that functions to constrict and dilate the pupil. A patient with true polycoria experiences handicapped vision as well as stimulation of the retina in response to bright lights.

Although less rare than true polycoria, pseudopolycoria is still very uncommon. In cases of pseudopolycoria there is a 'passive constriction' that differentiates the extra pupil from the true pupil during constriction and dilation. The extra pupil in pseudopolycoria is different than the extra pupil in true polycoria because it shows defects that are independent of the sphincter muscles. Pseudopolycoria is often associated with Seckel syndrome, posterior polymorphous dystrophy, and juvenile glaucoma. Pseudopolycoria consists of splitting of the iris that are not contingent with the sphincter muscles at the root of the iris.

But pupula duplex anomaly is often misdiagnosed. For instance, people with Axenfeld-Rieger syndrome often have a pupil that is off-center (corectopia) or extra holes in the iris that can look like multiple pupils [2].

[1] Islam et al: True polycoria or pseudo-polycoria? in Acta Ophthalmologica Scandinavica - 2007
[2] Zamora and Salini: Axenfeld-Rieger Syndrome - 2022

Salish Sea Human Feet Phenomenon

Since 2007, at least 20 detached human feet have been found on the coasts of the Salish Sea in British Columbia (Canada) and Washington (USA). In total the discoverey of 21 lone feet have been documented.
The most recent discovery was in 2019, when people on Jetty Island in Everett, Washington called police to report a boot with a human foot inside, which the coroner was able to match to Antonio Neill, who was missing since December 12, 2016[1].

However, prior to the recent avalance of feet washing ashore, there have been earlier instances going back more than a century, such as a leg in a boot that was found on a Vancouver beach in 1887[2].

In Canada, the Coroners Service said in 2017 that foul play had been ruled out by authorities in all investigations and that the feet came from people who died either in accidents or by suicide, and the feet detached during the normal decomposition process. The feet were usually found in sneakers, which the coroner thought were responsible for both keeping the feet buoyant enough to eventually wash ashore, and for giving the feet enough protection from decomposition to be found relatively intact.

In the summer of 2007, forensic scientist Gail Anderson was conducting a study to understand how quickly a homicide victim would decompose in the ocean[3]. Because ethics rules preclude using a human body, she used a dead pig instead. Pigs have often been used in forensic research as stand-ins for a human body; they are roughly comparable in size and are quite similar biologically.

Anderson conducted her study in the Salish Sea. Her team dropped the dead pig into the water, and it quickly sank to the seafloor. The pig carcass was quickly eaten by a hungry mob shrimp, lobsters, and crabs, starting with the softer areas

It turns out that these underwater scavengers will work around bones and other tough obstacles, preferring to pick apart softer tissues. And unlike the bony ball-and-socket joints that join our legs to our hips, our ankles are made up mostly of soft ligaments and other connective tissue. So it follows that a sunken, shoe-wearing cadaver in the Salish Sea is likely to be chewed apart by scavengers, and to have its feet disarticulated from the rest of the body in short order.

What’s more, feet wearing sneakers would almost certainly float. Not only have gas-filled pockets become common in sneaker soles (and they’re visible in some sneakers found in the Salish Sea), but around that time, the foams used in sneaker soles started to be noticeably lighter, with more air mixed in. In other words, they’ve become buoyant.

[1] Human foot in boot washes ashore on Everett island, article appeared in the Herald. See here.
[2] Snyders and O'Rourke: Namely Vancouver: A Hidden History of Vancouver Place Names - 2002
[43] Anderson and Bell: Impact of marine submergence and season on faunal colonization and decomposition of pig carcasses in the Salish Sea in PLoS ONE - 2016