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.

[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

Spontaneous Human Combustion

Spontaneous Human Combustion is the belief of the combustion of a living (or recently deceased) human body without an apparent external source of ignition. Strange, you might think, that a human body can catch fire without an apparent external source of ignition.
And, if it is too good to be true, it probably isn't.

This idea and the term 'Spontaneous Human Combustion' were both first proposed in 1746 by Paul Rolli, a Fellow of the Royal Society, in an article he translated from the Italian concerning the mysterious death of the Italian Countess Cornelia Zangheri Bandi (1664-1731). Her death was less mysterious if you know that some accounts of the incident report that the countess used to sprinkle camphorated brandy on her body to relieve pain.

The current scientific consensus is that purported cases of Spontaneous Human Combustion must involve external sources of ignition.

Already in 1823, research found commonalities among recorded cases of Spontaneous Human Combustion[1]. These included the following characteristics: the victims are usually chronic alcoholics; they are usually elderly females,; the body has not burned spontaneously, but some lighted substance has come into contact with it; the hands and feet usually fall off; the fire has caused very little damage to combustible things in contact with the body; the combustion of the body has left a residue of greasy and fetid ashes, very offensive in odour.

Another investigation showed that the burned bodies were always close to plausible sources for the ignition, such as candles, lamps, fireplaces, and so on[2]. Such sources were often omitted from published accounts of these incidents, presumably to deepen the aura of mystery surrounding an apparently 'spontaneous' death. The investigations also found that there was a correlation between alleged Spontaneous Human Combustion deaths and the victim's intoxication (or other forms of incapacitation) which could conceivably have caused them to be careless and unable to respond properly to an accident. Where the destruction of the body was not particularly extensive, a primary source of combustible fuel could plausibly have been the victim's clothing or a covering such as a blanket or comforter.

However, where the destruction was extensive, additional fuel sources were involved, such as chair stuffing, floor coverings, the flooring itself, and the like. The investigators described how such materials helped to retain melted fat, which caused more of the body to be burned and destroyed, yielding still more liquified fat, in a cyclic process known as the 'wick effect' or the 'candle effect'.

[1] Dr John Ayrton Paris and John Samuel Martin Fonblanque: A Treatise on Medical Jurisprudence (1823)
[2] Joe Nickell and John Fischer: Spontaneous Human Combustion in The Fire and Arson Investigator - 1984

Visual Snow Syndrome

Imagine an old-school television that receives no (or a very weak) transmission signal. You will hear white noise and you will see a sort of random snow pattern or static.

Your brain may also be having a form of visual hallucination that is characterized by the perception of small, bilateral, simultaneous, diffuse, mobile, asynchronous dots usually throughout the entire visual field, but it can be partial, and it is present in all conditions of illumination, even with the eyes closed. The dots remain individual and do not clump together or change in size. 

This syndrome is called Visual Snow Syndrome. It is uncommon neurological condition with an unknown etiology[1]. The condition is typically always present and has no known cure. Visual snow symptoms commonly appear during the late teenage years and early adulthood. Migraine and tinnitus are common comorbidities and are both associated with a more severe presentation of the syndrome.

Visual snow exists in one of two forms: the pulse type and the broadband type. In the pulse type the dots are the same color as their background, black or white, and the noise is monopolar. In black pulse visual snow, the dots are always darker than their background, whereas in white pulse the dots are always lighter than their background. In the broadband type the dots noise is bipolar and occurs in contrast to the background: with a light background the dots will appear dark, and with a dark background the dots will appear light.

The underlying mechanism is believed to involve excessive excitability of neurons in some parts of the brain. Research has been limited due to issues of case identification and diagnosis, and the limited size of any studied cohort. Initial functional brain imaging research suggests visual snow is a brain disorder.

There is no established treatment for Visual Snow Syndrome. Medications that may be used to treat the condition include lamotrigine (normally used to treat focal epilepsy), acetazolamide (normally used to treat epilepsy) or verapamil (normally used for the prevention of migraines and cluster headaches). However, these do not commonly result in benefits and the evidence for their use is very limited.

[1] Puledda et al: Visual snow syndrome: A clinical and phenotypical description of 1,100 cases in Neurology - 2020. See here.

Tea and Toast Syndrome

Tea and Toast Syndrome is a form of malnutrition commonly experienced by elderly people who are unable or unwilling to prepare meals. An elderly person with nobody left to cook for, or without the skills to cook, will revert to a diet of simple foods such as bread, cheese and crackers, and canned foods. The diet will often dwindle to tea and toast, resulting in a deficiency of vitamins and other nutrients.
Patients also present with hyponatremia, which occurs when the concentration of sodium in the blood is abnormally low. Sodium is an electrolyte, and it helps regulate the amount of water that's in and around your cells[1].

Some signs and symptoms of malnutrition in older adults may include: unintended weight loss, tiredness and fatigue, muscle weakness or loss of strength, constipation, dizziness, syncope, gastritis, peptic ulcers, paleness of the skin, poor wound healing, depression, problems with memory, a weak immune system, and anemia. In addition, the lack of vital nutrients will also create complications of other illnesses, even the common cold, can be much more severe.

The syndrome often manifests itself as hyponatremia, a low concentration of the electrolyte sodium in the bloodstream, due to the lack of salt in the diet. Hyponatremia can lead to various neurological problems ranging from headaches and a decreased ability to think, to seizures and coma in the most severe cases.

According to an article in the New York Times, as many as 60% of seniors living at home are either malnourished or at risk of becoming malnourished[2].

Factors that lead to the syndrome include poverty, social isolation, psychological issues such as depression, chronic illnesses that cause a lack of appetite, dental problems that result in difficulty chewing and swallowing foods, a decline in cognitive functioning, alcoholism, and physical disabilities and limitations.

Potential signs and symptoms of the tTea and Toast Syndrome can include those of 'normal' malnutrition such as general weakness and cognitive impairment.

[1] Filippatos et al: Hyponatremia in the elderly: challenges and solutions in Clinical Interventions in Aging – 2021. See here.
[2] Eric Nagourney: Tea and Toast and a Danger That Can Be Hard to Spot in New York Times - April 12, 2005

Fragile Masculinity Hypothesis

Research shows that many men feel pressure to look and behave in stereotypically masculine ways — or risk losing their (perceived) status as “real men.” Masculine expectations are socialized from early childhood and can motivate men to embrace traditional male behaviours while avoiding even the hint of femininity. This unforgiving standard of maleness makes some men worry that they’re falling short. These men are said to experience “fragile masculinity.”
The political process provides a way that fragile men can reaffirm their masculinity. By supporting tough politicians and policies, men can reassure others (and themselves) of their own manliness[1].

The researchers wanted to see whether fragile masculinity was associated with how Americans vote — and specifically whether it was associated with greater support for Trump in the 2016 general election and for Republicans in the 2018 midterm elections[2].

But measuring fragile masculinity poses a challenge. You cannot simply do a poll of men, who might not honestly answer questions about their deepest insecurities. Instead DiMuccio and Knowles relied on Google Trends, which measures the popularity of Google search terms. People are often at their least guarded when they seek answers from the Internet.

The researchers began by selecting a set of search topics that they believed might be especially common among men concerned about living up to the ideals of manhood: “erectile dysfunction,” “hair loss,” “penis enlargement,” “penis size,” “steroids,” “testosterone” and “Viagra.”

Then, they measured the popularity of these search topics in every media market in the country during the years preceding the past three presidential elections. In the map below, darker colors show where these searches were most prevalent in 2016.
[Darker areas indicate a higher volume of search activity. Source: Google Trends]

The research showed that support for Trump in the 2016 election was higher in areas that had more searches for topics such as “erectile dysfunction.”

[1] DiMuccio, Knowles: Precarious Manhood Predicts Support for Aggressive Policies and Politicians in Personality and Social Psychology Bulletin – 2021
[2] DiMuccio, Knowles: The Political Significance of Fragile Masculinity in Current Opinion in Behavioral Sciences - 2020

Cannabis Hyperemesis Syndrome

Cannabis Hyperemesis Syndrome (CHS) is sometimes also called Cannabinoid Hyperemesis Syndrome affects people who use cannabis (marijuana). Cannabis Hyperemesis Syndrome causes frequent, severe nausea and vomiting. You have a higher risk of developing Cannabis Hyperemesis Syndrome if you use cannabis at least once a week. Your risk also increases if you have used cannabis since adolescence. The only way to cure Cannabis Hyperemesis Syndrome is to stop using cannabis.

Cannabis hyperemesis syndrome is a condition caused by long-term cannabis (marijuana) use. People who have Cannabis Hyperemesis Syndrome experience reoccurring episodes of sometimes explosive nausea, vomiting, dehydration, and abdominal pain, with frequent visits to the emergency department.

Cannabis Hyperemesis Syndrome is more than just a side effect of marijuana. It is a condition that can lead to health complications if left untreated[1].

Cannabis Hyperemesis Syndrome is a form of functional gut-brain axis disorder characterized by bouts of episodic nausea and vomiting worsened by cannabis intake[2]. It is considered as a variant of Cyclical Vomiting Syndrome seen in cannabis users especially characterized by compulsive hot bathing/showers to relieve the symptoms.

[1] Nourbakhsh et al: Cannabinoid Hyperemesis Syndrome: Reports of Fatal Cases in Journal of forensic sciences – 2019
[2] Perisetti et al: Cannabis hyperemesis syndrome: an update on the pathophysiology and management in Annals of Gastroenterology – 2020

Systemic Inflammatory Response Syndrome

Defining the symptoms of Systemic Inflammatory Response Syndrome (or SIRS) led to a collection of other syndromes, such as Multiple Organ Dysfunction Syndrome (MODS), Compensatory Anti-Inflammatory Response Syndrome (CARS), and Mixed Antagonists Response Syndrome (MARS).
In 1992, the American College of Chest Physicians and Society of Critical Care Medicine convened to address the confusion over the (im)proper use of the terms and definitions for sepsis, where the use of the terms bacteremia, septicemia, sepsis, sepsis syndrome and septic shock were being used almost interchangeably. They agreed to a new set of definitions applied to patients in different stages of sepsis: bacteremia, SIRS, sepsis, severe sepsis, septic shock and Multiple Organ Dysfunction Syndrome (MODS). They also proposed to add the Compensatory Anti-Inflammatory Response Syndrome (CARS), and Mixed Antagonists Response Syndrome (MARS) to the set of clinical definitions, as the massive inflammatory reactions understood of SIRS and MODS was only half the picture.

The first acute immune reaction phase Systemic Inflammatory Response Syndrome (SIRS) is described as a subset of a cytokine storm or cytokine dysregulation, an inflammatory state with both pro- and anti-inflammatory components affecting the whole body, frequently a response of the immune system to infectious or non-infectious insult.

SIRS can be caused by ischemia, inflammation, trauma, surgery complications, infection or several insults combined. Nearly every ICU patient (sometimes reported greater than 90%) fits the SIRS criteria and it is considered a serious condition related to systemic inflammation, potentially leading to organ dysfunction or organ failure.

The criteria for SIRS includes at least two of the following:
- Body temperature hypothermic less than 36°C, or fever greater than 38°C
- Tachycardia (abnormal heart rate) greater than 90 bpm
- Tachypnea (high respiratory rate) greater than 20 breath per minute
- White blood cell count elevated (leucocytosis >12,000/l) or depressed (leucopenia <4 l="">
Also observed are:
- Hyperglycemia (blood glucose >6.66mmol/L [120mg/dL] in absence of diabetes mellitus
- Altered mental status

Severe SIRS is frequently complicated by Multiple Organ Dysfunction Syndrome (MODS). Sepsis often accompanies SIRS and the two share very similar symptoms.

Mixed Antagonist Response Syndrome (MARS), an immunological dissonance where at times there may be surges of hyperactivity (SIRS) and immunosuppression (CARS) which can become increasingly destructive and if severe enough leads to MODS, septic shock or a state of anergy. An uncorrected escalating deviation in either direction may result in death.

A 2012 study on sepsis-induced mice demonstrated that concurrent release of pro-inflammatory and anti-inflammatory cytokines occurs irrespective of the sepsis phase, severity or outcome[1]. In that study, the progression of sepsis was monitored which revealed the lethal outcome in sepsis is not caused by a single mediator but is likely driven by concurrent deregulation of numerous immuno-inflammatory pathways.

[1] Osuchowski et al: Sepsis chronically in MARS: systemic cytokine responses are always mixed regardless of the outcome, magnitude, or phase of sepsis in Journal of Immunology – 2012. See here.

Vaccine Acquired Immunodeficiency Syndrome

The internet was once seen as a valuable tool to obtain medical information from experts. Now, it seems that it has become a repository of garbage where every idiot can dump the most preposterous (and potentially dangerous) theories. One of these crackpot theories, presented as a fact by conspiracy theorists, is Vaccine Acquired Immunodeficiency Syndrome, shortened to VAIDS.
The claim is that COVID-19 vaccines are causing a new illness called Vaccine Acquired Immunodeficiency Syndrome.

It baffles the critical mind that people would even consider this theory, because your immune system doesn't know the difference between a virus and a vaccine. The only difference between the two is that the vaccine contains only a tiny part of a dead virus. It can't replicate in your body, giving your immune system ample time to react.

Still, widely circulating social media posts falsely identified Vaccine Acquired Immunodeficiency Syndrome as an emerging condition that is “similar to AIDS but caused by the Corona-19 vaccines.”

AIDS is a generalized body-wide compromise of a specific subset of immune cells (mostly CD4+ lymphocytes) caused specifically by infection with the HIV-1 virus. There is no vaccine-induced counterpart of AIDS.

Vaccines do not cause immunodeficiency. They don’t deplete any immune cells. The opposite is true: they stimulate immune cells to be activated, divide and produce molecules like antibodies and soluble factors to recognize a pathogen and rid the body of it. Research from the Centers for Disease Control and Prevention and others shows the COVID-19 vaccines boost the immune response. The mRNA vaccines work by training the immune system to recognize the spike protein on the surface of the virus that causes COVID-19, allowing it to generate an immune response, experts say.

Given that billions of people around the world have already been vaccinated against COVID-19, if such a 'thing' as Vaccine Acquired Immunodeficiency Syndrome existed, scientists would have detected it by now. Wouldn't they...

Empty Nose Syndrome

Empty Nose Syndrome is a potential complication of nasal surgery. It is a disorder that affects the nose and nasal passages. People with this condition will have normal-appearing, clear nasal passages, yet they will experience a wide range of symptoms[1].
A person who has had surgery on their nose or nasal passages may be at risk of developing Empty Nose Syndrome. Procedures to correct or repair the nasal structure can result in scarring. This scarring may reduce the nasal passages having a feeling that they cannot inhale a complete breath through their nose. These patients may also feel they have symptoms of suffocation, which can alter their sleep cycle and drastically reduce their quality of life.

Sometimes there is no direct cause or easy diagnosis of Empty Nose Syndrome. It remains relatively controversial and research tends to suggest that mental health disorders are comorbid with this syndrome[2]. However, many people report similar symptoms to this condition after surgery, which makes Empty Nose Syndrome an important disorder to study and treat. Corrective surgical methods are still experimental.

Additional symptoms of Empty Nose Syndrome may include a feeling that the inhaled air is too dry or too cold, a nasal obstruction, even though the passageways are clear, regular nasal bleeds, extreme dryness or crusting, headaches and dizzyness.

In the medical literature Empty Nose Syndrome is often referred to as a form of secondary atrophic rhinitis.

[1] Coste et al: Empty nose syndrome in European Annals of Otorhinolaryngology, Head and Neck Diseases - 2012
[2] Kanjanawasee et al: Empty Nose Syndrome Pathophysiology: A Systematic Review in Otolaryngology: Head and Neck Surgery - 2021

New England Vampire Panic

The New England Vampire Panic was a period of terror and mass hysteria during the 19th century, caused by an outbreak of consumption (tuberculosis or TB) blamed on vampires, mostly in the state of New England (United States).
Tuberculosis generally affects the lungs, causing a chronic cough with blood-containing mucus, fever, night sweats and weight loss.

Across the states of Connecticut, Maine, Massachusetts, New Hampshire, Rhode Island and Vermont, outbreaks of tuberculosis spread amongst family members and households. So severe was the epidemic, that it claimed around 2 percent of the region’s population between 1786 to 1800.

When a patient died, it was assumed that they consumed the life of their surviving relatives who also became ill from tuberculosis. To protect the survivors and ward off the symptoms of consumption, the bodies of those who died were exhumed to examine for traits of vampirism.

It wasn’t until the late 17th and 18th century that the folklore for vampires as we imagine, began to be told in the verbal traditions and lore of many European ethnic groups. They were described as the revenants of evil beings, suicide victims, witches, corpses possessed by a malevolent spirit or the victim of a vampiric attack that has resulted in their own viral ascension to vampirism. During the 18th century, vampire sightings across Eastern Europe had reached its peak, with frequent exhumations and the practice of staking to kill potential revenants.

In New England, vampiric traits were determined by how fresh the corpse appeared, especially if the heart or other organs still contained evidence of liquid blood. After a vampiric corpse was identified, the remains were either turned over in the grave, or in some cases the organs were burnt, and the affected family members would inhale the smoke to cure the consumption. In rare cases the deceased would be decapitated and their remains reburied.

The term “vampire” wasn’t a common term used in the 19th century communities across New England, instead it was likely applied by newspapers and outsiders at the time due to the similarity with contemporary vampire beliefs in eastern Europe.

In an anthropological study by Michael Bell of the New England phenomenon, he stated that: No credible account describes a corpse actually leaving the grave to suck blood, and there is little evidence to suggest that those involved in the practice referred to it as ‘vampirism’ or to the suspected corpse as a ‘vampire’, although newspaper accounts used this term to refer to the practice.”[1]

[1] Bell: Food for the Dead: On the Trail of New England's Vampires – 2001

Detroit Syndrome

Detroit Syndrome is a form of age discrimination in which workers of a certain age are replaced by those who are younger, faster, and stronger, not to mention endowed with new skills better suited for the modern workplace. Observers even detect a three-stage process, which is seen as very disrespectful to workers who've been working long hours for years. This process starts by devaluing these workers, then discounting them, and finally dumping them[1].
The syndrome, first reported in 1997, gets its name from the American city of Detroit, and more specifically from its former reputation as a manufacturing hub for automobiles, in which newer models would replace the older ones on a regular basis.

Seen in a somewhat broader sense, it is also a sign of an economic failure. Of cities like Detroit that did not embrace the modern times quickly enough.

Detroit's failing economy was inextricably linked to the auto industry and weapons complex. The corporations had grown complacent and did not see the cheaper, better quality Japanese cars as a threat. The US government allowed these companies to get over-leveraged, and most were (and are) drowned in debt. Automation and the replacement of skilled workers by robots meant that poverty increased and a brain-drain resulted in a dwindling population.

The present desolate and crumbling inner city of Detroit can be the future of any other (now) thriving center of technology or government that misreads the signs of the times.

[1] Petrick, Quinn: Management Ethics: Integrity at Work - 1997

Venice Syndrome

Anyone, who has never visited Venice, probably will think it's a beautyful and romantic city. They are wrong, because the entire medieval city is crumbling with neglect, smells of decay, and is sinking. Still, it's not a reason to commit suicide. Unlike its inhabitants, you can simply leave the city.
Tourists are apparently choosing the Italian city as a place to commit suicide. They seem to have fallen prey to what Venetian psychologist Diana Stainer calls the Venice syndrome or laguna syndrome[1].

She studied 77 cases of attempted suicide by foreign tourists between 1988 and 1995 and concluded that it was no accident that they opted for 'Death in Venice'. But, she suspects, it's just the tip of an iceberg. A further 10 attempted suicides were not considered in the study and another 16 people killed themselves during the period in question. "This phenomenon is almost certainly underestimated," Stainer said.

"Some of the suicides clearly wanted to make a theatrical gesture, perhaps a plea for help. What better choice than an oneiric city like Venice.

With an average age of 36 and evenly split between the sexes, the subjects generally took drug overdoses or attempted to drown themselves in a canal. One Frenchman cut his wrists in the midst of a crowd of fellow tourists.

Nine German speakers - who are most likely to be exposed to the influence of Thomas Mann - tried to end their days in Venice during Stainer's study, while the footsteps of the ailing Dirk Bogarde were followed by eight Frenchmen and two Britons, Dr Stainer said.

Visitors have always been fascinated by the link between Venice and death. For the art critic John Ruskin even the gondolas looked like "floating tombs". Composer Richard Wagner felt as though he was in a funeral procession for plague victims when he ventured out on one of the distinctive black-painted boats.

"It is a city of ghosts and fantasies, outside time and space, Annibale Crosignani, a psychiatrist, thinks. “That is why sensitive people such as artists can become overwhelmed, passing without pause from life to death. For them, sensitive to the appeal of aesthetics, it is deadly beautiful and beautiful to die in."

[1] Stainer et al: Death in Venice. Does a laguna syndrome exist? in Minerva Psichiatrica – 2001

Burgundy-blood Phenomenon

The Burgundy-blood Phenomenon is caused by burgundy-blood algae. This species of algae was originally classified as Oscillatoria rubescens, but in 2002 it was re-assigned to the genus Planktothrix and was renamed to Planktothrix rubescens.
The name 'Burgundy-blood' has a somewhat mythical origin: It is attributed to the blood of the Burgundians slain in the Battle of Morat (1476), where a Swiss army delivered a crushing defeat on the Burgundians near Lake Morat (or the Murtensee in German). Supposedly, the lake coloured red from the blood of the slain Burgundian soldiers whose bodies were thrown in the lake.

Burgundy blood algae are a type of filamentous cyanobacteria or 'blue-green algae'. The are ruddy because of their red pigment phycoerythrin. They are accessory to the main chlorophyll pigments responsible for photosynthesis.

Planktothrix grows in long unbranched cell threads, that are called filaments or trichomes. The straight filaments have limited mobility and show phototaxis, the ability to move directionally in response to a light source.

Flowering can occur under favourable conditions. During flowering this species produces a type of microcystin to protect itself. After mass reproduction, the toxin microcystin can pose a threat to aquatic organisms, to the drinking water supply, and to the environment at large.

In cold, Alpine lakes there have always been always blooms of this species that give the water a reddish hue. These Burgundy-blood algae lives in planktonic form in fresh water, especially in deep and stratified cold water lakes. These bacteria were also found in the deeper layers of Alpine lakes, and an occasional ascent was observed. The species can layer itself through gas bubbles (vesicles) within the water column[1].

Increased pollution supplies additional nutrients to these Alpine lakes, causing the Burgundy-blood Phenomenon to occur more frequently and in thicker layers, killing vast amounts of marine live.
Biologists even speculate that Burgundy-blood Phenomenon might even have been the driving cause of the first plague that is described in the Bible as 'the water turning into blood'. Toxic algae forced the frogs out of water. As frogs died mosquitoes, flies and various other insects flourished without existence of their predators. This led to the fifth and sixth plagues where the livestock was diseased. With the increase in insects there was rise of various epidemics, such as malaria. This, in turn, caused a large number of people falling ill.

[1] Walsby et al: The Burgundy-blood phenomenon: a model of buoyancy change explains autumnal waterblooms by Planktothrix rubescens in Lake Zürich in New Phytologist – 2005. See here.

Watermelon Snow Phenomenon

The Watermelon Snow Phenomenon is also known as Snow Algae, Pink Snow, Red Snow, or Blood Snow. This phenomenon was thought to have been caused by Chlamydomonas nivalis, a species of green algae that, in addition to chlorophyll, contains a secondary red carotenoid pigment, called astaxanthin. This pigment protects the chloroplast from intense visible and ultraviolet radiation, as well as absorbing heat, which provides the algae with liquid water as the snow melts around it.
Unlike most species of fresh-water algae, this species appears to be cryophilic ('cold-loving') and thrives in freezing water.

This type of snow is common during the summer in alpine and coastal polar regions worldwide. There, at altitudes between 3,000 and 3,600 meters, the temperature is low throughout the year, and so the snow will linger from winter storms. Compressing the snow by stepping on it or making snowballs leaves it looking red. Walking on watermelon snow often results in getting bright red soles and pink trouser cuffs.

Snow algae dominate glacial biomass immediately after the onset of melting, and its pigmentation can significantly darken the surface of a glacier. This plays a substantial role in glacial melt[1].

The Watermelon Snow Phenomenon has puzzled mountain climbers, explorers, and naturalists for thousands of years, some speculating that it was caused by mineral deposits or oxidation products that were leached from rocks. They were wrong.
[Image: Will Beback: Watermelon snow pits]

Recent research has shown that the algae responsible for most of the red snow fields on earth do not belong to the genus Chlamydomonas, but had to be placed in a separate, new genus, Sanguina. This genus now contains two known species, Sanguina nivaloides (producing red snow), and Sanguina aurantia (causing orange snow)[2].

During the winter months, when snow covers the algae, they become dormant. In spring, nutrients, increased levels of light, and meltwater will stimulate germination.

[1] Lutz et al: The biogeography of red snow microbiomes and their role in melting arctic glaciers in Nature Communications – 2016
[2] Procházková et al: Sanguina nivaloides and Sanguina aurantia gen. et spp. nov. (Chlorophyta): the taxonomy, phylogeny, biogeography and ecology of two newly recognised algae causing red and orange snow in FEMS Microbiology Ecology – 2019. See here.

Second Impact Syndrome

When a person suffers a second concussion before symptoms from an earlier concussion have subsided, the brain swells rapidly shortly thereafter. This is rare condition, but when it does happen, it is most often fatal. The few who do not die from such an event are usually left severely disabled for life. This is called the Second Impact Syndrome (SIS).
It is a devastating event because young, otherwise healthy patients can die within a few minutes of suffering the second concussion. Death or lifelong disability occurs because the brain suddenly loses its ability to regulate cerebral spinal fluid pressure, leading to severe swelling of the brain and possible herniation of the brain.

The impact of the second event does not have to be strong to trigger second impact syndrome. A minor blow to the head, chest or back that snaps the head enough to cause the brain to move inside the skull can trigger the usually lethal damage.

When a concussion patient whose symptoms have not yet resolved sustains a second impact, they may not even lose consciousness at the moment of the impact, but they may look stunned. They may even complete a game and make it to the sideline themselves, but then collapse within a minute or two. The patient’s condition then deterioreates rapidly with loss of consciousness, loss of eye movement, dilated pupils, then respiratory failure. This can all take place within a few minutes.

Obviously the most sensible approach to avoid a Second Impact Syndrome from occuring is to prevent the first concussion from happening, and then take enough time for the (first) concussion to heal. Any concussed patient who still shows signs of concussion should not be allowed in any activities where another impact is possible.

Signs and symptoms of Second Impact Syndrome include fatigue, headache, disorientation, nausea, vomiting, feeling “in a fog” or “slowed down,” as well as other difference from the patient’s normal behaviour and function.

Post-earthquake Dizziness Syndrome

Major earthquakes are often followed by a significant number of aftershocks. But this quakes not only have destructive effects on the environment, but also have some largely unknown physical and psychological effects on the humans that experience them.
Significant outbreaks of dizziness occurred after an major earthquake. This is now called the Post-earthquake Dizziness Syndrome. However it is unclear why major earthquake causes dizziness.

A trial on equilibrium dysfunction and psychological states associated with equilibrium dysfunction in individuals exposed to repetitive aftershocks versus those who were rarely exposed[1]. Greater equilibrium dysfunction was observed in the aftershock-exposed group under conditions without visual compensation. Equilibrium dysfunction in the aftershock-exposed group appears to have arisen from disturbance of the inner ear, as well as individual vulnerability to state anxiety enhanced by repetitive exposure to aftershocks.

The scientific results seem indicate potential effects of autonomic stress on equilibrium function after major earthquake. The findings may contribute to risk management of psychological and physical health after major earthquakes with aftershocks and allow development of a new empirical approach to disaster care after such events.

Post-earthquake Dizziness Syndrome is an earthquake-induced disequilibrium that may be further influenced by physical stressors, including sensory disruptions induced by earthquake vibrations, changes in living conditions, and autonomic stress[2].

Maybe the Post-earthquake Dizziness Syndrome can be partly seen as a surface-based version of the Mal de Débarquement Syndrome.

[1] Miwa et al: Post-earthquake dizziness syndrome following the 2016 Kumamoto earthquakes, Japan in PLoS One – 2021. See here.
[2] Motoyashu et al: Disturbances in equilibrium function after major earthquake in Science Reports – 2012. See here.

Sundown Syndrome

Sundown Syndrome is also known as sundowning. It is a neurological phenomenon associated with increased confusion and restlessness in people with delirium or some form of dementia. It is most commonly associated with Alzheimer's disease, but also found in those with other forms of dementia.
The term 'sundowning' was first used by Louis K. Evans in 1987 due to the timing of the person's increased confusion beginning in the late afternoon and early evening[1].

For people with Sundown Syndrome, a multitude of behavioural problems begin to occur and are associated with long term adverse outcomes. People are generally able to understand that this behavioural pattern is abnormal. Research shows that 20–45% of people with Alzheimer's will experience some variation of confusion related to Sundown Syndrome.

Some preliminary research tries to link the Sundown Syndrome to accidents[2].

Symptoms are not limited to but may include:
– Increased general confusion as natural light begins to fade and increased shadows appear;
– Agitation and mood swings. Individuals may become fairly frustrated with their own confusion as well as aggravated by noise. Individuals found that yelling and becoming increasingly upset with their caregiver is not uncommon;
– Mental and physical fatigue increase with the setting of the sun. This fatigue can play a role in the individual's irritability;
– An individual may experience an increase in their restlessness while trying to sleep. Restlessness can often lead to pacing and or wandering which can be potentially harmful for an individual in a confused state;
– Hallucinations (visual and/or auditory) and paranoia can cause increased anxiety and resistance to care.

Because the Sundown Syndrome is still a relatively novel syndrome, sufficient research has yet been carried out. Possibly the aberrant behaviour can be seen as 'normal' in patients with variant types of dementia. This uncertainty in all aspects of this syndrome also results in a a wide range of reported prevalence. The latest edition of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) does not regard the Sundown Syndrome as an accepted disorder.

[1] Evans: Sundown syndrome in institutionalized elderly in Journal of the American Geriatric society – 1987
[2] Renner et al: Diurnal variation and injury due to motor vehicle crashes in older trauma patients in Traffic Injury Prevention -2011

Ganser Syndrome

Ganser Syndrome is a rare and somewhat controversial diagnosis. It was first described by Sigbert Ganser (1853-1913) in 1897.  Sometimes called 'prison psychosis', because it was first observed in prisoners. With this condition, a person deliberately and consciously acts as if they have a physical or mental illness when, in fact, they are not really sick. People with Ganser Syndrome mimic behaviour that is typical of a mental illness, such as schizophrenia.
People with such disorders act as if they have an illness by deliberately producing, feigning, or exaggerating symptoms, because of an inner need to be seen as ill or injured[1]. No clear benefit can be found. They are even willing to undergo painful tests and operations in order to obtain the sympathy and special attention given to people who are truly ill. Factitious disorders are technically considered mental illnesses, because they are associated with severe emotional difficulties.

People with Ganser Syndrome have short-term episodes of odd behaviour similar to that shown by people with other mental illnesses. The person may appear confused, make absurd statements, and report hallucinations such as the experience of sensing things that are not there or hearing voices. A classic symptom of Ganser Syndrome is vorbeireden (German for: to talk past). This is when the person gives approximate answers (or near misses) to very simple questions. In addition, a person with this condition may report physical problems such as an inability to move part of the body, called 'hysterical paralysis'. Loss of memory (amnesia) of the events that occurred during an episode is common.

Little is known about this unusual disorder, but it is believed to be a reaction to extreme stress. There are also physical problems that may predispose the symptoms of Ganser syndrome such as alcoholism, head injury, and stroke.

I think that Ganser Syndrome is simply an atypical form of Munchausen's syndrome, which is a psychological disorder where someone pretends to be ill or deliberately produces symptoms of illness in themselves. Their main intention is to be at the centre of attention. In the Ganser Syndrome one can theorize that an inmate may want to break the eternal dullness of incarnation by pretending to be ill and thus temporarily breaking that eternal dullness.

Cocores et al: The Ganser syndrome: evidence suggesting its classification as a dissociative disorder in International Journal of Psychiatry in Medicine - 1984

Refeeding Syndrome

The Refeeding Syndrome is a bit like a man lost in a desert and when he finally reaches safety and water, he will drink too much in one go. Bedouins will tell you that you should drink with care. They're right, because too much too quickly can dilute the concentration of sodium in the blood, a condition called hyponatremia. When this happens, the balance of sodium in the fluids outside your body's cells is disrupted, fluid moves into the cells in an attempt to fix the imbalance and your cells swell. Brains cells are particularly prone to swelling. Symptoms of hyponatremia include confusion, convulsions, fatigue, loss of appetite, irritability and even death.
Refeeding is the equivalent of finding an oasis after prolonged fasting. Prolonged fasting occurs as a result of following idiotic diets, hunger strikes or religious fasting. Mostly, however, one finds the refeeding syndrome in severely malnourished patients in hospitals. When you are restricting your food intake over a prolonged period of time you essentially starve yourself. The body quickly switches from using carbohydrate to using fat and protein as the main source of energy. Not only metabolic changes occur but also hormonal changes. The net result of all this is that the metabolic rate decreases by as much as 20-25%.

These hormonal and metabolic changes are aimed at preventing protein and muscle breakdown. Muscle and other tissues decrease their use of ketone bodies and use fatty acids as the main energy source. This results in an increase in blood levels of ketone bodies, stimulating the brain to switch from glucose to ketone bodies as its main energy source. The liver decreases its rate of gluconeogenesis, thus preserving muscle protein.

So, what happens if you stop fasting and start eating again. Some potentially fatal shifts in fluids and electrolytes that may occur in malnourished patients receiving (artificial) refeeding[1]. These shifts result from hormonal and metabolic changes and may cause serious clinical complications. The hallmark biochemical feature of refeeding syndrome is hypophosphataemia or extremely low levels of phosphate in the blood. However, the syndrome is complex and may also feature abnormal sodium and fluid balance; changes in glucose, protein, and fat metabolism; thiamine deficiency; hypokalaemia; and hypomagnesaemia.

The true incidence of refeeding syndrome is unknown—partly owing to the lack of a universally accepted definition and research[2]. In a study of 10,197 hospitalised patients the incidence of severe hypophosphataemia was 0.43%, with malnutrition being one of the strongest risk factors.

[1] Mehanna et al: Refeeding syndrome: what it is, and how to prevent and treat it in British Medical Journal – 2008. See here.
[2] Camp, Allon: Severe hypophosphatemia in hospitalised patients in Mineral & Electrolyte Metabolism – 1990

Crocodile Tear Syndrome

When humans are showing crocodile tears they display false, insincere emotions. Think of it as a form of superficial or hypocritical sympathy.
The phrase derives from an ancient belief that crocodiles shed tears while consuming their prey, and as such is present in many modern languages, especially in Europe where it was introduced through Latin. While crocodiles do have tear ducts, they simply weep to lubricate their eyes, typically when they have been out of water for a long time and their eyes begin to dry out. However, some evidence suggests this could also be triggered by feeding.

There is also an almost discarded theory that the 'tears' come from crocodiles eyes when they just came out of the water and it looks like they have been crying, when in truth they have not.

But, in reference to the legend, Crocodile Tear Syndrome can in fact be a real syndrome.

Officially called Bogorad's Syndrome it is a condition which causes sufferers to shed tears while consuming food. It is a rare complication of facial paralysis. It's characterized by a flow of tears (lachrymation) on the same side of the palsy in connection with stimulation of salivation, for instance when eating. It is caused by a misdirection of the regenerating autonomic fibers to the lacrimal gland instead of to the salivary gland. It is therefore the result of 'faulthy wiring' during regeneration after paralisis.

The syndrome is named after the Russian neuropathologist F. A. Bogorad, who first described the condition in 1926.