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.

Lorikeet Paralysis Syndrome

Rainbow lorikeets (Trichoglossus haematodus) in the western Australian states New South Wales and Queensland are becoming paralyzed, often resulting in death.
Researchers from the University of Sydney identified the prevalence, distribution, and manifestation of the Lorikeet Paralysis Syndrome. It is a seasonal disease, occurring between October and June, with the highest number of cases happening between December and February. It affects thousands of rainbow lorikeets each year in northern New South Wales and southern Queensland.

The syndrome can cause limb, neck, and tongue paralysis, and an inability to blink or swallow, rendering birds unable to fly and feed, and therefore, survive.

Not only can the syndrome prevent them from feeding and flying—it can render them prone to injury and predation," Professor David Phalen said. "This means they are more likely to run into objects or be hit by cars and be attacked by cats than those without the syndrome."

To make matters worse, severely diseased birds are not responding well to treatment. Affected lorikeets only have a 60 percent chance of recovery, and their treatment requires intensive care followed by extensive rehabilitation. The prognosis is better for milder cases, which have a good (up to 84 percent) chance of recovery. An effective treatment could involve restoring kidney function, correcting electrolyte abnormalities, and relieving pain associated with muscle injury.

"The number of cases each year varies from hundreds to thousands, making it one of the most important wildlife diseases and animal welfare concerns in Australia," professor Phalen explained

The researchers are now calling on the public to help identify the likely source of the disease—a plant toxin.

Green Nail Syndrome

Green Nail Syndrome is an inflammation of the skin around the nail (paronychia) caused by an infection with Pseudomonas aeruginosa, a bacterium. It can develop in individuals whose hands or feet are frequently submerged in water, detergents or damp soil. The bacteria grow and multiply rapidly in moist environments such as sinks, swimming pools, and sponges.
As indicated by the name of this syndrome, the most common symptom of Green Nail Syndrome is the discolouration of the infected nail as it turns a dark green colour, due to the bacteria secreting the green pigments pyoverdine and pyocyanine. The patient can also suffer from tenderness surrounding the infected nail along with redness and swelling.

Normally, the seal between the nail and finger acts as a physical barrier to prevent this kind of infection, however hyper-hydration or damage to the epidermis can impair the barrier, allowing the colonisation of the bacteria.

Treatment for Green Nail Syndrome varies greatly depending on the severity of the infection and the length of time it has been present. The least invasive treatment includes soaking the nail in alcohol or vinagar and regularly trimming the nail back, in order to dry out the area and prevent further bacterial colonisation.

For moderate cases of Green Nail Syndrome topical antibiotics (silver sulfadiazine, gentamicin, ciprofloxacin, bacitracin and polymyxin B) or oral antibiotics (ciprofloxacin) are prescribed. In severe cases, surgical removal of the infected nail may be required.

Resignation Syndrome

Resignation Syndrome, also known as Traumatic Withdrawal Syndrome or Uppgivenhetssyndrom in Swedish, causes children to stop walking, talking and eating. They assume a coma-like state, lying prone, with their eyes closed, disconnected from the world around them. They are fed via feeding tubes. Thus far, no known cases have been identified outside Sweden.

The Resignation Syndrome is possible factitious, dissociative syndrome that induces a catatonic state, first described in Sweden in the 1990s. The condition affects predominately psychologically traumatized children and adolescents in the midst of a strenuous and lengthy migration process[1][2]

All 169 of these children are the offspring of asylum seekers, and each family had had their application for asylum rejected. What’s doubly strange is that all these asylum seekers were Yazidis, from war-torn Syria.

Young people reportedly develop depressive symptoms, become socially withdrawn, and become motionless and speechless as a reaction to stress and hopelessness. In the worst cases, children reject any food or drink and have to be fed by feeding tube; the condition can persist for years. Recovery ensues within months to years and is claimed to be dependent on the restoration of hope to the family.

[Buy the book here]

More recently, this phenomenon has been called into question, with two children witnessing that they were forced by their parents to act apathetic in order to increase chances of being granted residence permits. As evidenced by medical records, healthcare professionals were aware of this scam, and witnessed parents who actively refused aid for their children but remained silent at the time.

In March 2020, a report citing the Swedish Agency for Medical and Social Evaluation, SBU, said "There are no scientific studies that answer how to diagnose abandonment syndrome, nor what treatment works."

[1] Sallin et al: Resignation Syndrome: Catatonia? Culture-Bound? in Frontiers in Behavioral Neuroscience – 2016
[2] Von Knorring, Hultcrantz: Asylum-seeking children with resignation syndrome: catatonia or traumatic withdrawal syndrome? in European Child and Adolescent Psychiatry. – 2020

Red Ear Syndrome

Red Ear Syndrome is a rare disorder of unknown etiology which was first described in 1994. The defining symptom of Red Ear Syndrome is - yes, you guessed it correctly - redness of one or both external ears, accompanied by a burning sensation[1].
Attacks of skin redness and burning sensation or pain in one or both external ears are the only common symptoms. Pain is often most pronounced at the ear lobe, and sometimes radiates to the jawbone and cheek. The pain is normally mild, but has occasionally been described as severe, as a dull ache, as a stabbing pain, as a sharp pain, and as a jabbing pain. The attacks can last seconds or hours, with 30 minutes to an hour being typical. Most patients have daily attacks, ranging from 20 a day to a few a year.

It is believed this syndrome may represent an auriculo-autonomic headache or be part of the group of disorders known as trigeminal autonomic cephalgias, which includes cluster headaches. It is more often associated with migraine in younger people, while late-onset Red Ear Syndrome may result from pathology of the upper cervical spine or trigeminal autonomic cephalgia.

Most patients with Red Ear Syndrome have both spontaneous and triggered attacks. Triggers most often include heat, rubbing the ear, physical exercise, and neck movement. Other stimulations able to provoke episodes of Red Ear Syndrome include light touching of the ear, brushing of the hair, chewing, tooth grinding and showering.

Red Ear Syndrome is considered rare, but the exact prevalence is unknown. There are only a bit more than 100 cases described in the medical literature. A variety of treatments have been tried with a limited success.

[1] Lambru et al: The red ear syndrome in Journal of Headache and Pain – 2013

Hwabyung

Hwabyung or Hwabyeong (depending on transcription) is a syndrome that is only known form Korea. It is a (sort of) mental illness which arises when people are unable to confront their anger as a result of conditions which they perceive to be unfair.
Hwabyung is known as a Korean culture-bound syndrome. In a survey, 4.1% of the general population in a rural area in Korea were reported as having hwabyung[1].

The etymology of the word hwabyung is a combination of hwa (the Sino-Korean word 火 for fire which can also contextually mean anger) and byung (the Sino-Korean word 病 for syndrome or illness).

Physical symptoms include palpitations, anorexia, dry mouth, insomnia, (imagined) thoracic or chest pressure, respiratory difficulties, epigastric mass, headache, a whole-body sensation of heat (distinct from heat intolerance, and a symptom of hyperthyroidism).

Psychological symptoms include being easily startled, externalization of anger, also known in Korean as bun (憤, "eruption of anger"), a Korean culture-related sentiment related to social unfairness, generally sad mood, frequent sighing, a feeling of eok-ul (抑鬱, [feeling of] unfairness), being easily agitated, feelings of guilt, and feelings of impending doom.

Diagnosed patients may also have a medical history of prior major depressive disorder. Strangely, they are most likely to be middle-aged, post-menopausal women with low socio-economic status.

Because hwabyung is a culture-bound syndrome one would imagine to point to the stress of the Korean work ethics. Korea has one of the highest average work weeks and overtime hours in the world. With their rigorous work ethic, one can expect employees to go beyond their own standards to keep up, resulting in continuous stress.

The syndrome is believed to be the result of the continued repression of feelings of anger without addressing their source.

Min: Hwabyung in Korea: Culture and Dynamic Analysis in World Cultural Psychiatry Research Review - 2009

Sea Star Wasting Syndrome

Sea stars, also known as starfish, have a reputation for being resilient animals that can regenerate lost limbs. However, in 2013, sea stars off of the North American Pacific Coast began rapidly dying in huge numbers, and no one knew why.
[Image: Linus Mylund]

Similar sea star mass die-offs have been recorded for decades, but this event was one of the largest wildlife mass-mortality events ever recorded[1]. Sick sea stars become covered in lesions, permanently losing their limbs and melting into blobs of decayed tissue. This illness, termed sea star wasting syndrome (SSWS), was widely thought to be caused by a viral infection. However, this could not be replicated in the lab and was ultimately disproven[2].

Now, in a new study, researchers have found the mysterious illness was caused by microorganisms sucking up oxygen from the water around infected sea stars, essentially suffocating them[3]

The researchers had previously investigated and ruled out other factors, such as water temperature, as the cause for Sea Star Wasting Syndrome. However, when they examined the water immediately surrounding sick sea stars to the environments around healthy sea stars, they found that nutrient-loving bacteria living on the sea stars had used up all the oxygen that they need to breathe.

Although Sea Star Wasting Syndrome is caused by an ecological interaction rather than an infection, it can still be transmitted between sea stars. As dying sea stars decay, they generate organic matter that can promote bacterial growth on nearby sea stars in a dangerous feedback loop.

Sea stars play essential roles in many ecosystems and help maintain local biodiversity. Knowing how this disease develops can help researchers treat sick sea stars in the lab, helping to preserve delicate ecological relationships.

[1] Schultz et al: Evidence for a trophic cascade on rocky reefs following sea star mass mortality in British Columbia in PeerJ - 2016
[2] Hewson et al: Investigating the Complex Association Between Viral Ecology, Environment, and Northeast Pacific Sea Star Wasting in Frontiers in Marine Science - 2018. See here.
[3] Aquino et al: Evidence That Microorganisms at the Animal-Water Interface Drive Sea Star Wasting Disease in Frontiers in Marine Science - 2021. See here.

White Bear Problem

The White Bear Problem is a psychological syndrome that describes the art of saying inappropriate things at an appropriate time.
It is remarkably like as if there resides a mischievous inner demon inside of you that whispers to us to make a fool of ourselves – an imp dubbed Gegenwille ('counter will') by Sigmund Freud[1]. Harvard social psychologist Dan Wegner has spent considerable time investigating such 'ironic' mental processes.

Suppressing unwanted thoughts is a strangely difficult thing to do, as Fyodor Dostoevsky trenchantly observed in his 'Winter Notes on Summer Impressions'. “Try not to think of a polar bear,” he challenged his readers, “and you will see that the cursed thing will come to mind every minute.” In his books and scientific papers, Wegler calls this syndrome 'ironic process theory', 'ironic rebound', or 'the white bear problem'[2]. It refers to the psychological process whereby deliberate attempts to suppress certain thoughts make them more likely to surface.

More alarmingly, the same goes for actions. Remind yourself not to tell the widow at the wake that you’re dying for a drink, and as like as not, you will. Try not to spill the longed-for glass of wine on that nice carpet: oops, there it goes. The harder you try to stop yourself making a fool of yourself, the more likely it is that you will.

This syndrome, also called Foot-in-Mouth Problem in our modern times, frequently surfaces in politics, where ignorant politicians try to answer a question on a subject that they have absolutely no knowledge about. So, they string a couple of words together, hoping to obfuscate the answer, but often their stupidity and ignorance are obvious for everyone but themselves.

[1] Breuer, Freud: Studien über Hysterie - 1895
[2] Wegner: Setting free the bears: escape from thought suppression in American Psychologist – 2011

Why shepherds in nativity scenes have goiters

Shepherds in Christmas Nativity scenes that were painted, carved or sculpted hundreds of years ago sometimes have goiter, an enlargement of the thyroid gland caused by iodine deficiency. The condition was common in those days in northern Italy, where the soil and water are depleted of iodine.

"Goiter is more often seen in poor people," says retired surgeon Renzo Dionigi of the University of Insubria in Varese, Italy, who notes that the working classes in this region would historically not have a varied diet that might supply this vital nutrient. “That's why, probably, the poor shepherds were depicted with goiters,” he explains.
[Adoration of Shepherds by Alessandro  Bonviccino]

In the northern Italian Sacri Monti ('Sacred Mountains') churches from the 16th and 17th centuries often have depictions of goiters. In one Nativity tableau from 1694 (see image above), for example, a young horn player with a large goiter plays for the Holy Family. And in one fresco over the main door of the Aosta Cathedral, a shepherd with goiter plays his bagpipe for the newborn Jesus.

Dionigi and his son also recently reported on two wooden shepherds, both with enormous goiters, that were once part of a 16th-century Nativity scene (see image below).

Another report noted a large, obvious goiter on one of the shepherds visiting the baby Jesus in the 16th-century Adoration of Shepherds by Renaissance painter Alessandro Bonvicino.

Dionigi's favourite artistic goiter appears on a woman portrayed in The Crucifixion of St. Andrew, by Caravaggio, now at the Cleveland Museum of Art (see image below).
Massive goiters sometimes show up on artists' portrayals of tormentors and executioners, apparently as a symbol of evil. But often, goiters just indicates that persons are poor or needy.

In one 17th-century terra-cotta sculpture from northern Italy, a person with an enormous goiter begs St. Francis for healing. "That's the hugest goiter I have ever seen in any sculpture," says Dionigi. "The size of that goiter in that sculpture is something like half a meter."

Exerpted from: Nell Greenfieldboyce - 2010. See here.

Folie à Deux

Folie à deux, which translates from French as 'dual madness' or 'madness of two' (and not 'madness for two' as Wikipedia erroneously claims), has lately been renamed as shared psychosis or Shared Delusional Disorder (SDD). The syndrome has not been included in the most recent edition of the Diagnostic and Statistical Manual of Mental Disorders, the DSM-5.
Here, I will continue to address the problem as folie à deux, as it is still the best known terminology. Folie à deux is a psychiatric syndrome in which the symptoms of a delusional belief (or belief system) is shared by two persons. It is not magically transmitted as some sources seem to think, but if both individuals are susceptible to the same delusion at the same time, both may suffer from the same psychiatric problems. One (the inducer) influences the other (acceptor).

This syndrome is most commonly diagnosed when the two or more individuals of concern live in close proximity, may be socially, physically or religiously isolated, and have little interaction with other people.

Even though folie à deux is a rare disorder, socially or physically isolated psychiatrists have managed to discover a number of sub-classifications, such as folie imposée, folie simultanée and folie partagée.

As with most psychological disorders, the extent and type of delusion varies, but the non-dominant person's delusional symptoms usually resemble those of the inducer. Prior to therapeutic interventions, the inducer typically does not realize that they are causing harm but instead believe they are helping the second person to become aware of vital or otherwise notable information. The cause or cause of folie à deux are still unknown, but the main contributors are pre-existing psychological issues, stress and social isolation.

The best known, most depressing case is that of the Swedish twin sisters Ursula Eriksson and Sabina Eriksson (both born 3 November 1967). Their behaviour quickly became more erratic in 2008. Sabina stabbed a man to death, fled and then jumped from a 12-metre high bridge. She was taken to hospital with two broken ankles and a fractured skull. Her sister tried to kill herself by running onto the motorway, which succeeded and a passing lorry crushed her legs. A distressing documentary was made of these incidents and can be watched here
.

Intermittent Explosive Disorder

Intermittent Explosive Disorder, abbreviated to IED, is a behavioural disorder characterized by explosive outbursts of anger and violence, often to the point of rage, that are disproportionate to the current situation. Symptoms include impulsive shouting, screaming or excessive reprimanding triggered by relatively inconsequential events.
This impulsive aggression is not premeditated, and is defined by a disproportionate reaction to any provocation, real or perceived. Some individuals have reported affective changes prior to an outburst, such as increased tension, mood changes, energy changes, etc.

Individuals, diagnosed with Intermittent Explosive Disorder, report their outbursts as being brief (lasting less than an hour), with a variety of bodily symptoms (sweating, stuttering, chest tightness, twitching, palpitations).

Aggressive acts are frequently reported accompanied by a sensation of relief and in some cases even pleasure, but often followed by remorse.

The disorder is currently categorized in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) in the category 'Disruptive, Impulse-Control, and Conduct Disorders'.  The disorder itself is not easily characterized and often exhibits co-morbidity with other mood disorders, particularly bipolar disorder.

Psychiatrists try to control or treat these outbursts through cognitive behavioural therapy and psychotropic medication, though the pharmaceutical options have shown limited success.

But now there is some new evidence that Intermittent Explosive Disorder might be the result of an earlier brain infection with Toxoplasma gondii, a protozoan parasite found in cat faeces or undercooked meat[1].
[Image: phys.org - Toxoplasma gondii]

In the study of some 350 adults, those with Intermittent Explosive Disorder were twice as likely to have been infected by the toxoplasmosis parasite compared with healthy individuals with no psychiatric diagnosis.

The study adds to a growing body of evidence suggesting that toxoplasmosis — usually a mild or non-symptomatic infection with Toxoplasma gondii — may somehow alter people's brain chemistry to cause long-term behavioural problems.

Previous studies have linked toxoplasmosis to schizophrenia, bipolar disorder, impulsivity, and suicidal behaviour[2].

[1] Desmettre: Toxoplasmosis and behavioural changes in Journal Français d'Ophtalmologie – 2020
[2] Elsheikha et al: The known and missing links between Toxoplasma gondii and schizophrenia in Metabolic Brain Disease - 2016

Fresh Water Skin Disease (in Dolphins and Whales)

Dolphins and whales are used to living in salty seawater. Their skin is adapted to a saline environment. So, what happens when they are exposed for extended periods of time to water with lower than normal levels of salt, a situation called hypo-salinity?

Their skin cannot cope with those alien levels of salinity and severe skin lesions and ulcers will develop.

The problem is called fresh Fresh Water Skin Disease (FWSD) and is a disease of marine cetaceans in coastal and estuarine environments. It has been observed in dolphins that were displaced into freshwater lakes, and in normally-salty lakes and estuaries where salinity has dropped suddenly due to flooding or extensive rains during a prolonged tropical cyclone season[1].

The symptoms of Fresh Water Skin Disease (FWSD) are widespread skin lesions and ulcers. Chronic lesions may have overgrowths of algal and/or fungal mats. Extended exposure can lead to over-hydration, electrolyte imbalance, organ failure, and death.

At the moment, the syndrome has been observed with
[1] bottlenose dolphins (Tursiops truncatus) in Lake Pontchartrain (Louisiana, USA), a brackish lagoon, from 2007, that were thought to have been trapped by Hurricane Katrina in 2005[2];
[2] Burrunan dolphins (Tursiops australis), living in the Australian Gippsland Lakes in 2007. The sudden decrease in salinity was the result of heavy downpours after a slow build-up of salinity levels after during ten years of drought;
[3] Indo-Pacific bottlenose dolphins (Tursiops aduncus) at the Australian Swan Canning Riverpark (Swan and Canning rivers) in 2009[3];
[4] common bottlenose dolphin (Tursiops truncatus) in Texas following Hurricane Harvey in 2017;
[5] Chilean dolphins (Cephalorhynchus eutropia) in waters off Patagonia (Tierra del Fuego);
[6] Guiana dolphins (Sotalia guianensis) in coastal waters off Brazil;
[7] humpback whales (Megaptera novaengliae) in the Pacific Ocean off northern California (USA)[4].

Climate changes, whether the result of global warming or of global cooling, is resulting in more extreme weather patterns. Which means the problems of those dolphins and whales are just beginning and much worse is to come.

[1] Guignan et al: Fresh water skin disease in dolphins: a case definition based on pathology and environmental factors in Australia in Scientific Reports – 2020. See here.
[2] Mulin et al: Common bottlenose dolphins (Tursiops truncatus) in Lake Pontchartrain, Louisiana, 2007 to mid-2014 in National Oceanic and Atmospheric Administration (NOAA) – 2015. See here.
[3] Holyoake et al: Technical report on the Bottlenose dolphin (Tursiops aduncus) unusual mortality event within the Swan Canning Riverpark, June-October 2009 in ResearchGate – 2010
[4] Gulland et al: Health assessment, antibiotic treatment, and behavioral responses to herding efforts of a cow-calf pair of humpback whales (Megaptera novaeangliae) in the Sacramento River Delta, California in Aquatic Mammals – 2008

Did you see it?

Your brain is a strange place. It can ponder the origins of life and the beginning or the end of the universe. It can also create astonishing ways of killing and curing. But your brain isn't perfect and sometimes it plays some little tricks on you. Just to let you know that it has a mind of its own.
Most of us probably know the psychological term déjà vu (French for 'already seen'), but there are some related phenomenons, such as presque vu (French for 'almost seen') and jamais vu ('never seen').

Deja vu is the illusion that you have the distinct impression that you've already seen something before or experienced some situation before, but it just was the very first time you've seen or experienced it.

Presque vu is a so-called 'tip of the tongue' phenomenon. You have a strong feeling that you are on the very brink of a powerful epiphany, insight, or revelation, but it never materialises. The feeling is that of a forgotten name you know you know and are just about to say it, but your brain just cannot put its finger on it.

Jamais vu is the illusion that you are experiencing a situation that you seem to recognise in some way or another, but that nonetheless seems novel and unfamiliar. It involves a sense of eeriness and the observer's impression of seeing the situation for the first time, despite rationally knowing that they have been in the situation before.

Bouffée Délirante

Bouffée délirante is an historic and unique French diagnostic term for a short-lived psychosis. The key diagnostic features are acute, floridly psychotic symptoms with complete remission.

It probably can be seen as a culture-bound syndrome as the term has a long history in France, various French-speaking islands in the Caribbean, and erstwhile French colonies in Africa. Some suggest that religious rituals and expectations of the family play a major role in the genesis and maintenance of this sort of delusions[1].

The meaning of the term 'Bouffée délirante' is somewhat obscure. Bouffée is from the verb bouffer, which originally meant 'a puff of air' and is the source of 'buffoon'. But it also had the meaning of 'flash' in the sense of 'short-lived'. Délirante is akin to delirium or psychosis. So, the term can be translated as a 'short-lived psychosis'.

Bouffée délirante is an acute, brief nonorganic psychosis that typically presents with a sudden onset of fully formed, thematically variable delusions and hallucinations against a background of some degree of clouding of consciousness, unstable and fluctuating affect, and spontaneous recovery with some probability of relapse.

The suggested criteria for a diagnosis of Bouffée délirante are: abrupt onset, polymorphic delusions, emotional changes, mood swings, depersonalization, derealization and/or hallucinations, complete remission within weeks or a few months, exclusion of organic causation, alcohol or drug use, and no psychiatric antecedents with the exception of a previous episode of bouffée délirante[2].

As no other country recognises bouffée délirante, international scientists have tried to fit the syndrome into the Diagnostic and Statistical Manual of Mental Disorders 5th edition (DSM-5). The diagnostic category brief psychotic disorder is probably the closest analog of bouffée délirante[3].

However, in some societies similar psychiatric illnesses exist. In certain German speaking countries one can get the diagnosis of cycloid psychosis, while in Scandinavian countries a diagnosis of psychogenic psychosis can be given.

[1] Bhavsar, Bhugra: Religious delusions: finding meanings in psychosis in Psychopathology – 2008
[2] Johnson-Sabine et al: Bouffée délirante: an examination of its current status in Psychological Medicine – 1983
[3] Chabrol: Chronic hallucinatory psychosis, bouffée délirante, and the classification of psychosis in French psychiatry in Current Psychiatry Reports - 2003

Tardive Psychosis

Tardive Psychosis is a (still) not widely accepted form of psychosis, proposed in 1978 by Guy Chouinard, professor of psychiatrie at the University of Montréal [1].

Tardive Psychosis (tardive means 'late in appearing') was defined as a condition caused by long term use of widely prescribed dopaminergic antipsychotics, noticeable when the medication had become decreasingly effective, requiring higher doses, or when not responding to higher doses. These antipsychotics deplete the levels of dopamine in the brain, which is related to the known side effect caused by their long-term use. This might lead to a worsening of psychosis beyond the original level.
[Vincent van Gogh: Starry Night]

Tardive Psychosis should be understood as drug-induced brain damage that leads to a global decline in brain function. The motor dysfunction is often accompanied by an increase in psychotic symptoms, a decline in cognitive function, and an increased risk of early death[2].

So, you are prescribed medication for your mental problems. The medications, over time, have devastating effects and will lead to symptoms that are worse than the original ones. Then you need wean off that medication and will have to use new medication with still unknown side effects.

Evaluation suggests that tardive psychosis as a whole is a possibly combination of 'several different and not necessarily correlated phenomena related to neuroleptic treatment of schizophrenia'.

[1] Chouinard et al: Neuroleptic-induced supersensitivity psychosis in American Journal of Psychiatry - 1978
[2] Robert Whitaker: A Short History of Tardive Dyskinesia: 65 Years of Drug-Induced Brain Damage That Rolls On and On in Mad in America - 2020. See here.

Don Quixote's Psychosis

We all know Don Quixote, the chivalrous Spanish nobleman who fought windmills. He appears in a two books by Miguel Cervantes, entitled 'El ingenioso hidalgo Don Quijote de la Mancha' (or 'The Ingenious Gentleman Don Quixote of La Mancha') and published in 1605 and 1615.

A little known fact is that the personal name of Don Quixote was Alonso Quixano. Don Quixote was the name he invents after falling into madness ('insanity').

Alonso Quijano read many chivalric books and the stories, as we are told, caused his madness. But reading does not cause madness. But hunger does.

The appearance of Don Quixote does offer some clues. His 'squire' Sancho Panza describes him as follows: 'Don Quijote is the worst-looking man he has ever seen, thin from hunger and missing most of his teeth'.

Besides Sancho Panza's description, we find the following descriptions of him in the text: 'His age was about 50, with a solid (recio) complexion, his flesh shriveled (seco), a gaunt face' (Part I, Chapter 1) and 'He was tall, a shrunken (seco) face, long, wrinkled arms and legs, half bald, his nose like that of an eagle, but curved, and with a large and droopy moustache' (Part II, Chapter 14).

So, can hunger result in illusions, hallucinations and even psychosis? It does and modern science now can help to diagnose Don Quixote's psychological problems[1][2][3].

[1] Mittal, Khan: Starvation causes acute psychosis due to anterior thalamic infarction in Southern Medical Journal – 2010
[2] Morylowska-Topolska et al: Schizophrenia and anorexia nervosa - reciprocal relationships. A literature review in Psychiatria Polska – 2017
[3] Koven, Abry: The clinical basis of orthorexia nervosa: emerging perspectives in Neuropsychiatric Disease and Treatment - 2015

Wendigo Psychosis

You might have watched the movie 'The Lone Ranger' featuring Johnny Depp as the somewhat eccentric Tonto. In the movie Tonto mentions Wendigo, an evil, cannibalistic spirit in the stories of the Algonquian peoples of the Northeast and Great Lakes regions of the United States and Canada. In its core, the wendego (many other spellings of the name exist) is a personification of winter, hardship, and hunger[1].
In some, more recently formed traditions, humans that are overpowered by greed could also turn into (a) wendigo. The myth thus served as a method of encouraging cooperation and moderation. Other sources say wendigos were created when a human resorted to cannibalism to survive.

The creature also lends its name to the controversial modern medical term Wendigo psychosis, described by some psychiatrists as a culture-bound syndrome with symptoms, with symptoms like an intense craving for human flesh and fear of becoming a cannibal.

In some indigenous communities, encroaching environmental destruction and insatiable greed are also seen as a manifestation of Wendigo psychosis.

This belief is paralleled by other culture bound psychoses in which a mentally ill person develops cannibalistic urges. However, the very existence of this condition has been disputed in recent times.

[1] Robert Brightman: The Windigo in the Material World. See here (pdf).

Purple Urine Bag Syndrome

Purple Urine Bag Syndrome, abbreviated to PUBS, is a somewhat uncommon medical syndrome where purple discolouration of urine occurs in people with urinary catheters and co-existent urinary tract infection. Bacteria in the urine produce the enzyme indoxyl phosphatase. This converts indoxyl sulfate in the urine into the red and blue colored compounds indirubin and indigo[1].
The most commonly implicated bacteria are Providencia stuartii, Providencia rettgeri, Klebsiella pneumoniae, Proteus mirabilis, Escherichia coli, Morganella morganii, and Pseudomonas aeruginosa.

People that display Purple Urine Bag Syndrome usually do not complain of any symptoms. Purple discolouration of a urine bag is often the only symptom, frequently first noted by caregivers. It is usually considered a benign condition, although in the setting of recurrent or chronic urinary tract infection, it may be associated with drug-resistant bacteria.

Antibiotics such as ciprofloxacin should be administered and the catheter should be replaced. If constipation is present, this should also be treated.

Purple Urine Bag Syndrome is more common in female nursing home residents. Other risk factors include alkaline urine, constipation, and polyvinyl chloride catheter use.

[1] Sabanis et al: Purple Urine Bag Syndrome: More Than Eyes Can See in Current Urology – 2019. See here.

Toxic Squash Syndrome

Plants are more intelligent than we give them credit for. Because they don't like to be eaten, they learned to defend themselves. Plants produce chemicals to deter herbivores (or humans eating plants).
Of of these chemicals is cucurbitacin. Officially it is any chemical of a class of biochemical compounds that some plants — notably members of the family Cucurbitaceae, which includes the common pumpkins, cucumbers, zucchinis , melons, and gourds – produce. Cucurbitacins impart an extremely bitter taste.

But Mother Nature is intelligent and these chemicals are not only produced in pumpkins and gourds. They and their derivatives have been found in many plant families [including the cabbages (Brassicaceae), begonias (Begoniaceae), primulas (Primulaceae) and more], in some mushrooms (including Russula and Hebeloma) and even in some marine mollusks.

So, you might ask, I have eaten cucumbers or pumpkins for years and I've never had the displeasure of encountering a bitter taste in one of these fruits. You are quite right, because thousands of years of selective breeding has al but weeded out these bitter tasting chemicals. But the genes are still there. These genes are 'sleeping' or 'turned off'.

But sometimes these genes will become active again. They will be 'turned on'. Scientists have researched why these genes start producing cucurbitacins again and they think [1] cross-pollination with wild Cucurbitaceae species or [2] from plant growth stress due to high temperature and drought.

And suddenly and quite unexpectedly, your beloved cucumber or pumpkin will be extremely bitter and even toxic (again).

Symptoms include nausea, diarrhoea, abdominal pain, vomiting, dizziness, and (in rare instances) hair loss. In most cases, the poisoning will run its unpleasant course much like other instances of food poisoning. However, in 2015 a 79-year old German man died and his wife was hospitalized after eating a significant amount of toxic zucchini in a stew. Seek medical attention if you become dehydrated, have excessive pain or dizziness, experience ongoing stomach issues or believe you have consumed more than a bite or two of food containing high amounts of cucurbitacin.

Brachycephalic Obstructive Airway Syndrome

Brachycephalic Obstructive Airway Syndrome (BOAS) is a pathological condition that affects short nosed dogs (Boxer, Bulldog, Pekinese, etc) and cats (Persian, Burmese, etc).
These breeds are especially bred for their short nose (and thus their flat face). The skeletal deformities result in severe breathing difficulties.

There are four different anatomical abnormalities that contribute to the disease: [1] an elongated soft palate, [2] pinched or narrow nostrils (stenotic nares), [3] malformation of the tracheal cartilage rings (hypoplastic trachea), and [4] tissue within the airway, just in front of the vocal cords, is pulled into the trachea (windpipe) and partially obstructs airflow (everted laryngeal saccules).

Because all of these components make it more difficult to breathe, in situations of exercise, stress or heat, an animal with these abnormalities may be unable to take deep or fast enough breaths to blow off carbon dioxide. This leads to distress and further increases respiratory rate and heart rate, creating a vicious cycle that can quickly lead to a life-threatening situation.

Other health problems affect these breeds too. They are overrepresented in skin and ear infections, prolapsed third eyelids and inwardly rolled eyelids (entropion), cryptorchidism, atopic dermatitis, corneal ulcers, umbilical hernias, dry eye (keratoconjunctivitis sicca), gastrointestinal disorders, periodontal disease, heart disease, cancer, and more. Their expected lifespan is just an appalling 7 years, several years shorter than the vast majority of other dogs.

The question is: do owners really love their pets or are these animals simply fashion assessories?

Dry Drowning Syndrome

The idea of Dry Drowning Syndrome (or Delayed Drowning Syndrome) originated when a small percentage of autopsies found no water in the lungs of people who had obviously died because of submersion in water. When water first enters the airway, it can trigger a spasm of the larynx, preventing water from going beyond and entering the lungs. Even a small amount of water in the lungs can destroy surfactant and lead to pulmonary edema. It is the lack of oxygen that causes harm, not the water itself.
Drowning requires going under water. It is not caused by just swallowing water or playing in water. 'Dry drowning' is not accepted medical terminology, and it is used inappropriately.

Parenting websites have been alarming parents about the possibility that their children might experience 'Dry Drowning Syndrome', with warnings like these:
a child can seem fine after getting out of the water, but start to have trouble breathing an hour—or even 24 hours—later.
Your child is in the pool, she swallows a bit of water and goes on playing—but a few hours later, she’s in the hospital on life support.
The website of Scary Mommy (what's in a name?) warns parents that:
Not all instances of drowning happen right away. Sometimes your child may go under water or unintentionally swallow water while swimming, and then only experience symptoms of drowning hours or days later. And yes, sometimes these symptoms – especially if not addressed right away – can lead to fatalities.
The CDC tells us “drowning kills more children 1-4 than anything else except birth defects,” so water safety is a serious concern for parents. Parents have been frightened by inaccurate, alarmist messages.
A 2017 article in Emergency Medicine News reported:
Earlier this month a young child died following days of vomiting. He had been in shallow water in a Texas dike about a week before his death. The story was picked up as an alleged case of a rare condition called dry drowning or secondary drowning…The media accounts went viral, spreading significant fear in parenting communities and among those learning about these alleged conditions from the news or social media…Unfortunately, there is significant misinformation in the media reports of this case, and we hope this evidence-based discussion of drowning and the best practice medical care of drowning patients will help set the record straight.
The authors go on to urge the media to use proper medical terminology and to abandon the terms near, dry, wet, delayed, and secondary drownings. They emphasize that anyone with respiratory symptoms after being in water should seek medical care, and they point out that There has never been a case published in the medical literature of a patient who received a clinical assessment, was initially without symptoms, and who later deteriorated and died.” 

Conclusion: “Dry Drowning Syndrome” is a myth
Rather than worrying unnecessarily about 'dry drowning', parents should worry about prevention. They should be encouraged to practice water safety, to include adult supervision, swimming lessons, life jackets and flotation devices, fences around home pools, and learning CPR.

Source.