we sleep to wake. . . but sometimes, sleep becomes brother to death. . . leads us helpless to a nightmare's dance. . . and we waken no more.

To die in one's sleep. . . so basic to the cauldron of human fears, subject matter to ancient rhymes and holy sonnets, the arts and literature, laden with layers of mythology, coloring folklore with creatures of the night, concoctions of superstitions, and nostrums of nightmare preventions. Cloaked in mystery and dread, it it has acquired a motley of names and acronyms – Sudden Unexplained Death Syndrome. SUDS, Sudden Unexpected Death in Sleep, Sudden Unexplained Nocturnal Death Syndrome, SUNDS, nightmare deaths, sudden night deaths – as science pokes through the muddle of myth and folklore, searching for etiologies and pathogenesis that can shed light into this mysterious fatal affliction that visits presumably healthy young men in their sleep, more commonly in the Southeast Asian and Pacific Rim countries and Polynesian populations believed to have migrated from South East Asia centuries ago.

First reported in the Philippines in 1917, 'sudden night deaths' or SUDS (sudden Unexpected Death in Sleep) has been attributed to bangungot (bangungut - from the Tagalog root words of "bangon," to rise; and "ungol," to moan) – a syndrome, wrapped in folklore and myth, that consists of a nightmare, commonly occurring in nocturnal sleep, frequently after a heavy meal that is often accompanied by alcohol, most often in young males, aged 25-44, presumably healthy, without any known cardiac illness.

How often bangungut becomes fatal is unknown. Many cases are never reported, especially in the rural areas where dying in your sleep is an accepted event in the folklore of death. Many know others who died in their sleep. Many more are 'survivors' of one or more attacks, with descriptive details of bangungot -type nightmares– of sleep paralysis, of falling from a mountain or into a deep abyss, of the creature in the dark standing by the bedside. How many of these are actually near-death or near-bangungut experiences or are they merely generic ingredients to culture-flavored nightmares?

Note: I have to begrudge the Ilocandia myth makers. Why the need to invent "Batibat?" To die in a bangungut nightmare is uugghh-dreadful enough. But to die with the the fat and vengeful "batibat" seating on your face. Oh, mercy me. "Batibat" clay sculpture by Alvin Barcelona, Brgy. Lumingon, Tiaong, Quezon (4"x5")

Although there are witness reports of "moaning, groaning, gasping, choking, frothing, and labored breathing," as often, patients are found dead, in seeming peaceful slumber, without the sounds of terror or any evidence of a terminal struggle.

In a "macho-culture" with a penchant for drinking, often to oblivion, and accompanying this libatory indulgence with a smorgasbord of "pulutan," pancreatitis became the popular and preferred "point-to diagnosis." (see pancreatitis, below).

In a country with more than 7000 islands and more than 70 indigenous communities, where albularyos and medicos minister to the end-days, diagnosing fainting spells by tawas and treating them with a bulong and/or orasyon, where the night worlds are ruled by the frightful creatures of myths and superstitions – the tikbalangs, kapres, asuwangs, white ladies and pontianaks, where death's ways are accepted with funereal fatalism as God's will, karma, or bangungut. — alas, the true incidence of bangungut / SUDS is probably a-long-time-coming before it gets revealed to the scrutiny of science.

SUDS IN OTHER COUNTRIES
Of course, nightmares are as old as sleep itself, and sleep-deaths are not unique to one particular race. Cultures wrap it in their own mythologies and superstitions. There are reports of SADS in other countries, unrelated to Southeast Asian populations. However, it was the Southeast Asian cultures and migrant populations that originally provided the mystique and attention to the nightmare-death syndrome.

RELATED REPORTS
• In the 1980s, Lancet reported SUDS deaths among Thai construction workers in Singapore.
• Sporadic reports of deaths among Cambodians and Laotian men in North America and refugee camps in Thailand.
• A 2006 UPS report in England of SADS being about eight times higher than previously thought. Aged 4 to 64, none had a history of heart disease, almost one in five had a family history of sudden unexplained deaths before the age of 45. Death was suspected to be from a genetic heart defect causing malignant abnormalities in heart rhythm.

A FEW SLEEP FACTOIDS
SLEEP PARALYSIS
Sleep paralysis is not unique to the bangungut syndrome. It is a common and ancient sleeping disorder attributed to demons and malevolent spirits, characterized by a feeling of immobility, being pinned down by an invisible force, unable to move and unable to scream for help. Inevitably, it becomes embellished with the creatures of culture and superstition. (See Batibat, above)

Sleep paralysis usually occurs at the threshold of wakefulness and sleep, hypnagogic when one is falling asleep, hypnopompic when one is waking up, with the accompaniments of falling sensation, chest pressure, and presences of shadowy creatures.

Dreaming occurs chiefly in REM states, to a lesser extent in NREM sleep. Sleep is cyclic with 4 or 5 REM periods during the night accounting for one-fourth of the total hour of sleep ( 1 1/2 to 2 hours). Studies suggest alcohol disturbs the REM cycles of sleep. What effects on the REM dreams? What effects on the stage 3 or 4 when sleep terrors (pavor nocturnus) occur?

Nightmares occur during REM sleep. Sleep terrors in stage 3 and 4 sleep.

NIGHT HAG
Night hag, or a waking dream, a modern-day name given to a sleep associated with nightmares and sleep paralysis. It is believed to be a nightmarish dream-state in the threshold of sleep and waking, sometimes replete with ogres and creatures, holding the person down or paralyzing him in fear. Some survive these episodes with "marks and bruises," attributing the experience to the paranormal.

NUTRITIONAL DEFICIENCIES AND MYTHS,
STRESS AND ENVIRONMENTAL FACTORS
Of the Thai workers in Singapore, nutritional deficiencies were implicated, particularly thiamine and potassium. However, there is no information as to whether potassium levels were obtained, or how severe the hypokalemia was.

Besides gorging and drinking before bedtime, certain foods myths abound. Some warn against big noodle meals before bedtime. Too, rice cakes at bedtime. In one province, seasoned imbibers are afraid to combine beer and balut, from an anecdotal account of a father and two sons who sccumbed to bangungut deaths - the deadly combination, prologue to their dreadful end.

Beer and balut
Gives you bangungut.

Stress has been considered in the etiology of SUDS, reported in usually high numbers in healthy young Southeast Asian men, especially in various refugee populations migrants communities. With increasing length of residence in the US, SUDS rates markedly declined. But if stress alone is causative, how to explain its relative absence in the many other races ravaged by war and poverty, and driven to dispersions and economic diaspora.

The occurrence of SUDS in Asian populations, the decline among SEA refugees after immigration to the US, the elevated risk among migrants in Manila and seasonality of occurrence (Munger and Booton) implicates stress, environmental factors and nutritional deficiencies

FOLKLORIC TREATMENTS
AND PREVENTIVE REMEDIES
• Move an extremity, a leg, or wiggling the big toe or thumb will drive the batibat away or snap him out of the 'paralysis.'
• Drinking several glasses of water before sleeping.
• Lying on the left side.
• Not going to bed too soon after a big meal (especially one washed down with lots of alcohol).
• Avoid balut as pulutan when drinking beer.
• Bedtime prayers.
• Put on lipstick, paint the nails, or wear women's nightclothes to bed at night to fool the pontianak, the lady ghoul.

THE SCIENCE
THE OLD AND THE NEW
Inevitably, science went forging and fishing into the sea of folklore and myths. In the recent decades, battling through ghouls and night hags, armed with the old and new tools of technology and the disciplines of research, digging into new world of genetic mutations, it has emerged partially victorious, providing us alternatives to the old and overused pancreatitis-diagnosis, with new theories and etiologies — the Whys-and-Whats and-Hows of unexpected sudden nocturnal deaths, and further adding to its lengthening lists of acronyms and syndromes (SADS: Sudden Arrhythmia Death Syndrome from Brugada, the Long QT, or Short QT syndromes).

THE OLD . . .
ACUTE HEMORRHAGIC
PANCREATITIS
In the Philippines, the cause of SUDS / bangungut has been linked to acute hemorrhagic pancreatitis attributed to a hearty or gluttonous meal often downed by a hefty amount of alcohol. A high salt diet, contributed to by native condiments - patis and bagoong - has been implicated. Stories are told of bangungut attacks with the combined indulgence of beer and balut.   

PANCREATITIS is the inflammation of the pancreas, the gland that sits behind the stomach, concerned with digestive enzyme functions and production of insulin. It is connected by a ductal system to the liver and the gallbladder, an anatomic detail of concern in gallstone disease. Pancreatitis can be either acute or chronic. In acute pancreatitis, there may be a history of excessive alcohol intake or a heavy meal preceding the attack or a history of biliary colic (gallstones) in the past. The rest are due to infections, vasculitis, drugs, trauma, hypercalcemia, hypertriglyceridemia. Although occasionally mild, often the symptomatology is rather dramatic in acute pancreatitis, with nausea, vomiting, fever, abdominal pain, distention, sweating, rapid pulse,and shock.
     Clinically, it is a hard-sell of a diagnosis if it is to be solely implicated for cause of bangungut deaths. As mentioned, the acute attacks have a rather dramatic constellation of symptoms, that runs the course of hours to days, with a severity that forces the patient to seek help or medical attention. Of course, the pancreatitis could have been "silent" if the alcohol was used in 'overdose' amounts, enough to cause respiratory depression, seizures, shock, coma, and death.
     Still, it will not explain the many cases of "bangungut" deaths in the seemingly "peaceful" scenarios of dying. Also, there are many similar "night deaths" where autopsies failed to show any pathologic cause. And for these, the usual fall-back is the waste-basket diagnosis of "cardio-respiratory arrest."

. . . AND THE NEW
The Brugada & QT Syndromes:
The long and short of it

The human body has a system of quasi independent electrical circuits that can be recorded through medically dedicated tools: the EMG-NCS (electromyography for muscle and nerve conduction studies), the EEG (electroencephalography for the study of brain waves) and the EKG or ECG (electrocardiography for a print out of the heart's electrical rhythm). Fascinating, all – electrical systems working in unison, with an endogenous power source that usually lasts a "lifetime of average use and abuse." Of these, it is the EKG that can provide information critical to the immediate assessment and management of life-and-death situations: heart attacks and potentially fatal cardiac irregularities. To boot, it can provide clues of rhythm disturbances and PQRST-wave configuration abnormalities that can alert the astute clinicians into raising red-flags, recognizing and preventing potential problems. The ECG has been the gateway tool in the diagnoses of clinical entities constituting a group called SADS (sudden arryhthmia death syndrome) recognizable by its potentially fatal electrocardiographic presentations (Wolff-Parkinson-White syndrome, idiopathic ventricular fibrillation, or arrhythmias caused by electrolyte imbalances). Recent studies and discoveries have focused on emerging entities — the Brugada syndrome, the long-QT and the short-QT syndromes — with its hereditary genetic defects affecting the cardiac ion channels, stripping some layers from the myths of sudden unexpected nocturnal deaths, providing science, etiologies and treatment options.

BRUGADA SYNDROME
In 1998, a hereditary (autosomal dominant) gene defect was found, involved in the coding of protein components in the sodium channels in heart cells. The channel defect causes abnormal electrical conduction in the heart with resultant ventricular arrhythmias, including full-blown ventricular fibrillation leading to death. Of the patients studied, many presented with unexplained fainting spells.
     
ECG PATTERNS
The Brugada syndrome presents with 3 different ECG patterns. The classic type 1 Brugada pattern consists of a right bundle branch block with a right precordial injury pattern (ST-segment elevations that descend and have an upward T-wave inversion ("coved type") in leads V1 through V3). Types 2 and 3 have "saddle-back" ST-T waves, with descending ST segments and an upright T wave; in type 2, the T wave is upright or biphasic. A slight prolongation of the QT interval may be noted in the right precordial leads due to the prolongation of the action potential in the right ventricular epicardium. The Brugada patterns differentiate from typical RBBB patterns by the absence of widened S waves. (Left insert: The V1– V3 tracings compare the normal on the left with the Brugada pattern on the right: a terminal R' wave in lead V1, a convex curve or "coved-type" ST elevation in V1 and V2 and a saddle-shaped ST-segment elevation in V3.)
      The classic (type 1) Brugada syndrome presents with the coved-type ST elevation in more than 1 right precordial lead ,V1 through V3, with or without a sodium channel blocker, with one of the following criteria: syncope, documented ventricular fibrillation, electrophysiologic inducibility of ventricular tachycardia, positive family history of cardiac death younger than age 45, nocturnal agonal respiration, self-terminating polymorphic ventricular tachycardia, and type 1 ST elevation in family members.
         Types 2 or type 3 Brugada syndrome presents with ST elevations: ≥1mm in type 2 and <1 mm in type 1 in more than one precordial lead, with conversion to type 1 Brugada ECG patters after the administration of a sodium channel blocker plus one of the type 1 criteria.

Fortunately, these ECG patters are rare. In Japan, it is found in less than 1% of the population; and in the U.S.,in less than 0.5%. Of these, most will not have any problems. But the EKG pattern, coupled with a history of unexplained fainting, a history of a relative dying young, raises a red-flag risk of sudden death.
     In the Philippines, a cross-sectional study done in 2003 to measure the prevalence of Brugada type EKG pattern reported finding the Brugada type 1 (coved) ECG pattern in 0.2% of the population and in 0.3% among males. The prevalence of any type Brugada ECG pattern was 2%. The risk of sudden death among individuals with this marker remains to be determined. (http://www.jclinepi.com/article/S0895-4356(07)00434-9/abstract)
     The syndrome has been linked to SUDS, causing sudden death in apparently healthy young people over the age 30.  A study of patients with SUNDS and their families, screened for genetic mutations in SCN5A, the gene known to cause the Brugada syndrome, suggested that SUNDS and the Brugada syndrome are phenotypically, genetically, and functionally the same disorder. <http://hmg.oxfordjournals.org/cgi/content/full/11/3/337>
     In Thailand, where the estimated prevalence of SUDS is 26-38 per 100,000 population, a study on patients with the Brugada syndrome showed a low heart rate variability at night that may predispose to the occurrence of ventricular fibrillation episodes.
     A study done to evaluate the significance of cardiac autonomic neuropathy (CAN) in the Brugada Syndrome concluded that CAN is an important risk factor in BS, and that men are susceptible to the development of cardiac events.
     The prognosis for high risk patients - abnormal EKG with history of syncopal attacks or near-sudden death resuscitation - is very poor, with a third at risk of a polymorphic ventricular tachycardia within two years. Treatment of choice is with an implantable cardioverter defibrillator. Risks for asymptomatic patients with typical electrocardiographic patterns are the same; a third will develop ventricular tachycardia or fibrillation within two years. Again, at present, only the implantable cardioverter-defibrillator protects against sudden cardiac death.

THE LONG QT SYNDROME (LQTS)
Like the Brugada syndrome, with its characteristic hereditary ion channel and ECG abnormality, hereditary prolongation of the QT interval is also associated with SADS (Sudden Arryhthmia Death Syndrome). LQTS is caused by mutations of the genes for cardiac potassium and sodium ion channels. The most common type is the autosomal dominant Romano-Ward syndrome. While it can present with syncope and seizures, In 30 to 40 percent of patients, sudden death is the only event. While the cardiac events are usually precipitated by physical and emotional stress, deaths can also occur in sleep. A history of unexplained sudden death in a young family member is a clue.
     QT prolongation is characteristic and predisposes to ventricular tachyarrhythmia – polymorphic ventricular tachycardia, or torsade de pointes, which can lead to ventricular fibrillation and sudden cardiac deaths. Sometimes, only a borderline prolonged QT interval is seen. Another clue is the presence of T-wave alternans, the severity of which correlates with cardiac events.
     Some of the highest rates of inherited long QT syndrome occurs in Southeast Asian and Pacific Rim countries.
     The syndrome has more treatment options than the Brugada syndrome: Beta blockers, potassium, avoidance of certain drugs, permanent pacemakers, and implantable defibrillators.

THE SHORT QT SYNDROME
A relatively new syndrome, first described in 1999, belonging to the ion-channel disorders called "channelopathies," hereditary short QT syndrome is an autosomal-dominant clinical-electrocardiographic entity with associated gene mutations. It is characterized by a short QT, frequently tall-peaked T-waves similar to a "hyperkalemic-T," inducible ventricular fibrillation, episodes of syncope, a high tendency for paroxysmal atrial fibrillation or life-threatening arryhthmias, without any underlying structural heart disease.

Three forms of the syndrome have been identified affecting different channels. Indicated therapy for those who have survived a cardiac arrest or those with a history of syncope, is the implantable cardioverter-defibrillator. In its absence or inaccessibility, drug therapy has the potential for prolonging the QT interval. However, drug therapy has been shown to be beneficial only for the first form, and ineffective for the other forms.

Although it has been linked to deaths in infants, children and young adults with a family background history of sudden cardiac death, it is possible that many survive into a later adulthood, into the mean age of deaths linked to SUDS/ SUNDS or bangungut.

In the past three decades science has made incredible head ways into unraveling the mysteries of unexpected sleep-deaths. Some sleep-deaths are now preventable. It might prove to be that many of these unexplained nocturnal deaths are attributable genetic aberrations that cause the heart's electrical system to go haywire. To search out these cohorts of patients who could benefit from the science is a formidable task. For many in the remote boondocks and rural areas, their night world will continue to be ruled by their myths, superstitions and folklore, their fears assuaged by nail polish and lipstick and doses of bedtime prayers.

SOURCES
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