Find information on thousands of medical conditions and prescription drugs.

Exploding head syndrome

Exploding head syndrome is a rare condition first reported by a British physician in 1988 (PMID 2899248) that causes the sufferer to occasionally experience a tremendously loud noise as if from within their own head, usually described as an explosion or a roar. This usually occurs within an hour or two of falling asleep, but is not the result of a dream. Although perceived as tremendously loud, the noise is usually not accompanied by pain. Attacks appear to increase and decrease in frequency over time, with several attacks occurring in a space of days or weeks followed by months of remission. Sufferers often feel a sense of terror and anxiety after an attack, accompanied by elevated heart rate. more...

Home
Diseases
A
B
C
D
E
Ebola hemorrhagic fever
Ebstein's anomaly
Eclampsia
Ectodermal Dysplasia
Ectopic pregnancy
Ectrodactyly
Edwards syndrome
Ehlers-Danlos syndrome
Ehrlichiosis
Eisoptrophobia
Elective mutism
Electrophobia
Elephantiasis
Ellis-Van Creveld syndrome
Emetophobia
Emphysema
Encephalitis
Encephalitis lethargica
Encephalocele
Encephalomyelitis
Encephalomyelitis, Myalgic
Endocarditis
Endocarditis, infective
Endometriosis
Endomyocardial fibrosis
Enetophobia
Enterobiasis
Eosinophilia-myalgia...
Eosinophilic fasciitis
Eosophobia
Ependymoma
Epicondylitis
Epidermolysis bullosa
Epidermolytic hyperkeratosis
Epididymitis
Epilepsy
Epiphyseal stippling...
Epistaxiophobia
EPP (erythropoietic...
Epstein barr virus...
Equinophobia
Ergophobia
Erysipelas
Erythema multiforme
Erythermalgia
Erythroblastopenia
Erythromelalgia
Erythroplakia
Erythropoietic...
Esophageal atresia
Esophageal varices
Esotropia
Essential hypertension
Essential thrombocythemia
Essential thrombocytopenia
Essential thrombocytosis
Euphobia
Evan's syndrome
Ewing's Sarcoma
Exencephaly
Exophthalmos
Exostoses
Exploding head syndrome
Hereditary Multiple...
Hereditary Multiple...
Hereditary Multiple...
Hereditary Multiple...
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z
Medicines

Attacks are also often accompanied by perceived flashes of light or difficulty in breathing.

Etiology

The cause of exploding head syndrome is not known, though some physicians have reported a correlation with stress or extreme fatigue. The condition may develop at any time during life and women are slightly more likely to suffer from it than men. Attacks can be one-time events, or can recur.

The mechanism is also not known, though possibilities have been suggested; one is that it may be the result of a sudden movement of a middle ear component or of the eustachian tube, another is that it may be the result of a form of minor seizure in the temporal lobe where the nerve cells for hearing are located. Electroencephalograms recorded during actual attacks show unusual activity only in some sufferers, and have ruled out epileptic seizures as a cause (PMID 1896728).

Those who claim to be subject to Kundalini events occasionally report similar auditory phenomena.

Whatever the mechanism, however, it appears that exploding head syndrome is a real phenomenon and not caused by psychological disturbances. It is not thought to be medically dangerous, although it is often distressing to experience. Note that EHS does not, in fact, cause the head to explode.

Treatment

Symptoms may be resolve spontaneously over time. It may be helpful to reassure the patient that this symptom is harmless. Clomipramine has been used in 3 patients, who experienced immediate relief from this condition (PMID 1896728).

Read more at Wikipedia.org


[List your site here Free!]


The environmental origins of TSEs: the ferrimagneto-prion theory
From Townsend Letter for Doctors and Patients, 7/1/04 by Mark Purdey

The White Sands Missile Range is an extensive spread of US military controlled cacti country that spans the southernmost extremes of the San Andres mountain ridge. There is an eerie atmosphere to the place.

A Department of Natural Resources truck kicks up the dust across the dried out canyon, its engines reverberating in the quiet air. It stops at the main entrance gates along the perimeter fence. One of the wildlife officers gets out and walks to security, seemingly oblivious to the distant thump of a missile exploding across the range. He is clearly preoccupied with the more important task of slaughtering animals who have succumbed to a so-called "hyperinfectious" disease. The truck is soon on its way, disappearing within the thousands of acres of parched military compound.

They've come to investigate yet another new eruption of chronic wasting disease (CWD) in the USA--the deer equivalent of 'mad cow disease.' This outbreak is particularly significant, in that it represents the first cases of a transmissible spongiform encephalopathy (TSE) disease recorded in a deer herd within the state of New Mexico. Furthermore, the affected herd has been confined within the perimeters of this missile range for several decades.

This latest epidemiological aberration delivers a serious challenge to the viability of the conventional consensus on the origins of CWD. It has shaken the cornerstones of institutionalized 'expertise,' bringing into question those veterinarians who have opted for the assumption that some unknown "hyperinfectious" agent is spreading via body to body contact through the deer populations.

So how did the 'infectious agent' jump the 500 mile gap between the long standing CWD hotspot zone in Colorado and the CWD-free deer residing within the White Sands Missile Range? The 'experts' were baffled. But, true to form, this latest challenge to the official theory was conveniently obfuscated into oblivion; outcast as some illusory mirage that just happened one day in the New Mexico desert.

But the answer is only evident to those who care to scratch a bit deeper than the dust. For they cannot help but notice some overt environmental features that exclusively predominate this unique location. A package of factors which are invariably shared by every single TSE cluster location around the world.

Before the military came, White Sands was an industrial center for the mining of the manganese oxide and wulfenite ores (NB; wulfenite contains the copper chelating molybdenum metal). And since the military have occupied the range, the US authorities have been actively engaged in monitoring the unique intensity of infrasonic shock bursts that are radiated by the explosions of their missiles. The poor deer herd has played guinea pig to an unwitting experiment that has cracked the causal riddle of spongiform disease.

The BSE debacle

Since 1986, the infamous novel neurodegenerative syndrome, BSE and vCJD, has insidiously blighted the heartbeat of British rural life. The disease has annihilated thousands of cattle and a growing number of young people, as well as creating a fierce battleground between nations, vested interests, political parties, farmers, victim support groups and consumers. More recently, the shock waves of the BSE debacle have ricocheted around the entire world, reaching as far afield as Japan and North America.

Yet despite the severity of the mad cow legacy, little genuine attempt has been made to crack the causal riddle of these diseases; thereby leaving us devoid of insight into measures that would best cure, control and, better still, prevent this disease.

But hard scientific evidence is being amassed which indicates that vCJD and BSE could both result from separate exposure of bovines and humans to the same package of toxic environmental factors--ferrimagnetic metals and low frequency sonic shock--and not from the ingestion of the one species by the other. If such a polemic hypothesis continues to accumulate momentum, a radical upheaval of the status quo mindset can be expected.

As a working livestock farmer and TSE researcher with first hand experience of BSE erupting in cattle that had been purchased and brought into my organic farm, I was struck by the fact that no cases of BSE had ever emerged in cows that had been born and raised on fully converted organic farms, despite those cattle having been permitted access to the feed that contained the incriminated meat and bone meal (MBM) ingredient--as part of their 20% conventional feedingstuff allowance decreed in the organic standards at that time.

In this respect, I developed a hunch that the resistance of organic livestock farmers to comply with a UK compulsory livestock chemical treatment program using systemic organo dithiophosphorus (OP) insecticides--toxic chemicals derived from the OP military nerve agents--might offer an explanation for the total absence of BSE in 'home raised' organic cattle across the UK.

In 1982 measures were passed that enforced twice annual application of a uniquely concentrated dose (20 mg/kg bodyweight) of a systemic acting organodithiophosphate insecticide for the control of warbles on UK cattle. Amongst a myriad of toxicological effects, the systemic types of dithiophosphate can chelate copper and open up the blood brain barrier; thereby disturbing the overall crucial balance of metals in the brain. I was therefore not surprised to witness BSE rearing its ugly head in the UK cattle herd in 1986; which, in my opinion, was partly a direct legacy of the UK government's compulsory 'high dose' warble fly campaign. The few other European countries who instigated warble fly campaigns (eg; France, Switzerland, Ireland, etc.) used lower doses of insecticide, and, not surprisingly, developed proportionately fewer cases of BSE as a result.

From then on, I became deeply skeptical of the conventional consensus on the origins of BSE and its human equivalent, vCJD. There were just too many radical flaws blighting the hypothesis that bovine ingestion of micro doses of scrapie contaminated MBM lead to BSE. Equally flawed was the follow up theory that human ingestion of BSE-contaminated beef caused vCJD.

The hyperinfectious hypothesis was based upon a single strand of evidence--that TSEs could be transmitted via injections of TSE-diseased brain tissues into unfortunate laboratory animals. Yet, various other diseases, such as familial Alzheimer's disease, thyroiditis and toxic metal encephalopathies have been transmitted in this way. So why aren't the health authorities panicking about the supposed 'hyperinfectious' capacities of these other diseases?

The Flaws in the Conventional Hypothesis

1. Thousands of tons of the BSE-incriminated meat and bone meal (MBM) feed were exported as cattle feed during the 1970s/1980s/1990s to countries that have remained BSE-free to date--eg, South Africa, Sweden, Eastern Europe, Middle East, India, Third World, etc.

2. Relaxation in the temperature/manufacturing techniques of the MBM rendering process in the UK was blamed for permitting the survival of the scrapie agent in the sheep brain material; thereby enabling the "agent" to jump across into cattle, producing BSE. But none of these alterations were exclusive to the UK plants. For instance, other scrapie endemic countries such as USA and Scandinavia had adopted the same continuous flow system of rendering five years before the UK, yet these countries have remained BSE-free. Furthermore, the pathogenic, 'infectious' capacity of the scrapie agent remains active after heating to temperatures up to 700 degrees--way above the 150 degree temperatures employed in the supposedly 'safe' rendering processes operating in pre BSE days.

3. Several live animal trials in the USA failed to induce BSE in cattle after feeding/injecting them with massive doses of scrapie-contaminated brain tissue. Furthermore, no cases of BSE have developed in 1000 cows that were experimentally challenged with high doses of MBM feed/innoculant on a Department of Agriculture farm at High Mowbray in Yorkshire, UK.

4. Forty thousand plus cows that were born after the UK's 1988 ban on MBM incorporation into cattle feed have still developed BSE.

5. Several countries such as Ireland, Portugal and France have witnessed a greater number of BSE cases in cows born after their respective bans on MBM than in cows born before their bans.

6. There have been no cases of BSE in other TSE-susceptible ruminants in the UK, such as goats and sheep, despite the customary inclusion of the same MBM protein source in their feeds.

7. Four of the original five kudu antelope that developed BSE at the London zoo had not had any possible access to MBM-containing feeds.

8. The UK government's former experimental farm at Liscombe on Exmoor was designed to raise suckler beef cattle on a pure grass/silage system--without resort to feeding any MBM containing concentrated feeds at all. Yet BSE struck down four animals on this holding.

9. It is customary for Icelandic sheep farmers to slaughter and eat their scrapie-affected sheep (brains included) immediately the first symptoms of this rapid wasting disease are recognised. Yet, no cases of CJD have been recorded in Icelandic sheep farmers.

10. The infamous mechanically retrieved meat products/baby foods blamed for causing vCJD in the UK were exported all over the world to countries where vCJD has not erupted to date.

11. BSE fails to fulfill 'Koch's postulates'--the yardstick for gauging whether a given disease stems from infectious origins.

Hyperinfectious Hysteria takes hold

Despite the myriad of epidemiological flaws and millions of pounds worth of research failing to ascertain any association between the origin of these diseases and the scrapie agent, the whole propaganda myth that BSE was caused by scrapie became impregnated as 'gospel' into mainstream public/professional mentality.

It is easy to see how the momentum of such a reductionist mindset took hold; the media loved the theory because they could drum up a viral holocaust-horror scoop. The farming industry could get their beef sales back on the road by deluding consumers that the causal agent had been eliminated. The vegetarian lobby found themselves with a powerful propaganda weapon on their plate, whilst the scientific institutions could carry on, drawing generous funding for their hyperinfectious witch hunt without the embarrassment of having to account for years of barking up the wrong tree. And the government could conveniently offload the blame onto the vagaries of some naturally occurring 'nasty' for which no vested interest or official directive could ever be held accountable.

Governments of the BSE-affected countries rapidly found themselves cornered into providing 'quick fix' remedies to appease the mounting intensity of political and economic pressures levied on them by their BSE-free neighbours.

Sound scientific reasoning has been forced to give way to the panic response; where wholesale slaughter regimes are enacted across the TSE affected regions, despite well documented historical evidence that these measures have repeatedly failed to eradicate TSEs in the longstanding scrapie and CWD hotspot regions across Iceland and Colorado--at great expense to the taxpayer, the farmer and animal life.

Cluster Buster

As a TSE field scientist, my observations and research findings led me to question the scientific validity of the conventional consensus on the origins of TSE. I felt convinced that some key package of environmental factors, such as the copper chelating OP warble fly insecticides, played a primary role in the cause of TSEs, and so I embarked on a global investigation in search of the etiological needles in the causal haystack.

I carried out total environmental analyses of the soil, water and foodchains in various ecosystems of Japan, Slovakia, Italy, Sardinia, Sicily, Iceland, Colorado, Wisconsin, etc, where longterm clusters of TSE have emerged in mammalian populations who are largely self-sufficient upon the local foodchain. I also sampled the adjoining TSE-free areas as controls.

My results indicated that high levels of specific metals such as manganese, uranium and strontium, in combination with deficiencies of copper, constituted an abnormal mineral imbalance that was common to every TSE cluster region that I had analysed. The levels returned to normal in TSE-free adjoining areas.

I also identified the co-presence of high intensities of low frequency sonic shockbursts in all of these TSE cluster environments, which stemmed from a variety of prominent sources; such as low flying military or concorde jets, quarry and military explosions, volcanic/earthquake tectonic rift lines, thunder and electric storms, etc.

I compiled and published a hypothesis which proposed that this abnormal mineral imbalance compromised the ability of the brain to protect itself against the neurotoxic effects of incoming sonic shocks from the external environment.

Copper prion proteins as the 'conductors' and Manganese prion proteins as the 'blockers' of electromagnetic energy flow

Whilst endorsing the well-established view that a malformed version of a native brain protein, known as the prion protein, plays a pivotal role in the pathogenesis of TSEs, I did not subscribe to the extreme view that this proteinaceous particle acted as the hyperinfectious TSE agent.

Given the mystery surrounding the healthy function of this elusive protein, I became interested in the fact that the normal prion protein had been shown to bond onto copper in the healthy brain, as well as performing a functional role in the mediation of the circadian rhythm. I proposed that the copper component of the normal healthy prion protein plays a role in the conduction of electromagnetic energy along the circadian/auditory pathways of magnetic superexchange; where a linear chain of paramagnetic copper atoms (bonded to prion proteins) provides a 'metal to metal to metal' motorway which distributes the electromagnetic energy of light and sound (received at the retina and cochlear) around the tissues for energizing the circadian mediated cycles of sleep, sex, behaviour, heartbeat, cell growth/repair and immune response--locations where the prion protein is intensively expressed.

So once the crucial supply of copper is curtailed in the brain--due to straightforward environmental copper deficiency or exposure to copper chelating OP insecticides, etc.--the prion protein's metal bonds become vacant, rendering the protein vulnerable to bonding with certain alternative replacement metals, such as manganese, uranium or strontium, which have binding affinity for the metal domains on prion protein. But once attached, these foreign substitutes may not act in the overall best interests of the organism, particularly if the invasive metal is in 'ferrimagnetic' and/or in 'radioactive' form.

For instance, once a ferrimagnetic manganese 3+ or strontium 90 atom substitutes at the vacant copper bonds on prion protein, the field-inducing influence of the ferrimagnetically-ordered atoms will progressively corrupt the circadian mediated pathways of electromagnetic superexchange throughout the brain; whereby a status of permanent magnetic charge is spread much like a domino-style, contagious corruption which jumps from metal bond to metal bond, from prion to prion. This phenomena is well illustrated by the classic college physics experiment, where a magnet is placed alongside a steel nail and the force field of the magnet rapidly magnetises the adjoining nail.

So once an individual's brain is contaminated by this freaky form of ferrimagnetic manganese or strontium, any subsequent exposure to external electromagnetic fields (eg, UV, sound waves, radar, cell phones, etc.) will permanently charge up the ferrimagnetically-ordered manganese prions to saturation point.

In this respect the TSE diseased brain can be likened to a solar powered battery on continuous charge; where the manganese loaded/copper depleted brain is no longer equipped to deal with the incoming surges of electromagnetic energy from the external environment. Instead of utilising this energy for the body's own vital requirements, its conduction is blocked and perverted into a potent force field for neuronal suicide; whereby the magnetically saturated atoms emit intensive magnetic fields, which, in turn, generate self-perpetuating 'cluster bombs' of free radical-mediated spongiform neurodegeneration. TSE ensues.

Does the rogue ferrimagnetic metal, co-partner of the misfolded prion protein, serve as the infectious/transmissible component in TSEs?

This theory explains why the so-called 'hyperinfectious' property of the prion is a misnomer. It is the toxic ferrimagnetic metal component of the prion that serves as the so-called 'infectious' pathogenic agent in TSEs. So whenever scientists inoculate unfortunate lab animals with TSE brain tissues (eg tissues contaminated with this rogue type of manganese or strontium atom) and effectively transmit TSE, they are actually transmitting a 'magnetic field inducing capacity' that is carried along with the ferrimagnetically ordered metal contaminant into the recipient animals, who, in turn, develop TSE.

Furthermore, the concept of the rogue ferrimagnetic manganese atom as the 'TSE agent' also explains why the so called 'infectious' pathogenic capacity of the prion can survive heating to temperatures in excess of 500 degrees--since ferrimagnetic metals will hold onto their magnetic charge until they are heated to temperatures beyond their respective 'curie point' temperature. (eg, 550 degrees for manganese 3+)--whence its magnetic energy is instantly drained.

Laboratory support for the TSE environmental origin theory

Several laboratory studies have come out in strong support of the mainstay of these environmental observations, suggesting that the abnormal mineral template common to TSE ecosystems represents more than an incidental finding. For instance, Cambridge University demonstrated that the prion protein adopts its TSE deformed shape after manganese has been added to copper depleted prion protein cell cultures, whilst the US Prion Surveillance Centre at Case Western University in Cleveland observed a ten fold increase in manganese levels and 50% reduction of copper in sCJD diseased brain tissues.

From the soil to the brain; the environmental dynamics of TSE pathogenesis

Interestingly, neuropathologists working on post-mortem TSE diagnosis in Sardinia, Iceland and Colorado, report worn down, soil-stained incisor teeth as well as a deposition of grit/soil in the gastro tracts of the carcasses of scrapie and CWD casualties that are sent in for analyses. These unusual phenomena could be explained by the fact that both CWD and scrapie have a tendency to erupt in overpopulated ruminant populations who are overgrazing short-cropped pastures in drought stricken areas; indicating that these hard pressed, grazing animals would be taking in significantly larger amounts of top soil than normal.

Likewise, CJD has a tendency to erupt in self sufficient and/or rural based human populations whose work and lifestyles necessitate closer contact with the soil.

My studies have observed that TSE clusters arise in mammalian populations who are dependent upon certain geological soil types that have been subjected to various environmental 'stress' influences (eg; infrasonic vibrational shocks, fire, lightning strikes, intensive ultraviolet radiation, drainage/liming). These influences can trigger a metamagnetic transition of certain iron, manganese 3+, uranium, strontium compounds in the soil (and atmospheres) which can open up a quantum capacity for absorption of select frequencies of phonons, photons or thermal energy that are incoming from the external environment. For instance, low frequencies of acoustic-vibration shock energy can actually metamorphose the octahedral crystalline lattice of some metallic compounds, inducing a metamagnetic transmutation of the atom from paramagnetic to ferrimagnetic form.

So in areas where the rogue ferrimagnetic manganese 3+, uranium or strontium species of metal is at high levels in the soil, any intake of top soil into the guts of grazing ruminants is likely to result in the increased uptake of these rogue metals into their biosystem, and, in certain circumstances, into their brain.

Furthermore, overpopulation of cervids in the CWD areas, has also led to increased browsing of juniper/pine and of locally farmed alfalfa crops as a means of bolstering their impoverished diet. These plants concentrate strontium and manganese to excessively high levels (Author's latest unpublished observations 2002/2003), so could represent a source of the rogue metals in conjunction with the more direct source from the soil.

Alternatively, the actual sonic shock induced metamagnetic transmutation could be triggered in the metal atoms within the living brain itself. A good example of this phenomena is possibly illustrated in the context of the racing pigeons who had flown into the 100 km shockwave boom carpet left in the wake of the Concorde supersonic aircraft and had permanently lost their sense of magnetic orientation as a result. Furthermore, cell culture studies have also shown that a sound wave challenge will proliferate the mysterious multireplicating property of the prion protein.

It is proposed that the long standing, less aggressive, traditional strains of TSE are largely caused by exposure to foodchains that are contaminated by naturally occurring sources of toxic ferrimagnetic metals (manganese, thorium, strontium from volcanic emissions, etc.) and deficiencies of copper; along with exposure to intensive shockbursts of naturally occurring sources of low frequency acoustic waves which emanate from the movement of tectonic fault lines (during earthquake, volcanic activities) or from thunder/lightning storms.

Whereas, the more aggressive, accelerated version of new strain TSEs (BSE/vCJD) that has emerged more recently in younger mammals, are caused by exposure to the more intensive artificial sources of these same ecofactors. In this respect, it is proposed that the UK's BSE and vCJD 1986-2000 epidemics were caused by the simultaneous exposure to:

1. The soils/atmospheres that were contaminated with high levels of radioactive strontium 90 after the emissions from the 1986 Chernobyl atomic leak were rained down over North Western Europe (UK, and to a lesser extent Brittany, Ireland, etc.)--the precise region which was shortly to become the first ever BSE hotspot region in the world.

2. The systemic acting 'copper chelating' types of organo dithiophosphate insecticide that were intensively used for warble fly/head lice/flea/food crop treatment around this time; thereby starving the prion protein of its copper co partner, subsequently rendering the protein's vacant metal domains to binding up with any replacement metals that are at 'superfluous' levels within the brain; eg; the rogue radioactive strontium 90.

The resulting mineral imbalance impairs the ability of the mammalian brain to deal with the ever increasing challenge of sonic shocks from the external environment.

The Canadian context

The Canadian authorities should make a concerted attempt to identify the true origins of their TSE cases. My own preliminary survey has identified some of the key TSE risk phenomena in the environments where TSE has erupted in Alberta and Saskatchewan to date. The two farmed deer diagnosed with CWD were both raised on a farm that was directly under the takeoff flight path of a recently closed military jet base on the northern side of Edmonton.

The 'nidus' of the new variant TSE cases that have erupted in Canada so far, have involved two mammals (a human and cow) that had both originated from around the Sandhills district of Saskatchewan. Identical to the other TSE hotspot regions across North America, the soil is copper deficient, high in uranium/strontium and is of the drought prone, sandy type. The vegetation is also predominated by the juniper bush. Interestingly, the largest military tank test shelling range in North America, Camp Wainwright, is also located in the middle of this area, where the low frequency acoustic shockbursts from the tank shelling practice reverberate throughout the summer period.

Interestingly, all Canadian cases of CWD in wild deer have also originated from the Sandhills area to date. In fact, the first case of CWD was purportedly observed in a deer that was picked up staggering around in dazed condition on the military range itself.

Understanding the true causes of TSEs provides the best insight into measures that would best cure, control and, more importantly, prevent these grotesque diseases. Given the potential financial losses that could be incurred by the Canadian/North American economy as a result of the recent outbreaks of TSEs in deer and cattle herds, it would seem wise for the appropriate authorities to break ranks with the mainstream reductionist mindset on the origins of TSE and adopt an alternative foolproof strategy for getting to the root of this problem, rather than 'cuckooing' out the same old stereotype protocol of control measures that have invariably failed to properly control a single outbreak of TSE to date.

Wholesale slaughter measures; the final farcical solution?

The epidemiological and experimental evidence amassed to date points to the fact that TSEs are caused by a clearcut combination of genetic and toxic environmental factors. And, despite the universal scaremongering over the 'hyperinfectious' nature of the prion, an impartial study of the epidemiological history of TSEs clearly demonstrates that this disease does NOT originate from animal to animal contact or through ingestion of feeds contaminated with TSE brain material. So why do the authorities continue to treat these diseases as if they stem solely from hyperinfectious origins?

The reasons for such an irrational, Pavlovian-like stance of the Establishment towards the environmental perspectives of TSEs probably hangs upon issues that are more to do with protecting academic egos, professional reputations and the vested interests of the TSE institutions/key advisors, than with promoting sound scientific argument. But the main reason must undoubtably stem from the fear of massive compensation claims, should issues such as government mandated use of copper chelating 'OP warblecides' (re the massive BSE epidemic in the UK) or leakage of radioactive metals from power or military facilities ever prove to be partially accountable for TSE causation at the end of the day.

Despite the repeated failure of wholesale livestock slaughter /fallowing regimes to eradicate long established TSE hotspot regions in Colorado and Iceland since the 1970s, governments are still adopting this same slaughter strategy as a first choice means of control today. But history has shown that TSEs will invariably re-erupt as soon as fresh livestock are introduced back into the slaughtered out areas; supporting the idea that the environmental causes of TSE are still well and truly wedded to the local food chain.

Such extreme measures do little more than remove the superficial evidence of the disease. They merely mislead the public into the illusory notion that TSE has been controlled (a good vote catching policy for any government). But who is questioning the scientific reasoning for executing this final farcical solution on these poor creatures. For the unilateral adoption of a policy of 'totalitarian overkill' of a few million healthy animals across the world has been received with almost complacent acceptance. Such perverse and senseless 'carry ons' have sadly become the daily 'non-stories' of our modern times. Reports pop up with ever increasing frequency of so called TSE precautionary slaughter control programmes being enacted after 3% or more animals in a flock prove positive to the TSE genotype test; an innocuous, endemic phenomena that has existed in the sheep flocks across countries like Australia for light years. Countries where clinical scrapie has never emerged, presumably because the TSE environmental triggers are not present there.

Nonetheless, despite the total absence of any sound scientific requirement, the prophylactic annihilation of livestock still carries on--a herd of water buffalo in Vancouver, deer herds across North America, sheep flocks from Vermont, hundreds of cows slaughtered in Germany, plus thousands of scrapie susceptible traditional sheep and goat herds erased from the European hillsides--all healthy animals.

Bibliography

Agrimi U, Riu G, Cardone F, Pochiari M, Caramelli M. Epidemic of TSE in sheep and goats in Italy. Lancet 1999; 353: 560-561.

Alpers MP, Kuru; Chapter 16 in Human Biology in Papua New Quinea 1992 Eds; Attenborough RD, Alpers MP. Clarendon Press, New York.

Annual Animal Health Reports; Warble Fly. 1988. MAFF, Toby Jug Site, Tolworth, Surrey.

Arendt S, Fritts DC. Acoustic radiation by ocean surface waves. J Fluid Mechanics 2000; 415: 1-21.

Ascher M, Ascher JL, Manganese Neurotoxicity; Cellular effects and blood brain barrier transport. Neurosci Biobehavioural reviews 1991 15 333-340

Barnett K and Palmer A. A retinopathy in sheep affected with Natural Scrapie. Res Vet Sci 1971 12 383-385.

Bartlet P, Haus E, Tuason T. Circadian rhythm in number of erythroid and granulocytic colony forming units in culture in bone marrow of BDFI male mice; in Haus E, Bastian F, CJD and other transmissible encephalopathies, Mosby Year Book 1991 St Louis.

Beauregard G, Lum J, Roufogalis B. effect of histidine modification on the aging of OP inhibited acetylcholinesterase. Biochem Pharm 1981;30 (21): 2915-2920.

Becker RO, Selden G. The Body Electric; Electromagnetism and the foundation of life. 1985. Quill, William Morrow, New York.

Bedard AJ; Infrasound originating near mountainous regions in Colorado. J Applied Meteorology 1978; 17:1014-1022.

Bounias M, Purdey M, An epidemiological evaluation of a possible link between BSE and systemic warblecide treatments in France. Under peer review.

Bowman HS, Bedard AJ. Observations of infrasound and subsonic disturbances related to severe weather. Geophys J Roy Astron Soc 1971; 26:215-242.

Bradley R, Wilesmith JW. Epidemiology and control of BSE. British Med Bulletin 1993; 49 (4): 932-959.

Brown D, Prion and prejudice; normal protein and the synapse. Trends in Neurosciences 2001 24 (2) 85-90.

Brown D, Hafiz F, Glassmith L, Wong BS, Jones I, Clive C, Haswell Consequences of manganese replacement of copper for prion protein function and protease resistance. EMBO J. 2000 19 (6) 1180-1186.

Brown D, Quin K, Herms J, Madlung A, Manson J, Strome R, Fraser P, Kruck T, Bohlen A, schulz-schaeffer W, Glese A, Westaway D, Kretzschmar H. The cellular prion protein binds copper in vivo. Nature 1997 Dec 390 684-687.

Brown P, Rau EH, Johnson BK, Bacote AE, Gibbs CJ, Gajdusek DC. New studies on the heat resistance of hamster adapted scrapie agent: Threshold survival after ashing at 600 degrees C suggests an inorganic template of replication. PNAS March 28, 2000; 97; (7) 3418-3421.

Bruce ME, Will RG, Ironside JW, McConnell I, Drummond D, Suttie A, McCardle L, Chree A, Hope J, Birkett C, Cousens S, Fraser H, Bostock CJ. Transmissions to mice indicate that new variant CJD is caused by the BSE agent. Nature, 2 October 1997, 389, 498-501.

BSE in Great Britain; A Progress Report; Nov 1995, Dec 2001. DEFRA, London, Uk.

BSE Inquiry, Volumes 2/5/9/10, October 2000; The Stationary Office Limited, PO Box 29, Norwich NR3 1GN.

BSE Inquiry; Volume 4 and 6. 2000. The Stationary Office, London, UK.

BSE Inquiry Sessions; M73; epidemiology of BSE 14/10/99.

Cagampang F, Whatley S, Powell J, Mitchel A, Campbell I, Cohen W. Circadian regulation of PrP messenger RNA in rat forebrain; a widespread and synchronous rhythm. Neurosci 1999 91 1201-1204.

Carlin RL; Magneto-chemistry. 1986. Springer Verlag, Berlin.

CJD Annual incidence rates by parish in Somerset. Public Health, Somerset Health Authority, Wellsprings Road, Taunton TA27PQ, UK.

CJD surveillance in the UK; 2000 9th Annual Report the National CJD Surveillance Unit, Western General Hospital, Edinburgh, EH42XU.

Crom R, Cluster of CJD cases in Tucson. Report; The epidemic Intelligence Service of the Arizona Department of Health Services, Phoenix. 1990.

Crystal Chemistry of Functional Materials 11; Symposium L. European materials research society, E-MRS Spring meeting 2002, June 18. Strasbourg, France.

Cutlip RC, Miller JM, Race RE, Jenny AL, Katz JB, Lehmkuhl BM, DeBey BM, Robinson MM. Intracerebral Transmission of scrapie to cattle. J Infectious Diseases 1994; 169: 814-820.

Dai P, Static and dynamic lattice effects in MnO3 compounds Lal-xCaxMnO3. Phys rev B 1996; 54:R3694.

Dalby J, Soil Association survey of the incidence of BSE on organic farms in the UK. 1996. Soil Association, Bristol House, 40-56 Victoria Street, Bristol, BS16BY, UK.

D'Alessandro M, Petraroli R, Ladogana A. Pocchiari M. High incidence of CJD in rural Calabria. 'Lancet 1998; 352: 1989-1990.

Donn WL, Rind D, Natural infrasound as an atmospheric probe. Geophys J R Astron Soc 1971; 26:111-133.

Disorders of mineral metabolism Vol 1; Trace Minerals 1981; Bronner F and Ford ED (Eds). AcademicPress, New York.

Donn WL. Exploring the atmosphere with sonic booms. Am Sci 1978; 66: 724-733.

Donn WL, Posmentier ES. Ground coupled airwaves from the great Alaskan earthquake. J Geophys Res 1964; 69: 5357-5361.

Duffey P, Comets and Concordes, Paladwr Press, Virginia, USA. 1999.

Farmer PM, Kane WC, Hollenberg-Sher J. Incidence of CJD in Brooklyn and Staten Island. 1974; 298

Forman H, Cadenas E, (eds). Oxidative stress and signal transduction. Chapman and Hall, New York. 1997

Free radicals in Biology and Medicine. Halliwell B, Gutteridge JMC, Eds 1989 2rd Edition. Clarendon Press, Oxford, UK.

Gabriela P. Sensitive detection of pathological PrP by cyclic amplification of protein misfolding. Nature June 14th 2001 411 810-813.

Goerke VH, Young JM, Cook RK. Infrasonic observations of the May 16 1963 volcanic explosion on the island of Bali J Geophys Res 1965; 70: 6017-6022.

Gordon I, Abdulla EM, Campbell IC, Whatley S. Phosmet induces upregulation of surface levels of cellular prion protein. Neuroreport; 1998 9 (7) 1391-1395.

Goudsmit MD, Morrow CH, Asher DM, Yanagihara RT, Masters CL, Gibbs CJ, Gajdusek DC. Evidence for and against the transmissibility of Alzheimer Disease. Neurology 1980 30 945-950.

Hagstrum JT. Infrasound and the avian navigational map. J Experimental Biol 2000; 203: 1103-1111.

Hogan R, Baringer J, Prusiner S. Progressive retinal degeneration in scrapie infected hamsters. Lab Invest 1981 44 34-42.

Hope J, Baybutt H. The Key role of the nerve membrane protein PrP in scrapie-like diseases. Seminars in the Neurosciences 1991 3 165-171.

Hornshaw M, McDermott J, Candy J, Lakey J. Copper binding to the N terminal tandem repeat region of mammalian and avian PrP; Structural studies using synthetic peptides. Biochem Biophys Res Communications. 1995 214 (3) 993-999.

Improvements in the control methods for warble fly in livestock; Eds; Boulard C, O'Brien D, Pithan K, Sampimon O, Sol J, Webster K. Cost 811 Project, Agriculture, European Commission, rue de la Loi 200, B-1049 Brussels.

Infrasound and low frequency vibration; Tempest W (ed). Academic Press, London. 1976.

Jenkins R, Katz CN, Le Bras R, Sereno T. Grand Truth analysis of explosions recordings at LSAR and TXIAR infrasound arrays. SAIC Tech Report 1998; /3035 25pp.

Kimmerle G, Loeser E. Delayed neurotoxicity of OP compounds and Cu concentrations in the serum of hens. Environ Quality Safety 1974; 3: 173-178.

Kirkwood JK, Cunningham AA. Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Vet Record 1994; 135: 296-303.

Lasmezas CI, Deslys JP, Robain O, Jaegly AS, Beringue V, Peyrin JM, Fournier JG, Hauw JJ, Rossier J, Dormont D. Transmission of the BSE agent to mice in the absence of detectable abnormal prion protein. Science 1997; 275: 402-404.

Liebisch A, Hypoderma Infection in cattle VET November 1988; from Lebhard Verlag GmbH, Labhardsweg 2a 7750 Konstanz, Germany.

Liszka L, Walodemark K. High resolution observations of infrasound generated by the supersonic flights of concorde, J Low Freq Noise Vibration. 1995; 14 (4): 63-70.

Marsh R. Transmissible mink encephalopathy, scrapie and downer cow disease; potential links. Proceedings of 3rd International workshop on BSE. Bethesda, Maryland. 1992 December 9-10th.

Mathews WB. Epidemiology of CJD in England and Wales. J Neurol Neurosurg Psych 1975; 38:210-213.

McKinley MP, Nerve growth factor induces gene expression of PrP and amyloid protein precursor in the developing hamster CNS. Prog Brain Res 1990; 86: 227-238.

Mitrova E. Some new aspects of CJD epidemiology in Slovakia. Euro J Epidemiol 1991 7 (5) 439-449

Mitrova F, Bronis M. Clusters of CJD in Slovakia; the first statistically significant temporo-spatial accumulations of rural cases. Eur J Epidemiol 1991; 7(5): 450-456.

Miyakawa T, Inoue K, Iseki E, Kawanishi C, Sugiyama N, Onishi H, Yamada Y, Suzuki K, Iwabuchi K, Kosaka K. Japanese CJD Patients exhibiting high incidence of the E200k PRNP mutation and located in the basin of a river. Neurological Research 1998; 20: 684-688.

Mohr Capt GC, Cole JN, Guild Lt Col E, Von Gierke HE. Effects of low frequency and infrasonic noise on man. Aerospace Medicine 1965; 36 (9): 817-824.

Moser M, Oesch B, McBride P, Manson J. Altered circadian activity rhythms and sleep in mice devoid of PrP. Nature 1996 380 639-642.

Neel L, Magnetism and the local molecular field. Nobel Lecture, December 11, 1970, p 318-341.

Orchard AF; Magnetochemistry. Oxford University Press, New York; 2003.

O'Reilly W. Rock and Mineral Magnetism, Blackie, Glasgow. 1984

Orlebar C. The Concorde Story. British Airways. Osprey Publishing Co. 1997.

Owen K. Concorde; new shape in the sky; fig 34. p 171. Jane's Publishing Co, London. 1982.

Palsson PA, Rida in Iceland and its epidemiology. In 'Slow transmissible diseases of the nervous system, vol 1, London Academic Press 1979, 357-366.

Prasher D, Luxon L. Biological effects of noise, Vol 1. Advances in Noise research. 1998 Whurr Publishers Ltd, 19b Compton Terrace London, N1 2UN, UK.

Prion diseases. Eds Collinge J, Palmer MS. Oxford; Oxford University Press 1997.

Purdey M, Are Organo phosphate pesticides involved in the causation of BSE. J Nutritional Med 1994 4 (1) 43-82.

Purdey M, BSE; Slow Virus or chronic pesticide initiated Modification of the prion protein? 2. An epidemiological perspective. Med Hypotheses 1996 46 (5) 445-454.

Purdey M; Mad Cows and Warble Flies. Ecologist 1992 24 (3) 100-104.

Purdey M, Ecosystems supporting clusters of sporadic TSEs demonstrate excesses of the radical generating divalent cation, manganese, and deficiencies of antioxidant co factors Cu, Se, Fe, Zn. Does a foreign cation substitution at Prp's Cu domain initiate TSE? Medical Hypotheses 2000 54 (2) 278-306.

Purdey M. Does an ultra violet photoxidization of the manganese loaded/copper depleted prion protein in the retina initiate the pathogenesis of TSE? Medical Hypotheses 2001 57 (1) 29-45.

Purdey M, High dose exposure to systemic phosmet insecticide modifies the phosphatidylinositol anchor on the prion protein; the origins of new variant transmissible spongiform encephalopathy? Medical Hypotheses 1998 50 (2) 91-111

Purdey M, The Mn loaded/Cu depleted brain fails to neutralise the incoming shockbursts of low frequency infrasound; The origins of BSE? Cattle Practice, BCVA 2002 10 (4) 311-335.

Purdey M, Does an infrasonic acoustic shock wave resonance of the manganese 3+ loaded/copper depleted prion protein initiate the pathogenesis of TSE? Medical Hypotheses; 2003, 60 (6) 797-820.

Qualitative Analysis of BSE risk factors in the US. USDA: APHIS: VS Animal Health Information, 555 South Howes, Fort Collins, Colorado 80521 1991; pp21.

Reiter R, Static and extremely low frequency electromagnetic field exposure: Reported effects on the circadian production of melatonin. J Cellular Biochem 1993 51; 394-403.

Rogalev A, Journal Phys Cond Matter 1999 11; 1115.

Scheving LE, Burns ER, Pauli JE, Circadian variation and cell division of the mouse alimentary tract, bone marrow and corneal epithelium. Anat Rec; 1978; 191: 479-486.

Schernmuly L, Klinke R. Infrasound sensitive neurones in the pigeon cochlear ganglion. J Comp Physiol A 1990; 166: 355-363.

Skinner BJ, Porter SC; The Dynamic Earth; 3rd Edition, Wiley and Sons, New York 1995.

Sun JZ, Krusin-Elbaum L, Gupta A, Xiao G, Duncombe PR, Parkin SSP. Magnetotransport in doped manganate perovskites. GMR, oscillatory coupling and related studies; 1998, 42 (1)

Tasker J, Grampian Pharmaceuticals; Statement and oral evidence to BSE Inquiry Hearing; November 5 1998. File BS051198. ASC. BSE Inquiry, Stationary Office, London.

Thompson R, Oldfield F; Environmental Magnetism; George Allen and Unwin. 1986.

Trabattoni G, Lechi A, Bettoni G, Macchi G, Brown P. Considerations on a group of 13 patients with CJD in the region of Parma, Italy. European Journal Of Epidemiology 1990, 6 (3) 239-243.

Trace Elements in Human and Animal Nutrition (Mertz W Ed) 1986 Academic Press, New York.

Uman MA. Lightning. Dover Publications, New York. 1969.

Von Gierke HE. Effects of sonic boom on people: review and outlook. J Acoustical Soc Am 1966; 39 (5) pt 2: S43-S50.

Von Gierke HE, Nixon CW. Human response to sonic boom in the laboratory and the community. J Acoustical Soc Am 1972; 51 (2) Pt 3: 766-782.

Warren CHE. Recent sonic-bang studies in the UK. J Acoustical Soc Am 1972 51 (2) Pt 3:783-789.

Webb DRB, Warren CHE. An investigation of the effects of bangs on the subjective reaction of a community. J Sound Vibration 1967; 6 (3) 375-385.

Will RG, Matthews WB, Smith PG et al. A retrospective study of CJD in England and Wales. 1970-1979: 11 Epidemiology. J Neurol Neurosurg Psychiatry 1986; 49: 749-755.

Williams ES, Young S. Spong. Encephalopathy in cervidae. Rev Sci Tech Off Int Epiz 1992 11(2)551-567.

Wong BS, Chen SG, Colucci M, Xie Z, Pan T, Liu T, Li R, Gambetti P, Sy MS, Brown DR. Aberrant metal binding by prion protein in human prion disease. J Neurochem 2001 78 1400-1408.

Correspondence:

Mark Purdey

High Barn Farm

Elworthy, Taunton, Somerset, TA43PX

United Kingdom

Tel: 0044-1984-656832

tsepurdey@aol.com

COPYRIGHT 2004 The Townsend Letter Group
COPYRIGHT 2004 Gale Group

Return to Exploding head syndrome
Home Contact Resources Exchange Links ebay