Risk of Brain Tumors From Wireless Phone Use

Journal of Computer Assisted Tomography November/December 2010; Vol. 34, No. 6; pp. 799-807 Rash Bihari Dubey, Madasu Hanmandlu, PhD, and Suresh Kumar Gupta, PhD FROM ABSTRACT: The debate regarding the health effects of low-intensity electromagnetic radiationfrom sources such as power lines, base stations, and cell phones has recently beenreignited.The impact of wireless communication on human health has not been completely assessed.Widespread concern continues in the community about the deleterious effects ofradiofrequency radiations on human tissues and the subsequent potential threat ofcarcinogenesis. Exposure to low-frequency electromagnetic field has been linked to a variety ofadverse health outcomes.This article surveys the results of early cell phone studies, where exposure durationwas too short to expect tumor genesis, and 2 sets of more recent studies with longer exposure duration: the Interphone studies and the Swedish studies led byHardell. KEY POINTS FROM THIS ARTICLE: 1) Health hazards due to the extensive use of cell phones among ever growingschemes of society are a matter of concern. 2) Effect of radiofrequency radiation on the human giving rise to brain tumor isbeing extensively studied all over the world. Investigations suggest that the use ofa mobile phone for 10 or more years can dramatically increase the risk ofdeveloping a tumor. 3) Mobile phones use electromagnetic radiation in the microwave range, andthis may be harmful to the human health. 4) The cell phone signal is absorbed deeply into the brains of children and up to2 inches into an adult skull. 5) There is serious neuronal damage in rat brains after an exposure to amicrowave radiation from a cell phone, at levels comparable with what peoplewould experience during normal use. 6) Most negative studies on cell phones and tumors have been substantiallyfunded by the cell phone industry. 7) These authors cite evidence that shows: * An association between cell phone use and the development of glioma, a typeof brain cancer. * There is a consistent pattern connecting cell phone use and the increased riskof developing brain cancer. * Long-term cell phone use increases the risk of tumors of the head. * The radiofrequency emissions from cell phones have been shown to damagegenetic material which is a common precursor to cancer. * The radiofrequency radiations from cell phones can damage the DNA insperm. Cell phone storage in front pockets has been linked to poor fertility and anincreased chance of miscarriage and childhood cancer. * Long-term cell phone use can increase the likelihood of being hospitalized formigraines and vertigo by 10% to 20%. * Independent research by a number of investigations has suggested a linkbetween brain tumors and cell phone use. * Cell phone radiation damages DNA, an undisputed cause of cancer. * Cell phone radiation causes the blood-brain barrier to leak. The leakage ofthe blood-brain barrier resulting from cell phone use increases the possibility ofbrain tumors. 8) The global system for mobile communications cell phones operates at afrequency of 900 or 1800 MHz. The interaction of cell phones with the base stationvia radiofrequency radiations occurs even when the phone is not in use.[Important] 9) Radiofrequency radiation in this range [of 900 or 1800 MHz] is non-ionizingradiation. It does not carry enough energy to completely move an electron from anatom or molecule. Instead, the energy is sufficient only for excitation, themovement of an electron to a higher energy state. 10) Exposure of the brain depends on the type of phone and position of theantenna but tends to be highest in the temporal lobe and insular region andoverlying skull, scalp, and parotid gland tissues. Irrespective of the type of phone,exposure is highest on the side of the head against which the cell phone is held andseems to be even higher in children owing to thinner scalps and skulls, increasedwater content of their brain, and lower brain volume. 11) The adult brain absorbs the cell phones radiation almost entirely on the sideof the head where the cell phone is held (ipsilateral); almost no radiation isdeposited on the opposite side of the head (contralateral). In adults, the ipsilateraltemporal lobe absorbs 50% to 60% of the total radiation. The ipsilateral cerebellumabsorbs 12% to 25% of the total radiation. 12) There are 11 published studies examining long-term cell phone use (ie, usefor 10 years) and the risk of developing a brain tumor. 13) Cell phone studies that claim they are safe may be flawed because of theymay have not considered these factors: * Cell phones radiation is higher in rural areas. * Cordless phones, walkie-talkies, ham radio transmitters, and other devicesare treated as unexposed, although in fact, they are exposed. * A large number of brain cancer subjects died before they could beinterviewed or were too ill to be interviewed, and therefore were not counted. 14) The independently funded Swedish studies led by Dr. Hardell have the mostcases that used a cell phone for 10 or more years. The Hardell team concludes: The higher the cumulative hours of use, the higher the radiated power, the higher the number of years since first use, the higher theexposure, and the younger the user, then the higher the risk of braintumor. (7 studies)The meta-analysis shows that long-term cell phone use canapproximately double the risk of developing a glioma or an acousticneuroma in the more exposed brain hemisphere.Long-term cell phone use elevates the users risk of developinga brain tumor. 15) The long-term epidemiological data suggest an increased risk of beingdiagnosed with an ipsilateral brain tumor related to cell phone use of 10 years ormore. 16) It is concluded that the current long-term epidemiological data areconsistent in determining an increased risk of brain tumors associated withipsilateral long-term cell phone use. 17) Based on extensive research done on RFR exposure till date, the FCC hasissued a warning label for cordless phones. 18) Because the expert groups have suggested that the radiation from mobilephones greatly exceeds safe levels even at normal use, even a short call can haveharmful effects. 19) There is now a considerable body of evidence proving that microwaveradiation from mobile and cordless phones causes brain tumors, disturbed brainfunction, and other health disturbances. 20) Steps one can take to reduce exposure to electromagnetic energy from cellphones: A)) Limit the use of cell phones to essential calls and keep calls short. B)) Children should be allowed to use a cell phone in cases of emergency only.Because of their developing skulls, the radiation can penetrate much more deeply. C)) Wear an air tube headset (not regular wired headset). The regular wiredheadset has been found to intensify radiation into the ear canal. The wire not onlytransmits the radiation from the cell phone but also serves as an antenna,attracting EMFs from the surroundings. D)) Do not put the cell phone in a pocket or a belt while in use or while it is on.The body tissue in the lower body area has good conductivity and absorbs radiationmore quickly than the head. One study shows that men who wear cell phones neartheir groin could have their sperm count dropped by as much as 30%. E)) If using the phone without a headset, wait for the call to connect beforeplacing the phone next to the ear. F)) Do not use the cell phone in enclosed metal spaces such as vehicles orelevators, where devices may use more power to establish connection. G)) Do not make a call when the signal strength is 1 bar or less, which means thephone must work harder to establish a connection. H)) Purchase a phone with a low specific absorption rate. Most phones have a lowspecific absorption rate level listed in its instruction manual. The low specificabsorption rate level is a way of measuring the quantity of radiofrequency energythat is absorbed by the body. I)) Use a scientifically validated electromagnetic field (EMF) protection device.There are advanced technologies available nowadays that strengthen the bioenergyfield and immune system against the effects of electromagnetic field (EMF). J)) Use text instead of talk. K)) Use landlines. L)) Keep the cell phone off most of the time. Let people leave messages and thencall them back from a landline. M)) Limit the use of cell phones in rural areas. 21) Cell phone radiation decreases as the square of the distance from the phoneincreases. As a result, even small changes in distance have a dramatic effect. Withthe use of a headset connected, the cell phone is not held directly against the ear,and thus, the absorbed cell phone radiation could be reduced by several orders ofmagnitude. 22) Using a cell phone for 10 years approximately doubles the risk of having adiagnosis of a brain tumor on the same (ipsilateral) side of the head as thatpreferred for cell phone use. 23) People should be very restrictive with using mobile phones, as there is asignificant body of compelling scientific evidence indicating serious hazards fromtheir use. 24) Therefore, it is advisable to reduce the use to very few and brief calls. Peopleyounger than 20 years should have mobile phones that allow short message servicemessages only, but no talking, because the risks are far higher in young people. 25) Moreover, it has been repeatedly confirmed that the radiation from basestations is harmful to health. 26) The existing International Commission on Non-Ionizing Radiation Protection(ICNIRP) and Federal Communications Commission (FCC) exposure limits are basedon a false premise that only thermal effects cause harm. 27) We conclude that the current standard of exposure to microwave duringmobile phone use is not safe for long-term exposure and needs to be revised.

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Risks of Copper and Iron Toxicity during Aging in Humans Chemical Research in Toxicology

February 15, 2010; Vol. 23; No. 2; pp. 319 – 326 George J. Brewer Departments of Human Genetics and Internal Medicine, University of Michigan Medical School (this article has 89 references) KEY POINTS FROM THIS ARTICLE: 1) Copper and iron are essential but also toxic metals. 2) Copper and iron toxicity are important in public health significance, yet arevirtually unknown to the general medical community and there is completeunawareness of the public. 3) The subtle toxicity of copper and iron affects almost all of us as we age. 4) Copper and iron contribute to the production of excess damaging freeradicals. 5) Diseases of aging such as Alzheimers disease, other neurodegenerativediseases, arteriosclerosis, diabetes mellitus, and others may all be contributed to byexcess copper and iron. 6) In the general population, those in the highest fifth of copper intake, losecognition at over three times the normal rate. [Very Important] 7) Inorganic copper in drinking water and in supplements is handled differentlythan food copper and is therefore more toxic. 8) Trace amounts of copper in drinking water, less than one-tenth of thatallowed in human drinking water by the Environmental Protection Agency, greatlyenhanced an Alzheimers-like disease in an animal model. 9) Humans use oxygen in the mitochondria to generate energy in the form ofadenosine triphosphate (ATP). Toxic byproducts of this metabolism are generated,called reactive oxygen species (ROS). 10) ROS can cause damage to most biological molecules, including DNA, protein,and lipids, resulting in damage to membranes and various cellular organelles. 11) Copper and iron are essential for life, and especially for their roles in energyproduction. But both copper and iron have their toxic side that allows them tocatalyze the generation of damaging reactive oxygen species (ROS). 12) Copper and iron are particularly damaging when they exist in theirfreestate. 13) 85-95% of the copper in human blood is safely bound to a molecule calledceruloplasmin (Cp). The other 5-15% is loosely bound to albumin and this 5-15% iscalled free copper. It is this free copper that causes generation of the toxic ROS. 14) Those living on the high side of the 5-15 µg/dL range may be suffering fromsubtle copper toxicity. 15) Organic food copper is bound to proteins and is processed by the liver, whichdoes not allow excess release into the free copper pool in the blood. 16) Inorganic copper consumed in drinking water or mineral supplementsbypasses the liver and contributes immediately to the free copper pool in the blood. 17) The higher the free iron, the greater the risks of developing the diseases ofaging. 18) Evolution favors reproduction. In youth, high levels of copper and ironincrease energy production, wound repair, compensate for blood loss, and thereforeincrease reproductive fitness. After about age 50 when reproduction is no longer afactor, high levels of copper and iron are toxic because they increase free radicalproduction, enhancing the degenerative diseases of aging. There is no natural selection against diseases of aging. 19) The levels of copper and iron considered normal for humans are acceptableduring the reproductive years but are too high after age 50 and contribute todiseases of aging. 20) Rabbits fed diets to develop Alzheimers disease would only do so if they alsodrank tap water; they did not develop Alzheimers disease on the same diet if theydrank only distilled water. The researchers determined that it was trace amounts ofcopper in the tap water that made the difference. 21) 0.12 ppm (parts per million) of copper added to distilled water triggerAlzheimers plaques. The Environmental Protection Agency (EPA) allows over 10times (1.3 ppm) that much copper in human drinking water. [Very Important] 22) The inorganic copper in drinking water contributes directly to the free copperpool in the blood. 23) Free copper levels are elevated in the blood of AD patients compared to age-matchedcontrols; the higher the free copper, the lower the cognitive ability. 24) The amino acid cysteine binds to copper and removes it from the brain.The ApoE protein has three alleles:ApoE2, has 2 copper binding cysteines and is protective against Alzheimers.ApoE3, has 1 copper binding cysteine.ApoE4, has no copper binding cysteines and increases the risk of Alzheimers. 25) Homocysteine interacts with copper to produce increased oxidant stress,oxidizing low-density lipoprotein (LDL) that contributes to the development of AD. 26) Parkinsons disease, Huntingtons disease, amyotrophic lateral sclerosis (LouGehrigs disease), and prion diseases such as Creutzfeldt-Jakob disease, are alldiseases of neurodegeneration, all have misfolded proteins that form inclusionbodies that are a copper dependent mechanism. 27) People in the highest quintile of copper intake with a high fat diet, lostcognition at a rate of 19 years in a six year period. In other words, they lostcognition at over three times the rate expected! These people were in the highestquintile of copper intake primarily because they took copper in their vitamin/mineral supplement pill. These data are frightening! Almost allvitamin/mineral supplementscontain copper. Copper deficiency is extremely rare; therefore, almost no one needscopper supplements, yet tens of millions of people are taking copper supplementsand in my view are running the risk of poisoning themselves with copper. 28) The interaction of copper and homocysteine generates oxidant stress andoxidize LDL, which is a component of the atherosclerotic plaque. 29) Abnormal copper metabolism increases diabetes and is involved in theetiology of diabetic neuropathy. 30) Increased copper has also been linked to Parkinsons disease, autism,Tourettes syndrome, age related macular degeneration and cancer. 31) Zinc is an anti-inflammatory and antioxidant agent. Supplemental zinc of 15mg or more significantly protects against advanced prostate cancer. 32) Increased iron levels play a major role in producing atherosclerosis. 33) Menstruating women have reduced iron load as a result of blood loss andhave strong protection against atherosclerosis compared to men. Post-menopausalwomen lose this protective effect. Blood donors have less atherosclerotic disease. 34) The interaction of iron and cholesterol promote oxidative damage, causingboth atherosclerosis and neurodegeneration. 35) The constant production of toxic free radicals, particularly reactive oxygenspecies, slowly produces mitochondrial damage. The slow loss of mitochondria andtheir energy production is associated with aging and may be the major cause ofaging; greater levels of free iron and free copper accelerate the production of toxicradicals. 36) The toxicity of free copper and free iron extends to the very basic processof aging itself. 37) To Minimize Copper and Iron Toxicity: * Avoid taking supplements containing copper and iron. Most multivitamin/multimineral pills have copper, and this copper is potentiallydangerous. Scan the label on your supplement bottle, and stop taking it if itcontains copper. Copper deficiency is extremely rare, and almost no one needscopper. Those with the highest quintile of copper intake lose cognition at over 3times the normal rate, and got there for the most part by taking copper supplements. * Men rarely need iron supplements unless they have chronic blood loss. Butsome menstruating girls and women, particularly if menstrual flow is heavy, maybecome iron deficient. * Both copper and iron are much more bioavailable from meat than fromvegetable foods. That means that these metals are much more easily absorbedfrom meat sources. Liver and shellfish are particularly high in copper content. Redmeat is particularly high in bioavailable iron. But copper and iron are readilybioavailable from all meat foods. * Those who averaged 2/3 of an ounce of red meat/day had 30% lessmortality than those who averaged 5 ounces of red meat/day. Processed meats alsoincreased mortality. Mortality was 20% higher in those who averaged 2 ounces ofprocessed meat per day (an average of one hot dog/day), compared to those whoate almost 15% that much. It is possible that the reduction in mortality seen in thestudy is at least partially due to the reduction of copper and iron intake. * Avoid drinking water with elevated copper content, one has to measure thecopper in their drinking water. 38) 80% of homes in the U.S. have copper water pipes. Whether toxic amountsof copper leaches from the copper pipes depends mostly on the acidity of the water.The more acidic the water, the more copper leaches from the pipes. If the plumbingsystem is used as the electrical ground for the house (which is legal in many places, but should not be), more copper can leach from the pipes. 39) There are various laboratories where copper in the water can be measured. Itis best to measure both the first draw water in the morning and water after allowingthe tap to run for five minutes. Because stagnant water may contain more copper,it is good to know if this is the case so that it can be avoided if necessary. 40) We recommend the drinking water contain no more than about 0.01 ppm.(The EPA allows 1.3 ppm!) 41) If the drinking water contains too much copper, a reverse osmosis devicecan be installed on the tap used for drinking and cooking water. Alternatively,distilled water, which contains no copper, can be purchased for drinking andcooking. 42) Bottled waters, which many people now drink, are an unknown for coppercontent, and at this point cannot be used to avoid copper in drinking water. 43) The intervention step required to further lower free copper is to take oral zincsupplements; zinc will lower free copper levels. It does so by strongly limitingcopper absorption. The minimal dose of zinc to do this is about 40 mg twice aday. The zinc dose must be separated from food and beverages other than waterby at least 1 h before and 2 h after. The best is zinc acetate and zinc gluconate. 44) Lowering free copper levels is beneficial in fibrotic, inflammatory, andautoimmune disease processes. 45) The intervention for lowering free iron is blood donation or removal of asignificant amount of blood on a regular basis. Men and menopausal women coulddonate 500 mL of blood every 2 months (or have that much removed if they arenot suitable blood donors), until their percent transferrin saturation is in the15-25 range. 46) If one is going to intervene by taking zinc to lower free copper and or donateblood to lower free iron, it is important to monitor free copper and/or free ironlevels. 47) It appears very likely that copper and iron toxicity are occurring in a largeproportion of our population. 48) Both copper and iron toxicity are likely contributing to Alzheimers disease. 49) There is a major epidemic of AD in the industrialized world, and this diseasedid not exist until 100 years ago. It still is rare in India and Africa. 50) The process of loss of cognition during aging may be greatly speeded up byincreased free copper exposure, and the very process of aging itself, if due to alifetime of oxidant stress, is likely increased by higher levels of free copper and freeiron since the toxicities of these two metals is through the production of oxidantstress. 51) Lower the risks of free copper and iron by throwing away supplementscontaining these metals, by lowering meat intake, and by avoiding drinking waterwith elevated levels of copper. 52) Rigorous methods of lowering free copper and free iron exposure includetaking zinc to lower copper and using blood donation to lower iron.

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Orofacial Injuries Due to Trauma Following Motor Vehicle Collisions: Temporomandibular Disorders

Journal of the Canadian Dental Association December 15, 2010; Vol. 76; a172 Joel B. Epstein, DMD; Gary D. Klasser, DMD; Dean A. Kolbinson, DMD; Sujay A.Mehta, DMD KEY POINTS FROM THIS ARTICLE: 1) Temporomandibular disorders are a collective term that embraces a numberof clinical problems that involve the masticatory muscles, the TMJ[temporomandibular joint], and associated structures. 2) Most literature strongly supports the association between motor vehiclecollisions, temporomandibular disorders, facial pain and headache. 3) Whiplash trauma may cause temporomandibular disorders via twomechanisms: A)) Direct orofacial trauma B)) Indirect or [inertial] injury; [this occurs without direct contact to the jaw] 4) TMDs have been clearly documented following an MVC involving directorofacial trauma and in a subset of WAD patients where no direct orofacial traumais recognized. 5) Temporomandibular disorders may not be identified at the time of firstassessment of the whiplash-injured patient, but may develop weeks or more afterthe collision. [This delay in the development of temporomandibularsymptoms following motor vehicle collisions is quite important]. 6) TMDs may not necessarily be diagnosed during a first assessment, but maymanifest weeks or months after an MVC. 7) Temporomandibular disorders in whiplash-injured patients occur predominantly in women. 8) Temporomandibular disorders in whiplash-injured patients may be associatedwith regional or widespread pain. [Important: some whiplash-injured patients,especially those with temporomandibular disorders, develop widespreadpain syndrome]. 9) Temporomandibular disorders following motor vehicle collisions may respondpoorly to independent therapy and may be best managed using multidisciplinaryapproaches. 10) Approximately 33% of those in a motor vehicle collision develop whiplash-associated disorders. 11) Whiplash-injured patients who also develop TMD have a measurably worserecovery prognosis than those who do not also develop TMD. 12) Temporomandibular disorders associated with whiplash injuries include: * Jaw pain or dysfunction * Headache * Dizziness * Hearing disturbances * Neck pain and dysfunction * Reduced or painful jaw movement 13) Temporomandibular disorders often include TMJ sounds (clicking, crepitus)and catching or locking with opening or closing. 14) There is a risk of delayed onset of temporomandibular disorders following amotor vehicle collision. Of whiplash-injured patients, approximately 4 times morepatients have temporomandibular disorders at 1 year compared to the firstevaluation following the collision. 15) The potential delay in onset of TMDs following an MVC raises concerns aboutdiagnosis, prognosis, management and medico-legal issues. 16) Regional and widespread physical symptoms as well as psychologicaldisturbances are common in motor vehicle collision patients. 17) Air bag deployment injuries include: * TMJ injury * Maxillofacial fractures * Burns * Eyes injuries * Ear injuries * Cranial VII paresis * Neuropathic facial pain (Cranial V injury) * Basal skull fractures * Transection of the internal carotid artery * Atlanto-occipital dislocation * Spinal cord injuries 18) Approximately 15 – 40% of patients with acute whiplash associated disordersdevelop chronic symptoms. 19) TMDs in WAD are more common in females and can be associated withregional or widespread pain that may reflect central, systemic and psychologicaleffects.

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Motor Vehicle Accidents: The Most Common Cause of Traumatic Vertebrobasilar Ischemia

Canadian Journal of Neurological Sciences November 2003; Volume 30, No. 4; pp. 320-325 Michel Beaudry, J. David Spence From the Department of Clinical Neurological Sciences, University of WesternOntario, London, Canada. FROM ABSTRACT: Background: Recent media exposure of strokes from chiropractic manipulation have focusedattention on traumatic vertebrobasilar ischemia. However, chiropracticmanipulation, while the easiest cause to recognize, is probably not the mostcommon cause of this condition. Methods: We reviewed all consecutive cases of traumatic vertebrobasilar ischemia referred toa single neurovascular practice over 20 years. Results: There were 80 patients whose vertebrobasilar ischemia was attributed to necktrauma. Five were diagnosed as due to chiropractic manipulation, but thecommonest attributed cause was motor vehicle accidents (MVAs), which accountedfor 70 cases; one was a sports injury, and five were industrial accidents.In some cases neck pain from an MVA led to chiropractic manipulation, so the causemay have been compounded.In most vehicular cases the diagnosis had been missed, even denied, by theneurologists and neurosurgeons initially involved.The longest delay between the injury and the onset of delayed symptoms was fiveyears. Conclusions: Traumatic vertebrobasilar ischemia is most often due to MVAs; the diagnosis isoften missed, in part because of the delay between injury and onset of symptomsand, in part, we hypothesize, because of reluctance of doctors to be involved inmedicolegal cases. SIGNIFICANT POINTS FROM THIS ARTICLE: 1) Recent neck trauma may cause extracranial carotid and vertebral dissection. 2) Genetic abnormalities of collagen, elastin and other supporting elements inthe blood vessel wall may predispose the patient to carotid and vertebral arterydissection with even minor trauma such as sneezing or Valsalva maneuvers. 3) When symptoms are delayed after trauma, the connection between traumaand vascular events are difficult to recognize. The longest described (in theliterature) delay between trauma and onset of vertebrobasilar symptoms is twomonths. 4) Delays of 7 weeks after injury and 37 days after a motor vehicle accident(MVA) have been reported for the vertebrobasilar distribution, and delay of manyyears has been described in the carotid artery distribution." 5) When vertigo is experienced following vertebral artery dissection, it is oftendifficult for the attending physician to think of cerebral vascular problem as opposedto a vestibular problem, particularly in a young patient. 6) Migraine can produce visual symptoms indistinguishable from those due totransient ischemia in the posterior cerebral artery territory, and migraine can alsobe triggered by trauma. 7) In this study, all of these were attributed to vertebrobasilar ischemia:70% showed loss of consciousness64% had some difficulty with short-term memory or episodes of transient global amnesia2.5% had sleep disturbances (narcolepsy, sleep-walking) 8) Several patients had a motor vehicle accident, and then had further vascularinjury by neck manipulation. [This suggests that absent the initial MVA, thechiropractic manipulation would not have been associated with the ischemia]. 9) The severity of the initial trauma was substantial for some patients, but wasmild for many. 10) We have been struck by how often neurologists and neurosurgeons miss orrefuse to recognize the diagnosis, and suspect that it is often dismissed because ofan aversion to medicolegal cases and legal practitioners. The unwillingness todiagnose this condition of traumatic vertebrobasilar ischemia in the setting of MVAsis in marked contrast to the willingness, even eagerness, to diagnose it in thesetting of chiropractic manipulation, often by the same physicians who are unwillingto recognize it in MVA cases. 11) The cases of sleep disturbance noted (sleepwalking and narcolepsy) wereattributed to ischemia of the brainstem reticular formation. 12) The diagnosis is often missed, in many cases because the neck injury is aminor event such as a chiropractic manipulation. 13) Another reason for failure to consider the association between the neck injuryand the subsequent vertebrobasilar ischemia is the delay in time, up to nearly fiveyears. 14) With extension of the neck, especially when adding a rotational component,the vertebral artery is stretched and/or compressed in the foramen transversariumof the atlas or before it pierces the atlanto-occipital ligament. 15) Trivial neck turning while looking backward while backing up a car or duringswimming, yoga or archery, or a Valsalsva maneuver during birthing, may initiatevertebral artery dissection. 16) Neck extension during surgical intubation has been shown to injure thevertebral artery. 17) Vertebrobasilar ischemia may occur after extension of the neck over the edgeof a hairdressers sink while having hair shampooed. 18) 72% of people have an asymmetric circulation, usually having one hypoplasticvertebral artery. 19) Rotation and extension of the neck obstructs flow in a dominant vertebralartery, which may predispose the patient to problems when the collateral circulationis poor. 20) Rarely, osteophytes may compress a vertebral artery causing recurrenttransient ischemic attack events. 21) Instability of the alar or other atlanto-axial ligaments may cause episodes ofvertebrobasilar ischemia provoked by turning of the head. 22) Arterial spasm may lead to ischemic symptoms, and pre-traumatic spasmincreases the incidence of dissection. 23) Migraine may cause ischemia symptoms similar or identical to arterydissection. 24) Artery dissections are best shown with either MRA (magnetic resonanceangiogram) or ultrasound. 25) Traumatic vertebrobasilar ischemia may present up to four and nearly fiveyears after the neck injury. It is, therefore, probably much more common than iscurrently suspected. 26) Though chiropractic manipulation is perhaps the best-known cause, it isimportant to recognize that MVAs are a much more common cause, which is oftenmissed. COMMENTS FROM DAN MURPHY * All chiropractors should be aware that motor vehicle collisions are a prime(and possibly the primary), trigger of vertebral artery dissections. * The symptoms of post-traumatic vertebral artery dissections can be delayedfor hours, days, weeks, months and even years. * The primary mechanism for vertebral artery dissection is a combination ofcervical extension and rotation. * There appears to be an increased risk of dissections in patients withmigraines.

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