Chiropractic Treatment for Spinal Subluxations

The chiropractic treatment uses a holistic healthcare and wellness approach. By holistic, we mean the overall health of a person which depends on a number of factors including the living environment and our habits.

Chiropractic is based on the principle that in a large number of patients, the main cause of disease and pains is primarily due to the misalignment of the vertebrae located in the spinal column. This misalignment accompanied by abnormal motion of the vertebrae is referred to as ‘subluxation’. The term was taken from Latin words and means ‘slightly’ (sub) and ‘to dislocate’ (luxare).

Thus, the main focus of chiropractic technique is to remove the subluxations in the spinal column so that the pressure and the irritation on the nerves are relieved. As a result, the mobility of various joints is restored and the body gradually returns to normalcy.

Roseville, a vibrant and dynamic city of America located just near St. Paul and Minneapolis is home to a number of chiropractic centers. This city in Ramsey County has a total area of nearly 13.8 sq miles while the population density is nearly 2,543.9 people per square mile (as per 2000 census).  

Any Chiropractor Roseville MN has is fully trained to diagnose and treat the spinal/vertebral subluxations in your body. In simple terms, chiropractors work towards curing a slight dislocation of the bones in the spine of the human body. The term subluxation is inclusive. It takes into its scope various functional, structural and neurological changes occurring in the body due to the misalignment of the bone.

Subluxations of the spine or the ‘Vertebral Subluxation Complex’ (VSC) is a complex phenomenon affecting the normal functioning of the body. Various chiropractors in Roseville MN very well understand the dangers to the human body caused by the vertebral subluxation. No wonder, they stress on proper functioning of the spine to keep the body healthy.  Chiropractors are the only health care professionals having training in the diagnosis and correction of the VSC with the help of chiropractic treatment.

Do you know how quickly the technique of chiropractic works in curing and correcting the vertebral subluxation? Chiropractors in Roseville MN apply a quick thrust to the vertebrae for correction of its position and its movement. The vertebral adjustments are a big relief for the suffering patients except for some minor discomfort experienced by few patients especially if they are feeling tensed at the time of the chiropractic treatment.

SKULL FRACTURES CAUSES,COMPLICATIONS AND TREATMENT

The first concern in a skull fracture is possible damage to the brain rather than the fracture itself; therefore, the injury is considered a neurosurgical condition. Signs and symptoms reflect the severity and extent of the head injury. Skull fractures may be simple (closed) or compound (open) and may displace bone fragments. They’re also described as linear, comminuted, or depressed.

A linear,or hairline, fracture doesn’t displace structures and seldom requires treatment. A comminuted fracture splinters or crushes the bone into several fragments. Adepressed fracture pushes the bone toward the brain; it’s considered serious only if it compresses or lacerates underlying structures. A child’s thin, elastic skull allowsa depression without a fracture.Skull fractures also are classified according to location, such as cranial vault or basilar. A basilar fracture occurs at the base of the skull and involves the cribriformplate and the frontal sinuses. Because of the danger of cranial nerve complications, dural tears, and meningitis, basilar fractures usually are far more serious thanvault fractures.

Causes

Like concussions and cerebral contusions or lacerations, skull fractures invariably result from a traumatic blow to the head. Motor vehicle crashes, bad falls, andsevere beatings (especially in children and elderly people) top the list of causes.

Complications

Skull fractures can lead to infection, intracerebral hemorrhage and hematoma, brain abscess, and increased intracranial pressure (ICP) from edema. A linear fractureacross a suture line in an infant increases the possibility of epidural hematoma.Recovery from the injury can be complicated by the residual effects of the injury, such as seizure disorders, hydrocephalus, and organic brain syndrome.

Assessment findings

The patient’s history—obtained from the patient, family members, eyewitnesses, or emergency personnel—reveals a traumatic injury to the skull. The patient mayhave lost consciousness and developed other neurologic changes. If conscious, he may complain of a persistent, localized headache. Assessment may reveal decreased pulse and respiratory rates as well as labored respirations. On inspection, a conscious patient with a linear fracture and aconcussion may appear dazed. If he has another type of skull fracture, he may appear anxious and, depending on his neurologic status, may have normal responsesor appear agitated and irritable.Because scalp wounds commonly accompany skull fractures, inspection of the scalp may reveal abrasions, contusions, lacerations, or avulsions. If the scalp waslacerated or torn away, you may note profuse bleeding. The patient, however, may be in shock from other injuries or from medullary failure if the head injury is severe.You’ll also note swelling and ecchymosis in the area of the injury, a sign that a fracture has occurred.Other findings on inspection may include bleeding in the nose, pharynx, or ears; under the conjunctivae; under the periorbital skin (raccoon’s eyes); and behind theeardrum. You may also observe Battle’s sign (postauricular ecchymosis).Inspection of the ears and nose may reveal cerebrospinal fluid (CSF) and brain tissue leakage. The halo sign—a blood-tinged spot surrounded by a lighter ringcaused by leakage of CSF—may also appear on the patient’s pillowcase or bed linens.Palpation of the head may reveal palpable fractures, areas of swelling and, possibly, hematoma. A vault fracture commonly causes soft-tissue swelling near the site,which makes the fracture difficult to detect without X-rays.During your neurologic assessment, you may observe altered level of consciousness (LOC) along with other classic signs and symptoms of brain injury. Theseinclude agitation and irritability, abnormal deep tendon reflexes, altered pupillary and motor responses, hemiparesis, dizziness, seizures, and projectile vomiting. Lossof consciousness may last for hours, days, weeks, or indefinitely. Keep in mind that linear fractures associated only with concussion don’t produce loss ofconsciousness.Your neurologic assessment also may reveal vision loss in a patient with a sphenoidal fracture, and unilateral hearing loss or facial paralysis in a patient with atemporal fracture.

Diagnostic tests

A computed tomography (CT) scan may locate the fracture. (Cranial vault fractures aren’t visible or palpable.) Reagent strips reveal the presence or absence of CSFin nasal or ear drainage. Cerebral angiography locates vascular disruptions from internal pressure or injury. Magnetic resonance imaging, a CT scan, and a radioisotope scan discloseintracranial hemorrhage from ruptured blood vessels.

Treatment

Although a simple linear skull fracture can tear an underlying blood vessel or cause a CSF leak, most linear fractures require only supportive treatment. Such treatment includes mild analgesics (acetaminophen) as well as cleaning, debriding, and suturing the wound after injection of a local anesthetic. Be sure to note thepatient’s coagulation time if he’s taking anticoagulants at home. An increased International Normalized Ratio (INR) may necessitate treatment with fresh frozenplasma.If the patient hasn’t lost consciousness, he should be observed in the emergency department for at least 4 hours. After this period, a patient with stable vital signs canbe discharged. He should receive an instruction sheet for 24 to 48 hours of observation at home. More severe vault fractures, especially depressed fractures, usually require a craniotomy to elevate or remove fragments that have been driven into the brain and toextract foreign bodies and necrotic tissue. This reduces the risk of infection and further brain damage.

Cranioplasty follows the use of tantalum mesh or acrylic platesto replace the removed skull section. The patient commonly requires antibiotics, tetanus prophylaxis, and (in profound hemorrhage) blood transfusions. The patientmay require sedating medication, such as Ativan (lorazepam) to help reduce seizures, or an anticonvulsant may be required.For status epilepticus, the patient may receive an anticonvulsant, usually 10 to 15 mg/kg of I.V. phenytoin sodium administered at a rate of not more than 50mg/minute. A maintenance dose should then be ordered to prevent the recurrence of seizures.A basilar fracture calls for immediate prophylactic antibiotics to prevent meningitis from CSF leaks. The patient also needs close observation for secondary hematomas and hemorrhages; surgery may be necessary. Also, a patient with either a basilar or a vault fracture requires I.V. or I.M. dexamethasone to reducecerebral edema and minimize brain tissue damage.

Explanation Of The 4 Types Of Cerebral Palsy

Cerebral palsy affects approximately 800,000 children and adults in the United States.

CP is a chronic condition that affects body movements and muscle coordination. It is caused by damage to one or more specific areas of the brain, usually occurring during fetal development, or during infancy.

Cerebral palsy was considered a distinct condition in 1861. Dr. William John Little, published the first paper describing the neurological problems of children with spastic diplegia (also known as cerebral palsy). This is still sometimes called Little’s Disease.

Two children out of every thousand born in America have cerebral palsy. At least 5000 infants and toddlers and about 1,400 preschoolers are diagnosed with cerebral palsy each year.

There are 4 types of CP. This next set of tips will discuss these types, and their differences.

Spastic

Spastic cerebral palsy is characterized by stiff or permanently contracted muscles. 70-80 percent of people with CP have this type.

Athetoid

Athetoid cerebral palsy is characterized by uncontrolled, slow movements. 10-20 percent of people have this type of CP.

Ataxic

Ataxic CP is characterized by a lack of coordination and balance. This type of CP accounts for 10 percent of all cases of CP. Ataxic CP (or any kind of CP) is not degenerative.

Mixed

Mixed CP is when one person has two or more types of CP. The most common type of mixed CP is Athetoid/Spastic-diplegic or Athetoid/Spastic-hemiplegic.

Diagnosing children with CP at a young age is important. Here are some of the symptoms to look for in a newborn child:

– Lack of alertness
– abnormal cry
– Trembling arms and legs
– Problems sucking and swallowing
– Weak muscle tone
– Favoring one side of the body
– Abnormal reflexes
– Seizures

Abnormal muscle tone is very common in people with cerebral palsy. Even as newborns, their muscles may change from low tone to high tone. They can also go from floppy to very stiff.

If you’re concerned that your child may have CP, look for developmental delays such as:

-Rolling over
-Sitting up
-Crawling
-Talking
-Walking

Understand that it takes time to diagnose cerebral palsy, especially specifying the type of CP. If it’s for a child, his doctor will want to take time to do tests and examine him several times before making the diagnosis.

Age and Race

According to research, the following people have a higher chance of having a child with CP:

-A mother or a father under 20 years old
-A mother over 40 years old
-African-American ethnicity

Blood Type

There is a rare circumstance where the mom’s and child’s blood is incompatible. This is called Rh or ABO blood type incompatibility, and it puts you at risk of having a child with cerebral-palsy.

Micro-Organisms

In rare cases, your infant’s central nervous system can be attacked by micro-organisms. This will put him at high risk of developing cerebral palsy.

Doctor Error

Unfortunately, there are some cases of cerebral-palsy where the doctor was at fault. There are now a ton of lawyers that are dedicated to bringing these doctors to justice. If you think a doctor was at fault for your child’s CP, you can talk to an attorney.

Here are some of the other risk factors associated with CP:

-Bleeding in the brain
-Infection
-Lack of oxygen

Solution for Bell's Palsy and Facial Paralysis

Named after Sir Charles Bell, a 19th century Scottish surgeon, Bell’s palsy refers to facial paralysis caused by an irritation to the cranial nerve VII (number 7).  It is this nerve that controls most of your facial muscles which include even those that control your smile, blink and wrinkle the forehead.

What causes Bell’s palsy?

The cause of Bell’s palsy or facial paralysis is not clearly known till date. It is not known till date as to why irritation occurs in the cranial nerve VII. There are many who believe that facial paralysis is caused due to extreme exposure to cold conditions though there is no evidence to suggest this. There are others who believe that facial paralysis happens due to an inflammation of the cranial nerve VII which may have been caused by a viral infection.

Recognizing the symptoms

One of the first symptoms of Bell’s palsy or facial paralysis is when you begin drooling after brushing your teeth or when you drink water. Likewise, when you notice that your mouth is not properly aligned and is slightly twisted. Some of the other symptoms include inability to whistle or blow your cheeks or have excess tearing in one eye.

Treating Facial paralysis

One of the major causes of concern in the treatment of Bell’s palsy refers to eye care. This is because the patient is unable to close one eye which can cause corneal abrasions or any other kinds of injuries. Irrespective of what kind of treatment you are taking, it is suggested that you always have a dark glass on and use eye drops to prevent the eyes from drying up.  Further, it has been observed that oral steroids like prednisone are very effective in reducing the course of this disease and at the same time improve the recovery rate quite effectively. In very severe cases surgery helps in relieving the pressure on the nerve, thereby preventing permanent nerve damage.

Causes, Symptoms and Treatment for Inguinal Hernia

An inguinal hernia, or a groin hernia, is a protrusion (lump) of the small intestine or fatty tissue into the groin through a weakness or tear in the abdominal wall.

When part of an organ protrudes through an abnormal opening or in an abnormal way, this is called a hernia. A groin (inguinal) hernia occurs when part of the intestine bulges through a weak spot in the abdominal wall at the inguinal canal. The inguinal canal is a passageway through the abdominal wall near the groin. Inguinal hernias are up to 10 times more common in men than in women. About one in four men develop a hernia at some point in life.

There are two types of inguinal hernias:

Indirect inguinal hernia – This type of hernia occurs when the internal opening of the inguinal canal, which usually closes around the time of birth, remains open. This allows a portion of the intestine to slip through the inguinal canal. Indirect inguinal hernias often are diagnosed within the first year of life, but may not show up until adulthood. This condition affects between 1% and 5% of normal newborns and up to 10% of premature infants.

Direct inguinal hernia This occurs when a portion of the intestine protrudes through a weakness in the abdominal muscles along the wall of the inguinal canal. These are common in adults, but rarely occur in children.

Causes

Usually, there is no obvious cause of a hernia, although they are sometimes associated with heavy lifting.

Hernias can be seen in infants and children. This can happen when the lining around the abdominal organs does not close properly before birth. About 5 out of 100 children have inguinal hernias (more boys than girls). Some may not have symptoms until adulthood.

In men, an inguinal hernia will commonly develop in the groin, specifically in a region called the inguinal canal. This is where the spermatic cord and blood vessels to the testicles pass out of the abdominal cavity and into the scrotum. A weakness in the abdominal tissues at this point can allow a loop of bowel to pass out of the abdomen by following the path of the spermatic cord (indirect inguinal hernia) or between the opening into the inguinal canal and the pubic bone (direct inguinal hernia).

Symptoms

A person can sometimes feel a hernia as it develops. There may be tenderness or a slight burning sensation in the area where the hernia is developing. Sometimes a person can push the hernia back into place. In other cases, the hernia may just disappear by itself. In still other cases, the hernia cannot be pushed back into place easily.

Exams and Tests

A doctor can confirm the presence of a hernia during a physical exam. The mass may increase in size when coughing, bending, lifting, or straining. The hernia (bulge) may not be obvious in infants and children, except when the child is crying or coughing.

Treatment of Hernia

Treatment tips for Hernia are as follows:

For small, non-strangulated and non-incarcerated hernias, various supports and trusses may offer temporary, symptomatic relief.
There are two surgically procedures available for the treatment of inguinal hernias – open surgery or laparoscopy.
Open surgery is the most common type of treatment, accounting for 95 percent of inguinal repairs.

Sciatica Nerve Pain During Pregnancy-What You Can Do

Back pain is one of humanity’s most frequent complaints. In the U. S. About nine out of ten adults experience back pain at some point in their life, and five out of ten working adults have back pain every year. One potential source of back pain is skeletal muscle of the back. The spine is a complex interconnecting network of nerves, joints, muscles, tendons and ligaments, and all are capable of producing pain. Sciatica Nerve Pain During Pregnancy.

There are diverse clinical trials sponsored both by industry and the National Institutes of Health. In addition, spinal cord stimulation, where an electrical device is used to interrupt the pain signals being sent to the brain and has been studied for various underlying causes of back pain. There are no clinical tests that can be objectively verified.

Injections, such as epidural steroid injections and facet joint injections, may be effective when the cause of the pain is accurately localized to particular sites. Body Awareness Therapy such as the Feldenkrais Method has been studied in relation to Fibromyalgia and chronic pain and studies have indicated positive effects. . Back pain is regularly cited by national governments as having a major impact on productivity, through loss of workers on sick leave.

Back pain in individuals with a history of cancer (especially cancers known to spread to the spine like breast, lung and prostate cancer) should be evaluated to rule out metastatic disease of the spine. Back pain in individuals with medical conditions that put them at high risk for a spinal fracture, such as osteoporosis or multiple myeloma, also warrants prompt medical attention. Most back pain syndromes are due to inflammation, especially in the acute phase, which typically lasts for two weeks to three months.

General factors aggravating the back pain of pregnancy include standing, sitting, forward bending, lifting, and walking. Biomechanical factors of pregnancy that are shown to be associated with low back pain of pregnancy include abdominal sagittal and transverse diameter and the depth of lumbar lordosis. Back pain in pregnancy may be severe enough to cause significant pain and disability and pre-dispose patients to back pain in a following pregnancy.

The avoidance of high impact, weight-bearing activities and especially those that asymmetrically load the involved structures such as: extensive twisting with lifting, single-leg stance postures, stair climbing, and repetitive motions at or near the end-ranges of back or hip motion can easen the pain. Some national governments, notably Australia and the United Kingdom, have launched campaigns of public health awareness to advise combat the problem, for example the Health and Safety Executive’s Transformed Backs campaign. Visit also Failed back syndrome Low back pain Posterior Rami Syndrome Tension myositis syndrome Upper back pain Pregnancy related pelvic girdle pain Spinal stenosis Scoliosis References T. Patel, A. A. Ogle. Ultrasound has been shown not to be beneficial and has fallen out of favor. Clinical Trials. Sciatica Nerve Pain During Pregnancy is noted.

Reporting 64405 for Third Occipital Nerve Blocks? Think Again

Also, learn what CPT codes you must choose for blocking lesser occipital nerve

Physiatrists who administer third occipital nerve blocks must not automatically assume that 64405* (Injection, anesthetic agent; greater occipital nerve) is the most suitable CPT code. Most medical coding consultants recommend reporting 64470-22 in place of 64405 to more precisely define these types of blocks.

Occipital Nerves Differ

When a physician specifies on the charge ticket that he or she carried out an occipital nerve block, your instinct might tell you to assign CPT code 64405. However 64405 is not at all times the most correct code. Physiatrists administer injections to the third occipital nerve to help diagnose and treat dissimilar forms of headache and neck pain.

The ‘third occipital nerve’ is not anatomically identical with the greater occipital nerve. Physicians use both injections to diagnose and/or treat some forms of headache. However coding hinge more on the anatomical structure and the procedure location than the patient’s symptoms or diagnosis.

The body contains three diverse sets of occipital nerves: the greater occipital, the lesser occipital, and the third occipital nerve (also referred to as the “least occipital nerve”). By reviewing the physiatrist’s documentation, you can identify which nerve he or she blocked and assign the correct code for the procedure.

The greater occipital nerve originates from the dorsal ramus of the C2 spinal nerve. It has movement (motor) functions that innervate in the posterior neck muscles and sensory functions for the skin of the posterior surface of the scalp. Physicians often inject the greater occipital nerve to diagnose and treat occipital neuralgia (723.8, other syndromes affecting cervical region). You should report CPT code 64405 for this procedure.

The lesser occipital nerve also originates from the C2 spinal nerve, but its source is the ventral ramus. It has only sensory functions that innervate the skin behind the ear. The CPT code for blocking lesser occipital nerve is 64450* (Injection, anesthetic agent; other peripheral nerve or branch).

The third occipital nerve (TON) is certainly the superficial medial branch of the C3 spinal nerve’s dorsal ramus. The TON, like the greater occipital nerve, has both motor and sensory functions. It innervates some of the neck muscles and the C2-3 facet joint. Pain stemming from this joint can be referred to the occiput and even as far as the frontal region and orbit.

Pinpoint the Correct Code

A physiatrist may inject all three occipital nerves to help diagnose or treat chronic headaches. The practitioner selects the suitable occipital nerve injection based on the patient’s medical history along with the condition (for example, a history of neck trauma such as whiplash [847.0, Sprains and strains of other and unspecified parts of back; neck], tender neck points [723.1, Other disorders of cervical region; cervicalgia], description and quality of headache, etc.).

 

For Read full article : http://www.supercoder.com/coding-newsletters/my-physical-medicine-rehab-coding-alert/reporting-64405-for-third-occipital-nerve-blocks-think-again-article

Ischias: Sciatic Nerve or Sciatica

On average, symptoms will only happen on one side of the body.
This is a very common form of back pain, however the term sciatica actually applies to a set of symptoms rather than the diagnosis of what is irritating the nerve.

Causes
The cause of sciatica is generally the compression of the lumbar spine nerve root L4 or L5, or compression of the sciatic nerve itself, which is far less common.

In the case of disc herniation, sciatica can occur due to the pressing down on one of the sciatic nerve roots. Spinal Stenosis can also be a cause of sciatica because of the narrowing of the spinal canal, where the spinal cord runs, and compression of the spinal cord. This can be caused by herniated discs, bone spurs and vertebral dislocation, which then pinches the spinal cord that travels to the sciatic nerve and irritating it with friction.

Piriformis Syndrome is another cause of sciatic symptoms. However, this only occurs in 15 percent of the population who have the sciatic nerve running through the piriformis rather than beneath it. In case of trauma, the muscle shortens and is compresses the sciatic nerve under the muscle. Unhealthy posture and excess time in chairs or sleeping in the fetal position, along with no stretching or exercise can cause sciatic irritation and pain as well. Another common cause of pain in the sciatic nerve is pregnancy, usually occurring late when the uterus is pressing on the sciatic nerve, as well as due to muscle tension caused by the weight of the fetus.

Treatment
One of the best ways to treat sciatic nerve problems is through the use of a chiropractor or osteopath. By seeing professionals who specialize in
repairing the spine, a patient will benefit greatly due to chiropractic
treatments that are meant to fix problems of the spine. While bed rest and staying off the back is one of the best things you can do, in terms of problems with the sciatic nerve, it is better to be safe than sorry, so those who suffer with pain should see a chiropractor.

Conclusion
One of the most painful spinal injuries can be to the sciatic nerve. The nerve can be compressed, or pinched, resulting in a great deal of pain to anyone who suffers from it. The pain can affect the lower half of one side of a person’s body, making them immobile.

However, by visiting a professional chiropractor for chiropractic treatment, an individual can eliminate the pain in the sciatic nerve and begin walking proud and tall again. There is no reason to suffer with pain that an individual can eliminate with a short visit to a chiropractor or osteopath.

As well, by visiting a chiropractor, an individual can ensure they do not do further damage to their spine due to a lack of treatment. Ont i
ryggen Ischias

Sudden infant death syndrome

Overview

Typically the infant is found dead after having been put to bed, and exhibits no signs of having suffered.

SIDS is a diagnosis of exclusion. It should only be applied to an infant whose death is sudden and unexpected and remains unexplained after the performance of an adequate postmortem investigation including

an autopsy;

investigation of the scene and circumstances of the death;

exploration of the medical history of the infant and family.

SIDS was responsible for 0.543 deaths per 1,000 live births in the U.S. in 2005. It is responsible for far fewer deaths than congenital disorders and disorders related to short gestation, though it is the leading cause of death in healthy infants after one month of age.

SIDS deaths in the U.S. decreased from 4,895 in 1992 to 2,247 in 2004. But, during a similar time period, 1989 to 2004, SIDS being listed as the cause of death for sudden infant death (SID) decreased from 80% to 55%. According to Dr. John Kattwinkel, chairman of the Center for Disease Control (CDC) Special Task Force on SIDS “A lot of us are concerned that the rate (of SIDS) isn’t decreasing significantly, but that a lot of it is just code shifting.

Nomenclature

Australia and New Zealand are shifting to the term Sudden Unexplained Death in Infancy (SUDI) for professional, scientific and coronial clarity.

The term SUDI is now often used instead of Sudden Infant Death Syndrome (SIDS) because some coroners prefer to use the term ndetermined for a death previously considered to be SIDS. This change is causing diagnostic shift in the mortality data.

SIDS Back To Sleep campaign: history and theory

In 1985 Davies reported that in Hong Kong, where Chinese custom called for supine infant sleep position (face up), SIDS was a rare problem. In 1987 the Netherlands started a campaign advising parents to place their newborn infants to sleep on their backs (supine position) instead of their stomachs (prone position). This was followed by infant supine sleep position campaigns in the United Kingdom, New Zealand, and Australia in 1991, the U.S. and Sweden in 1992, and Canada in 1993.

This advice was based on the epidemiology of SIDS and physiological evidence which shows that infants who sleep on their back have lower arousal thresholds and less slow-wave sleep (SWS) compared to infants who sleep on their stomachs. In human infants sleep develops rapidly during early development. This development includes an increase in non-rapid eye movement sleep (NREM sleep) which is also called quiet sleep (QS) during the first 12 months of life in association with a decrease in rapid eye movement sleep (REM sleep) which is also known as active sleep (AS). In addition, slow wave sleep (SWS) which consists of stage 3 and stage 4 NREM sleep appears at 2 months of age and it is theorized that some infants have a brain-stem defect which increases their risk of being unable to arouse from SWS (also called deep sleep) and therefore have an increased risk of SIDS due to their decreased ability to arouse from SWS.

Studies have shown that preterm infants, full-term infants, and older infants have greater time periods of quiet sleep and also decreased time awake when they are positioned to sleep on their stomachs. In both human infants and rats, arousal thresholds have been shown to be at higher levels in the electroencephalography (EEG) during slow-wave sleep.

In 1992, a SIDS risk reduction strategy based upon lowering arousal thresholds during SWS was implemented by the American Academy of Pediatrics (AAP) which began recommending that healthy infants be positioned to sleep on their back (supine position) or side (lateral position), instead of their stomach (prone position), when being placed down for sleep. In 1994, a number of organizations in the United States combined to further communicate these non-prone sleep position recommendations and this became formally known as the ack To Sleep campaign. In 1996, the AAP further refined its sleep position recommendation by stating that infants should only be placed to sleep in the supine position and not in the prone or lateral positions.

In 1992, the first National Infant Sleep Position (NISP) Household Survey was conducted to determine the usual position in which U.S. mothers placed their babies to sleep: lateral (side), prone (stomach), supine (back), other, or no usual position. According to the 1992 NISP survey, 13.0% of U.S. infants were positioned in the supine position for sleep. According to the 2006 NISP survey 75.7% of infants were positioned in the supine position to sleep.

Since 1998 there have been several studies published which report that infants placed to sleep in the supine position lag in motor skills, social skills, and cognitive ability development when compared to infants who sleep in the prone position. In a 1998 article entitled ffects of Sleep Position on Infant Motor Development. by Davis, Moon, Sachs, and Ottolini, the authors state e found that sleep position significantly impacts early motor development. The prone (stomach) sleeping infants in this study slept an average of 225.2 hours (8.3%) more in their first 6 months of life than the supine (back) sleeping infants.

In the 1998 article entitled oes the Supine Sleeping Position Have Any Adverse Effects on the Child? II. Development in the First 18 Months31] by Dewey, Fleming, Golding, and the ALSPAC Study Team the objective of the study was o assess whether the recommendations that infants sleep supine could have adverse consequences on their motor and mental development. They used the Denver Developmental Screening Test (DDST) and studied infants at 6 and 18 months. According to the study, at 6 months of age, the infants who were placed to sleep in the prone position had statistically significant higher social skills scores, gross motor scores, and total development scores than those infants who were put to sleep in the supine position. In the 2005 article entitled nfluence of supine sleep positioning on early motor milestone acquisition29] by Majnemer and Barr they used the Alberta Infant Motor Scale Scores (AIMS Scores) to analyze the impact of infant sleep position. They reported that ypically developing infants who were sleep-positioned in supine had delayed motor development by age 6 months, and this was significantly associated with limited exposure to awake prone positioning. But, the authors also note that awake prone (stomach) positioning is associated with prone (stomach) sleeping. No studies have been conducted which compare supine sleeping infants who have regular awake prone positioning (tummy time) to prone sleeping infants who have regular awake prone positioning (tummy time).

Placing infants on their stomachs while they are awake (tummy time) has been recommended to offset the motor skills delays associated with the back sleep position but positioning the infant on their stomach while awake will not impact the amount of slow wave sleep since tummy time only occurs when an infant is awake.

Undiagnosed conditions

Some conditions that may be undiagnosed and thus could be alternative diagnoses to SIDS include:

medium-chain acyl-coenzyme A dehydrogenase deficiency (MCAD deficiency), ;

infant botulism;

long QT syndrome (accounting for less than 2% of cases);

infections with the bacterium Helicobacter pylori;

shaken baby syndrome and other forms of child abuse.

For example an infant with MCAD deficiency could have died by ‘classical SIDS’ if found swaddled and prone with head covered in an overheated room where parents were smoking. Genes of susceptibility to MCAD and Long QT syndrome do not protect an infant from dying of classical SIDS. Therefore presence of a susceptibility gene, such as for MCAD, means the infant may have died either from SIDS or from MCAD deficiency. It is impossible for the pathologist to distinguish between them.

Risk factors

Very little is certain about the possible causes of SIDS, and there is no proven method for prevention. Although studies have identified risk factors for SIDS, such as putting infants to bed on their stomachs, there has been little understanding of the syndrome’s biological cause or causes. The frequency of SIDS appears to be a strong function of the infant’s sex, age and ethnicity, and the education and socio-economic-status of the infant’s parents.

According to a study published in October 2007 in the Journal of the American Medical Association, babies who die of SIDS have abnormalities in the brain stem (the medulla oblongata), which helps control functions like breathing, blood pressure and arousal, and abnormalities in serotonin signaling. According to the National Institutes of Health, which funded the study, this finding is the strongest evidence to date that structural differences in a specific part of the brain may contribute to the risk of SIDS.

In a British study released May 29, 2008 researchers discovered that the common bacterial infections Staphylococcus aureus (staph) and Escherichia coli (E. coli) appear to be the cause of some cases of Sudden Infant Death Syndrome. Both bacteria were present at greater than usual concentrations in infants who died from SIDS. SIDS cases peak between eight and ten weeks after birth, which is also the time frame in which the antibodies that were passed along from mother to child are starting to disappear and babies have not yet made their own antibodies.

Listed below are several factors associated with increased probability of the syndrome based on information available prior to this recent study.

Prenatal risks

maternal nicotine use (tobacco or nicotine patch)

inadequate prenatal care

inadequate prenatal nutrition

use of heroin, cocaine and other drugs

subsequent births less than one year apart

alcohol use

infant being overweight

mother being overweight

Teen pregnancy (if the baby has a teen mother, it has a greater risk)

infant’s sex (60% of SIDS cases occur in males)

Post-natal risks

mold (can cause bleeding lungs plus a variety of other uncommon conditions leading to a misdiagnoses and death). It is often misdiagnosed as a virus, flu, and/or asthma-like conditions.

low birth weight (in the U.S. from 1995-1998 the rate for 1000-1499 g was 2.89/1000 and for 3500-3999 g it was 0.51/1000)

exposure to tobacco smoke

prone sleep position (lying on the stomach, see sleep positioning below)

not breastfeeding

elevated or reduced room temperature

excess bedding, clothing, soft sleep surface and stuffed animals

Co-sleeping with parents or other siblings increases the risk for accidental smothering

infant’s age (incidence rises from zero at birth, is highest from two to four months, and declines towards zero at one year)

premature birth (increases risk of SIDS death by about 4 times. In 1995-1998 the U.S.SIDS rate for 3739 weeks of gestation was 0.73/1000; The SIDS rate for 2831 weeks of gestation was 2.39/1000)

anemia

Risk reduction for SIDS

Though SIDS cannot be prevented, parents of infants are encouraged to take several precautions in order to reduce the likelihood of SIDS.

Environment

Sleep positioning

Sleeping on the back has been recommended by (among others) the American Academy of Pediatrics (starting in 1992) to avoid SIDS, with the catchphrases “Back To Bed” and “Back to Sleep.” The incidence of SIDS has fallen sharply in a number of countries in which the back to bed recommendation has been widely adopted, such as the US and New Zealand. However, the absolute incidence of SIDS prior to the Back to Sleep Campaign was already dropping in the US, from 1.511 per 1000 in 1979 to 1.301 per 1000 in 1991.

Among the theories supporting the Back to Sleep recommendation is the idea that small infants with little or no control of their heads may, while face down, inhale their exhaled breath (high in carbon dioxide) or smother themselves on their beddinghe brain-stem anomaly research (above) suggests that babies with that particular genetic makeup do not react “normally” by moving away from the pooled CO2, and thus smother. Another theory[citation needed] is that babies sleep more soundly when placed on their stomachs, and are unable to rouse themselves when they have an incidence of sleep apnea, which is thought to be common in infants.

Arguments against infant back-sleeping include concerns that an infant could choke on fluids it brings up. Hospital neonatal-intensive-care-unit (NICU) staff commonly place preterm newborns on their stomach, although they advise parents to place their infants on their backs after going home from the hospital.

Other concerns raised about the Back to Sleep Campaign have included the possible increased risk of positional facial and head deformities (see positional plagiocephaly), possible interference with development of good sleep habits (which in turn may have other bad effects), and possible interference with motor skills development (as infants delay attempts to lift their heads, crawl, etc.).

Breastfeeding

A 2003 study published in Pediatrics, which investigated racial disparities in infant mortality in Chicago, found that previously or currently breastfeeding infants in the study had 1/5 the rate of SIDS compared with non-breastfed infants, but that “it became nonsignificant in the multivariate model that included the other environmental factors”. These results are consistent with most published reports and suggest that other factors associated with breastfeeding, rather than breastfeeding itself, are protective.” However, a more recent study shows that breast feeding reduces the risk of SIDS by approximately 50% at all infant ages.

Co-sleeping

In nearly all incidences, the higher the rate of co-sleeping, the lower the rate of SIDS and vice versa. http://thebabybond.com/Cosleeping&SIDSFactSheet.html The data has suggested that almost all SIDS deaths in adult beds would be occurring when other prevention methods, such as placing infants on their backs, are not used. Co-sleeping studied in the West has been present mostly in poorer families where other risk factors are present. While co-sleeping in other cultures such as in China is more prevalent and is done in combination with practices such as sleeping children on their back, correlating with a significantly lower rate of SIDS than the West.Further studies have suggested that factors associated with safe co-sleeping such as enhanced infant arousals are responsible for a positive contribution to SIDS prevention.

A 2005 policy statement by the American Academy of Pediatrics on sleep environment and the risk of SIDS deemed co-sleeping and bed sharing unsafe. One article reports that co-sleeping infants have a greater risk of airway covering than when the same infant sleeps alone in a cot.

Secondhand smoke reduction

According to the U.S. Surgeon General Report, secondhand smoke is connected to SIDS. Infants who die from SIDS tend to have higher concentrations of nicotine and cotinine (a biological marker for secondhand smoke exposure) in their lungs than those who die from other causes. Infants exposed to secondhand smoke after birth are also at a greater risk of SIDS. Parents who smoke can significantly reduce their children’s risk of SIDS by either quitting or smoking only outside and leaving their house completely smoke-free.

The maternal pregnancy smoking rate decreased by 38% between 1990 and 2002.

Sleeping area

Bedding

Product safety experts advise against using pillows, sleep positioners, bumper pads, stuffed animals, or fluffy bedding in the crib and recommend instead dressing the child warmly and keeping the crib “naked.”

Blankets should not be placed over an infant’s head. It has been recommended that infants should be covered only up to their chest with their arms exposed. This reduces the chance of the infant shifting the blanket over his or her head.[citation needed]

Sleep sacks

In colder environments where bedding is required to maintain a baby’s body temperature, the use of a “baby sleep bag” or “sleep sack” is becoming more popular. This is a soft bag with holes for the baby’s arms and head. A zipper allows the bag to be closed around the baby. A study published in the European Journal of Pediatrics in August 1998 has shown the protective effects of a sleep sack as reducing the incidence of turning from back to front during sleep, reinforcing putting a baby to sleep on its back for placement into the sleep sack and preventing bedding from coming up over the face which leads to increased temperature and carbon dioxide rebreathing. They conclude in their study “The use of a sleeping-sack should be particularly promoted for infants with a low birth weight.” The American Academy of Pediatrics also recommends them as a type of bedding that warms the baby without covering its head.The use of swaddling clothes, a traditional form of infant restraint which leaves only the head uncovered, is controversial.
Pacifiers

According to a 2005 meta-analysis, most studies favor pacifier use. According to the American Academy of Pediatrics, pacifier use seems to reduce the risk of SIDS, although the mechanism by which this happens is unclear. SIDS experts and policy makers haven’t recommended the use of pacifiers to reduce the risk of SIDS because of several problems associated with pacifier use, like increased risk of otitis, gastrointestinal infections and oral colonization with Candida species. A 2005 study indicated that use of a pacifier is associated with up to a 90% reduction in the risk of SIDS depending on the ambient factors, and it reduced the effect of other risk factors. It has been speculated that the raised surface of the pacifier holds the infant’s face away from the mattress, reducing the risk of suffocation. If a postmortem investigation does not occur or is insufficient, a suffocated baby may be misdiagnosed with SIDS.

Air circulation with fan use

According to a study of nearly 500 babies published the October 2008 Archives of Pediatrics & Adolescent Medicine, using a fan to circulate air correlates with a lower risk of sudden infant death syndrome. Researchers took into account other risk factors and found that fan use was associated with a 72% lower risk of SIDS. Only 3% of the babies who died had a fan on in the room during their last sleep, the mothers reported. That compared to 12% of the babies who lived. Using a fan reduced risk most for babies in poor sleeping environments. Author De-Kun li said that “the baby’s sleeping environment really matters” and that “this seems to suggest that by improving room ventilation we can further reduce risk.”

New link. A special, small fan for gentle, direct ventilation of the infants sleeping area, crib or bassinet.

Bumper pads

Bumper pads may be a contributing factor in SIDS deaths and should be removed. Health Canada, the Canadian government’s health department, issued an advisory recommending against the use of bumper pads, stating:

The presence of bumper pads in a crib may also be a contributing factor for Sudden Infant Death Syndrome (SIDS). These products may reduce the flow of oxygen rich air to the infant in the crib. Furthermore, proposed theories indicate that the rebreathing of carbon dioxide plays a role in the occurrence of SIDS.

Speculated associations

A number of theoretical causes have been proposed as a trigger for SIDS, but many of them are unproven or have not been thoroughly studied and peer-reviewed. As of June 2009 there were 113 such articles found in Medical Hypotheses as cited in PubMed.

Anemia

Anemia is not a documented SIDS risk factor per se because at the moment of death the blood hemoglobin begins to degrade. This degradation can be slow or rapid and it shows up as livor mortis, the mottled and reddened coloring that can develop within 30 minutes of death. Because SIDS usually occurs during sleep and is unnoticed, the time interval between moment of death and autopsy is unknown so no correction can be made to the hemoglobin value measured postmortem to estimate the antemortem value immediately before death. However anemia is a risk factor for apparent-life-threatening-events (ALTE) as described by Poets et al. (1992) referred to above where anemia is listed as a postnatal risk factor.

Oxygen Deprivation

A 2003 Study showed that a common cause of death of infants is because parents/caretakers leave the child “face-down” on the bed. Making it so the child cannot breathe. A child at the age of 1 month to 6 months…does not have the muscle development to move their head…therefore it is benefical if they lay the child head up. In addition, an autopsy would not show necrotic tissue in any part of the body, due to oxygen deprivation. Due to the fact that the infant typically has more hemoglobin then the standard adult. Making their blood capable of “holding on” to more oxygen.

Mattress bugs

A 2004 study hypothesized that bugs feeding on baby vomit and dust could be fatal for small children, creating ‘supertoxins’ which spur the baby’s body into overreacting, leading to anaphylactic shock.

Brain disorder

A recently published research article showed evidence that cells in the brainstem fail to develop receptors for serotonin in the womb. This abnormality can continue postpartum until the end of the first year. This would account for there being few to no SIDS deaths after the first year of infancy and the reason the risk is more for premature infants. Males have fewer serotonin receptors than females, perhaps contributing to the increased incidence of SIDS in the demographic.

In addition, a study was done in 2006. Showed that a possible cause of SIDS is because parents leave there infants in a position known as “Trendelenburg position.” This position can cause the brain stem to fall…and in a result, the brain becomes “crushed.” The proper poistion for an infant is either High Fowlers or Sims.

Vitamin C

In the 1970s, high doses of vitamin C were touted as a preventive measure for SIDS, although the claim was controversial even then. Subsequent study failed to support a preventive role for vitamin C in SIDS. To the contrary, a 2009 study found that high levels of vitamin C were strongly associated with SIDS, possibly through a pro-oxidant interaction with iron.

Toxic gases

In 1989, a controversial piece of research by UK Scientist Barry Richardson claimed that all cot deaths were the result of toxic nerve gases being produced through the action of fungus in mattresses on compounds of phosphorus, arsenic and antimony. These chemicals are frequently used to make mattresses fire-retardant.

A major plank in this explanation is the widely-observed phenomenon that the risk of cot death rises from one sibling to the next. Richardson claims that the cause is that parents are more likely to buy new bedding for their first child, and to re-use that bedding for later children. The more frequently used the bedding is, the more chance there will be that fungus has become resident in the material; thus, a higher chance of cot death. A paper by Peter Fleming and Peter Blair references evidence from other studies that both supports and refutes the increasing occurrence of SIDS with mattress sharing and suggests that this is still inconclusive.

Dr. Jim Sprott recommends new parents either buy bedding free of the toxic compounds or to wrap the mattresses in a barrier film to prevent the escape of the gases. Sprott claims that no case of cot death has ever been traced back to a properly manufactured or wrapped mattress.

However, a final report of The Expert Group to Investigate Cot Death Theories: Toxic Gas Hypothesis, published in May 1998, concluded that “there was no evidence to substantiate the toxic gas hypothesis that antimony- and phosphorus-containing compounds used as fire retardants in PVC and other cot mattress materials are a cause of SIDS. Neither was there any evidence to believe that these chemicals could pose any other health risk to infants.” The report also states that “in normal cot-like conditions it is not possible to generate toxic gas from antimony in mattresses” and “babies have also been found to die on wrapped mattresses.”

Contrary to media publicity, the 1998 UK Limerick Report did not disprove the toxic gas theorys a highly qualified environmental scientist has stated in the New Zealand Medical Journal. In fact, the Limerick Committee’s experiments proved the fungal generation of toxic gases (forms of stibine and arsine) from cot mattress materials.

According to Dr. Sprott, as of 2006, the New Zealand government has not reported any SIDS deaths when babies have slept on mattresses wrapped according to his method. While the Limerick report claims that babies have been found to die on wrapped mattresses, Dr. Sprott argues that a chemical analysis of the bedding should be performed. He additionally claims that this part of the report was flawed:

In February 2000 Dr Peter Fleming (a co-author of the Limerick Report and principal author of the UK CESDI Report) conceded that the claim that three babies in the United Kingdom had died of cot death on polythene-covered mattresses could not be substantiated.

Central Respiratory Pattern Deficiency

There is ongoing research in the pediatric/neonatal community that has begun to associate apnea-like breathing cessations in animal models with unusual neural architecture or signal transduction in central pattern generator circuits including the pre-Btzinger complex. It is possible that irregularities in neurotransmitter release (such as GABA, adenosine, and NMDA) or deficiencies in their associated receptors (including both GABAA, GABAB subtypes and NMDA-glutamate receptors) are linked to incomplete prenatal development as is evident in pre-term infants.[citation needed]

Cervical spinal injury from birth trauma

During birth, if the infant’s head is traumatically turned side to side, upper cervical spinal injury can result. Difficulty breathing is a classic sign of upper spinal cord and brain-stem injury. When infants with undiagnosed upper cervical spinal cord injury are continually placed on their stomach for sleep, they are forced to turn their head to the side to breathe. This is hypothesised to aggravate and prolong the spinal cord injury sustained during birth, preventing proper healing and ultimately leading to fatal breathing difficulty.[citation needed]

Sex

There is a consistent 50% male excess in SIDS per 1000 live births of each sex. Given a 5% male excess birth rate (105 male to 100 female live births) there appear to be 3.15 male SIDS per 2 female SIDS for a male fraction of 0.61. This value of 61% in the U.S. is an average of 57% black male SIDS, 62.2% white male SIDS and 59.4% for all other races combined. Note that when multiracial parentage is involved, infant “race” is arbitrarily assigned to one category or the other; most often it is chosen by the mother. The X-linkage hypothesis for SIDS and the male excess in infant mortality have shown that the 50% male excess could be related to a dominant X-linked allele that occurs with a frequency of that is protective of transient cerebral anoxia. An unprotected XY male would occur with a frequency of and an unprotected XX female would occur with a frequency of 49. The ratio of to 49 is 1.5 to 1 which matches the observed male 50% excess rate of SIDS.

Although many authors have found autosomal and mitochondrial genetic risk factors for SIDS they cannot explain the male excess because such gene loci have the same frequencies for males and females. Supporting evidence for an X-linkage is found by examination of other causes of infant respiratory death, such as suffocation by inhalation of food and other foreign objects. Although food is prepared identically for male and female infants, there is a similar 50% male excess of death from such causes indicating that males are more susceptible to the cerebral anoxia created by such incidents in exactly the same proportion as found in SIDS.

The study which indicated that there was a relationship between fewer serotonin binding sites and SIDS noted that the boys “had significantly fewer serotonin binding sites than girls.” However, such neurological prematurity decreases with age, but the male fraction of approximately 0.61 persists each month throughout the first year of life. Furthermore, this cannot explain the identical male fraction of 0.61 in other respiratory mortality causes such as respiratory distress syndrome or suffocation from inhalation of food or foreign objects cited above, that also exists for all ages 1 to 14 years in the U.S. from 1979 to 2005.

Child abuse

Several instances of infanticide have been uncovered where the diagnosis was originally SIDS. This has led some researchers to estimate that 5% to 20% of SIDS deaths are infanticides. In 1997 The New York Times, covering a book called The Death of Innocents: A True Story of Murder, Medicine and High-Stakes Science, wrote:

The misdiagnosis of infanticide as SIDS “happens all over,” Ms. Talan, a medical reporter at Newsday, said. “A lot of doctors and police don’t know how to handle it. They don’t take it as seriously as they should.” As a result of the book’s revelations, people are starting to scrutinize possible cases of this “perfect crime,” which involves no physical evidence and no witnesses.

A former pediatrician Roy Meadow from United Kingdom believes that many cases diagnosed as SIDS are really the result of child abuse on the part of a parent displaying Munchausen syndrome by proxy (a condition which he was first to describe, in 1977). During the 1990s and early 2000s, a number of mothers of multiple apparent SIDS victims were convicted of murder, to varying degrees on the basis of Meadow’s opinion. In 2003 a number of high-profile acquittals brought Meadow’s theories into disrepute. Several hundred murder convictions were reviewed, leading to several high-profile cases being re-opened and convictions overturned.

The Royal Statistical Society issued a media release refuting the expert testimony in one UK case in which the conviction was subsequently overturned.

Nitrogen dioxide

A 2005 study by researchers at the University of California, San Diego found that “SIDS may be related to high levels of acute outdoor NO2 exposure during the last day of life.” While nitrogen dioxide (NO2) exposure may be one of many possible risk factors, it is not considered causal, and the report cautioned that further studies were needed to replicate the result.

Vaccination

According to the US Centers for Disease Control and Prevention, several studies have failed to provide sufficient evidence of a causal link between vaccinations and SIDS. They state:

From 2 to 4 months old, babies begin their primary course of vaccinations. This is also the peak age for sudden infant death syndrome (SIDS). The timing of these two events has led some people to believe they might be related. However, studies have concluded that vaccines are not a risk factor for SIDS.

Inner ear damage

Records of hearing tests (oto-acoustic emissions, OAEs) administered to certain infants show that those who later died of SIDS had differences in the pattern of these tests compared with normal babies. To be specific the OAE signal to noise ratio was reduced in the right ear in the SIDS babies. (Rubens DD et al Early Human Development 84, 225-9 (2008)) . It should be noted this was a small study (n=31 cases and 31 controls), had serious limitations (several significant factors were not controlled), and has been criticised from various perspectives. The authors’ suggestion for the cause of SIDS is that the deaths are caused by disturbances in respiratory control (from other than suffocation). The vestibular apparatus of the inner ear has been shown to play an important role in respiratory control during sleep. It is speculated that this inner ear damage could be linked to SIDS. It is speculated that the damage occurs during delivery, particularly when prolonged contractions create greater blood pressure in the placenta. The right ear is directly in the “line of fire” for blood entering the fetus from the placenta, and thus could be most susceptible to damage. If the findings are relevant, it may be possible to take corrective measures. Researchers are beginning animal studies to explore the connection.

Side effects of SIDS risk reduction recommendations

Dr. Rafael Pelayo from Stanford University and a number of other pediatric sleep researchers in the U.S. have stated that they believe that the American Academy of Pediatrics’ recommendations regarding cosleeping and pacifier use may have unintended consequences. They have stated that the SIDS prevention strategy of the American Academy of Pediatrics which keeps infants at a low arousal threshold and reduces the time in quiet sleep may be unhealthy for children. They state that slow wave sleep is the most restorative form of sleep and limiting this sleep in the first 12 months of life may have unintended consequences to both the sleep and the infant.

According to a 1998 study by British researchers that compared back sleeping infants to stomach sleeping infants there were developmental differences at 6 months of age between the two groups. At 6 months of age the stomach sleeping infants had higher gross motor scores, social skills scores, and total development skills scores than the back sleeping infants. The differences were apparent at the 5% statistical significant level. But, at 18 months the differences were no longer apparent. The researchers deemed the lower development scores of back sleeping infants at 6 months of age to be transient and stated that they do not believe the back sleeping recommendations should be changed. Other scientists have stated that the conclusion that the negative effects of back sleep at 18 months of age is transient is based upon very little evidence and that no long-term randomized trials have been completed.

Other side effects of the back sleeping position include increased rates of shoulder retraction, positional plagiocephaly, and positional torticollis. Some scientists dispute that plagiocephaly is a negative side effect. Dr. Peter Fleming, who is co-author of the study that deemed delays at 6 months of age to be transient, has stated that he does not think plagiocephaly is a negative side effect of back sleep. In an interview with the Guardian Dr. Fleming stated “I do not think it is a medical problemt is more of a cosmetic one. Mothers may feel it is a syndrome and a problem when it really is nonsense.” A research study on children with plagiocephaly found that 26% had mild to severe psychomotor delay. This study also showed that 10% of infants with plagiocephaly had mild to severe mental development delay.

Because of the delays caused by back sleep some medical professionals have suggested that the “normal” ages at which children had previously attained developmental milestones should be pushed back. This would enable medical professionals to consider “normal” children who previously were considered developmentally delayed.

Additional studies have reported that the following negative conditions are associated with the back sleep position: increase in sleep apnea, decrease in sleep duration, strabismus, social skills delays, deformational plagiocephaly, and temporomandibular jaw difficulties. In addition, the following are symptoms that are associated with sleep apnea: growth abnormalities, failure to thrive syndrome in infants, neurocognitive abnormalities, daytime sleepiness, emotional problems, decrease in memory, decrease in learning, and a delay in nonverbal skills. The conditions associated with deformational plagiocephaly include visual impairments, cerebral dysfunction, delays in psychomotor development and decreases in mental functioning. The conditions associated with gross motor milestone delays include speech and language disorders. In addition, it has been hypothesized that delays in motor skills can have a negative impact on the development of social skills. In addition, other studies have reported that the prone position prevents subluxation of the hips, increases psychomotor development, prevents scoliosis, lessens the risk of gastroesophageal reflux, decreases infant screaming periods, causes less fatigue in infants, and increases the relief of infant colic. In addition, prior to the ack to Sleep campaign many babies self-treated their own torticollis by turning their heads from one side to the other while sleeping in the prone position. Supine sleeping infants cannot self-treat their own torticollis.

Further reading

Joan Hodgman; Toke Hoppenbrouwers (2004). SIDS. Calabasas, Calif: Monte Nido Press. ISBN 0-9742663-0-2. 

Notes

^ Health Canada SIDS Healthy Babies SIDS Page.

^ a b c d e http://wonder.cdc.gov

^ a b c Bowman L, Hargrove T. Exposing Sudden Infant Death In America. Scripps Howard News Service. http://dailycamera.com/news/2007/oct/08/saving-babies-exposing-sudden-infant-death-in/

^ NZ Ministry of Health

^ Davies DP (December 1985). “Cot death in Hong Kong: a rare problem?”. Lancet 2 (8468): 13469. PMID 2866397. http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(85)92637-6. 

^ a b c Hgberg U, Bergstrm E (April 2000). “Suffocated prone: the iatrogenic tragedy of SIDS”. Am J Public Health 90 (4): 52731. doi:10.2105/AJPH.90.4.527. PMID 10754964. PMC 1446204. http://www.ajph.org/cgi/pmidlookup?view=long&pmid=10754964. 

^ Rusen ID, Liu S, Sauve R, Joseph KS, Kramer MS (2004). “Sudden infant death syndrome in Canada: trends in rates and risk factors, 19851998”. Chronic Dis Can 25 (1): 16. PMID 15298482. 

^ a b Kattwinkel J, Hauck F.R., Moon R.Y., Malloy M and Willinger M Infant Death Syndrome: In Reply, Bed Sharing With Unimpaired Parents Is Not an Important Risk for SuddenPediatrics 2006;117;994-996

^ Louis J, Cannard C, Bastuji H, Challamel MJ (May 1997). “Sleep ontogenesis revisited: a longitudinal 24-hour home polygraphic study on 15 normal infants during the first two years of life”. Sleep 20 (5): 32333. PMID 9381053. 

^ Navelet Y, Benoit O, Bouard G (July 1982). “Nocturnal sleep organization during the first months of life”. Electroencephalogr Clin Neurophysiol 54 (1): 718. doi:10.1016/0013-4694(82)90233-4. PMID 6177520. 

^ Roffwarg HP, Muzio JN, Dement WC (April 1966). “Ontogenetic Development of the Human Sleep-Dream Cycle”. Science (journal) 152 (3722): 604619. doi:10.1126/science.152.3722.604. PMID 17779492. 

^ Anders TF, Keener M (1985). “Developmental course of nighttime sleep-wake patterns in full-term and premature infants during the first year of life. I”. Sleep 8 (3): 17392. PMID 4048734. 

^ Bes F, Schulz H, Navelet Y, Salzarulo P (February 1991). “The distribution of slow-wave sleep across the night: a comparison for infants, children, and adults”. Sleep 14 (1): 512. PMID 1811320. 

^ Coons S, Guilleminault C (June 1982). “Development of sleep-wake patterns and non-rapid eye movement sleep stages during the first six months of life in normal infants”. Pediatrics 69 (6): 7938. PMID 7079046. 

^ Fagioli I, Salzarulo P (April 1982). “Sleep states development in the first year of life assessed through 24-h recordings”. Early Hum. Dev. 6 (2): 21528. doi:10.1016/0378-3782(82)90109-8. PMID 7094858. 

^ a b Myers MM, Fifer WP, Schaeffer L, et al. (June 1998). “Effects of sleeping position and time after feeding on the organization of sleep/wake states in prematurely born infants”. Sleep 21 (4): 3439. PMID 9646378. 

^ a b Sahni R, Saluja D, Schulze KF, et al. (September 2002). “Quality of diet, body position, and time after feeding influence behavioral states in low birth weight infants”. Pediatr Res. 52 (3): 399404. PMID 12193675. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0031-3998&volume=52&issue=3&spage=399. 

^ a b Brackbill Y, Douthitt TC, West H (January 1973). “Psychophysiologic effects in the neonate of prone versus supine placement”. J Pediatr. 82 (1): 824. doi:10.1016/S0022-3476(73)80017-4. PMID 4681872. 

^ a b Amemiya F, Vos JE, Prechtl HF (May 1991). “Effects of prone and supine position on heart rate, respiratory rate and motor activity in fullterm newborn infants”. Brain Dev. 13 (3): 14854. PMID 1928606. 

^ a b Kahn A, Rebuffat E, Sottiaux M, Dufour D, Cadranel S, Reiterer F (February 1991). “Arousals induced by proximal esophageal reflux in infants”. Sleep 14 (1): 3942. PMID 1811318. 

^ Ashton R (April 1973). “The influence of state and prandial condition upon the reactivity of the newborn to auditory stimulation”. J Exp Child Psychol 15 (2): 31527. doi:10.1016/0022-0965(73)90152-5. PMID 4735894. http://linkinghub.elsevier.com/retrieve/pii/0022-0965(73)90152-5. 

^ Rechtschaffen A, Hauri P, Zeitlin M (June 1966). “Auditory awakening thresholds in REM and NREM sleep stages”. Percept Mot Skills 22 (3): 92742. PMID 5963124. 

^ Neckelmann D, Ursin R (August 1993). “Sleep stages and EEG power spectrum in relation to acoustical stimulus arousal threshold in the rat”. Sleep 16 (5): 46777. PMID 8378687. 

^ “American Academy of Pediatrics AAP Task Force on Infant Positioning and SIDS: Positioning and SIDS”. Pediatrics 89 (6 Pt 1): 11206. June 1992. PMID 1503575. 

^ U.S. Department of Human Services. “BACK TO SLEEP” CAMPAIGN SEEKS To Reduce Inicidence of SIDS In African American Populations PressRelease. http://www.hhs.gov/news/press/1999pres/991026.html Tuesday, October 26, 1999

^ “Positioning and sudden infant death syndrome (SIDS): update. American Academy of Pediatrics Task Force on Infant Positioning and SIDS”. Pediatrics 98 (6 Pt 1): 12168. December 1996. PMID 8951285. 

^ a b National Infant Sleep Position Household Survey. Summary Data 1992. http://dccwww.bumc.bu.edu/ChimeNisp/NISP_Data.asp updated: 09/04/07

^ National Infant Sleep Position Household Survey. Summary Data 2006. http://dccwww.bumc.bu.edu/ChimeNisp/NISP_Data.asp updated: 09/04/07

^ a b c Majnemer A, Barr RG (June 2005). “Influence of supine sleep positioning on early motor milestone acquisition”. Dev Med Child Neurol 47 (6): 3706; discussion 364. doi:10.1017/S0012162205000733. PMID 15934485. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0012-1622&date=2005&volume=47&issue=6&spage=370. 

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^ Yang Z, Lantz PE, Ibdah JA (December 2007). “Post-mortem analysis for two prevalent beta-oxidation mutations in sudden infant death”. Pediatr Int 49 (6): 8837. doi:10.1111/j.1442-200X.2007.02478.x. PMID 18045290. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1328-8067&date=2007&volume=49&issue=6&spage=883. 

^ Nevas M, Lindstrm M, Virtanen A, et al. (January 2005). “Infant botulism acquired from household dust presenting as sudden infant death syndrome”. J. Clin. Microbiol. 43 (1): 5113. doi:10.1128/JCM.43.1.511-513.2005. PMID 15635031. 

^ Millat G, Kugener B, Chevalier P, et al. (May 2009). “Contribution of long-QT syndrome genetic variants in sudden infant death syndrome”. Pediatr Cardiol 30 (4): 5029. doi:10.1007/s00246-009-9417-210.1007/s00246-009-9417-2. PMID 19322600. 

^ Stray-Pedersen A, Vege A, Rognum TO (October 2008). “Helicobacter pylori antigen in stool is associated with SIDS and sudden infant deaths due to infectious disease”. Pediatr. Res. 64 (4): 40510. doi:10.1203/PDR.0b013e31818095f7. PMID 18535491. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0031-3998&volume=64&issue=4&spage=405. 

^ Bajanowski T, Vennemann M, Bohnert M, Rauch E, Brinkmann B, Mitchell EA (July 2005). “Unnatural causes of sudden unexpected deaths initially thought to be sudden infant death syndrome”. Int. J. Legal Med. 119 (4): 2136. doi:10.1007/s00414-005-0538-810.1007/s00414-005-0538-8. PMID 15830244. 

^ Du Chesne A, Bajanowski T, Brinkmann B (1997). “[Homicides without clues in children]” (in German). Arch Kriminol 199 (1-2): 216. PMID 9157833. 

^ a b Paterson DS, Trachtenberg FL, Thompson EG, et al. (November 2006). “Multiple serotonergic brainstem abnormalities in sudden infant death syndrome”. JAMA 296 (17): 212432. doi:10.1001/jama.296.17.2124. PMID 17077377. 

^ Gardner, Amanda (2008-05-30). “Bacterial Infection May Boost SIDS Risk”. Washington Post. http://www.washingtonpost.com/wp-dyn/content/article/2008/05/29/AR2008052903472.html#. Retrieved 2009-10-15. 

^ Buttigieg J, Brown S, Zhang M, Lowe M, Holloway AC, Nurse CA (May 2008). “Chronic nicotine in utero selectively suppresses hypoxic sensitivity in neonatal rat adrenal chromaffin cells”. Faseb J. 22 (5): 131726. doi:10.1096/fj.07-9194com. PMID 18070822. 

^ Kraus JF, Greenland S, Bulterys M (March 1989). “Risk factors for sudden infant death syndrome in the US Collaborative Perinatal Project”. Int J Epidemiol 18 (1): 11320. PMID 2722353. http://ije.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=2722353. 

^ Henriksen T (May 1999). “Foetal nutrition, foetal growth restriction and health later in life”. Acta Paediatr Suppl 88 (429): 48. PMID 10419226. 

^ Kandall SR, Gaines J, Habel L, Davidson G, Jessop D (July 1993). “Relationship of maternal substance abuse to subsequent sudden infant death syndrome in offspring”. J. Pediatr. 123 (1): 1206. PMID 8320605. 

^ Spiers PS, Wang L (July 1976). “Short pregnancy interval, low birthweight, and the sudden infant death syndrome”. Am. J. Epidemiol. 104 (1): 1521. PMID 937342. http://aje.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=937342. 

^ Zhou FC, Fang Y, Goodlett C (August 2008). “Peptidergic agonists of activity-dependent neurotrophic factor protect against prenatal alcohol-induced neural tube defects and serotonin neuron loss”. Alcohol. Clin. Exp. Res. 32 (8): 136171. doi:10.1111/j.1530-0277.2008.00722.x. PMID 18565153. 

^ Byard RW (September 2007). “Marked obesity in infancy and relationship to sudden infant death”. J Paediatr Child Health 43 (9): 64950. doi:10.1111/j.1440-1754.2007.01179.x. PMID 17688652. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1034-4810&date=2007&volume=43&issue=9&spage=649. 

^ Carroll-Pankhurst C, Mortimer EA (March 2001). “Sudden infant death syndrome, bedsharing, parental weight, and age at death”. Pediatrics 107 (3): 5306. PMID 11230594. http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=11230594. 

^ American Sudden Infant Death Syndrome Institute

^ Mage DT, Donner M (February 1997). “A genetic basis for the sudden infant death syndrome sex ratio”. Med. Hypotheses 48 (2): 13742. PMID 9076695. http://linkinghub.elsevier.com/retrieve/pii/S0306-9877(97)90280-2. 

^ Weinberg ED (June 2000). “Association of primary Pneumocystis carinii infection and sudden infant death syndrome”. Clin. Infect. Dis. 30 (6): 991. doi:10.1086/313796. PMID 10880335. http://www.journals.uchicago.edu/cgi-bin/resolve?CID000127. 

^ Hunt CE (November 2007). “Small for gestational age infants and sudden infant death syndrome: a confluence of complex conditions”. Arch. Dis. Child. Fetal Neonatal Ed. 92 (6): F4289. doi:10.1136/adc.2006.112243. PMID 17951549. http://fn.bmj.com/cgi/pmidlookup?view=long&pmid=17951549. 

^ Office of the Surgeon General of the United States Report on Involuntary Exposure to Tobacco Smoke (PDF)

^ Willinger M, Hoffman HJ, Hartford RB (May 1994). “Infant sleep position and risk for sudden infant death syndrome: report of meeting held January 13 and 14, 1994, National Institutes of Health, Bethesda, MD”. Pediatrics 93 (5): 8149. PMID 8165085. 

^ McKenna JJ, McDade T (June 2005). “Why babies should never sleep alone: a review of the co-sleeping controversy in relation to SIDS, bedsharing and breast feeding”. Paediatr Respir Rev 6 (2): 13452. doi:10.1016/j.prrv.2005.03.006. PMID 15911459. http://linkinghub.elsevier.com/retrieve/pii/S1526054205000230. 

^ Moon RY, Horne RS, Hauck FR (November 2007). “Sudden infant death syndrome”. Lancet 370 (9598): 157887. doi:10.1016/S0140-6736(07)61662-6. PMID 17980736. 

^ Fleming PJ, Levine MR, Azaz Y, Wigfield R, Stewart AJ (June 1993). “Interactions between thermoregulation and the control of respiration in infants: possible relationship to sudden infant death”. Acta Paediatr Suppl 82 (Suppl 389): 579. doi:10.1111/j.1651-2227.1993.tb12878.x. PMID 8374195. 

^ Mage DT (1996). “A probability model for the age distribution of SIDS”. J Sudden Infant Death Syndrome Infant Mortal 1: 1331. 

^ Poets CF, Samuels MP, Wardrop CA, Picton-Jones E, Southall DP (April 1992). “Reduced haemoglobin levels in infants presenting with apparent life-threatening events retrospective investigation”. Acta Paediatr. 81 (4): 31921. PMID 1606392. 

^ Mitchell EA, Hutchison L, Stewart AW (July 2007). “The continuing decline in SIDS mortality”. Arch Dis Child. 92 (7): 6256. doi:10.1136/adc.2007.116194. PMID 17405855. 

^ a b c d[citation needed]

^ Aris C, Stevens TP, Lemura C, et al. (October 2006). “NICU nurses’ knowledge and discharge teaching related to infant sleep position and risk of SIDS”. Adv Neonatal Care 6 (5): 28194. doi:10.1016/j.adnc.2006.06.009. PMID 17045948. 

“Erratum”. Adv Neonatal Care 6 (6): 340. December 2006. 

^ Hauck FR, Herman SM, Donovan M, Iyasu S, Merrick Moore C, Donoghue E, Kirschner RH, Willinger M (2003). “Sleep environment and the risk of sudden infant death syndrome in an urban population: the Chicago Infant Mortality Study”. Pediatrics 111: 120714. doi:10.1542/peds.111.5.S1.1207 (inactive 2008-06-25). PMID 12728140. http://pediatrics.aappublications.org/cgi/content/abstract/111/5/S1/1207. 

^ Vennemann MM, Bajanowski T, Brinkmann B, et al. (March 2009). “Does breastfeeding reduce the risk of sudden infant death syndrome?”. Pediatrics 123 (3): e40610. doi:10.1542/peds.2008-2145. PMID 19254976. http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=19254976. 

^ Wenda Trevathan, Euclid O. Smith, James Joseph McKenna (1999). Evolutionary Medicine. Oxford University Press US. pp. 559. ISBN 0195103556. 

^ McKenna, James J. (1996), “Sudden Infant Death Syndrome in Cross-Cultural perspective: is Infant-Parent Cosleeping Protective?”, Annual Review of Anthropology 25: 20116, doi:10.1146/annurev.anthro.25.1.201, http://arjournals.annualreviews.org/doi/abs/10.1146/annurev.anthro.25.1.201 

^ Mosko S, McKenna J, Dickel M, Hunt L (December 1993). “Parent-infant cosleeping: the appropriate context for the study of infant sleep and implications for sudden infant death syndrome (SIDS) research”. J Behav Med 16 (6): 589610. doi:10.1007/BF00844721. PMID 8126714. http://www.springerlink.com/content/l44150210255t523/. 

^ Task Force on Sudden Infant Death Syndrome (November 2005). “The changing concept of sudden infant death syndrome: diagnostic coding shifts, controversies regarding the sleeping environment, and new variables to consider in reducing risk”. Pediatrics 116 (5): 124555. doi:10.1542/peds.2005-1499. PMID 16216901. http://aappolicy.aappublications.org/cgi/content/full/pediatrics;116/5/1245. 

^ Ball H (September 2009). “Airway covering during bed-sharing”. Child Care Health Dev 35 (5): 72837. doi:10.1111/j.1365-2214.2009.00979.x. PMID 19531119. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0305-1862&date=2009&volume=35&issue=5&spage=728. 

^ Chapter 5; pages 180194, secondhand smoke is connected to SIDS.

^ “Smoking during pregnancynited States, 19902002”. MMWR Morb Mortal Wkly Rep. 53 (39): 9115. October 2004. PMID 15470322. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5339a1.htm. 

^ Smartmoney.com on bedding

^ .

^ L’Hoir MP, Engelberts AC, van Well GT, et al. (1998). “Risk and preventive factors for cot death in The Netherlands, a low-incidence country”. Eur. J. Pediatr. 157 (8): 6818. doi:10.1007/s004310050911. PMID 9727856. 

^ “The Changing Concept of Sudden Infant Death Syndrome: Diagnostic Coding Shifts, Controversies Regarding the Sleeping Environment, and New Variables to Consider in Reducing Risk”. American Academy of Pediatrics. http://aappolicy.aappublications.org/cgi/content/full/pediatrics;116/5/1245#SEC15. Retrieved 2008-11-06. 

^ van Gestel, Josephus Petrus Johannes; Monique Pauline Loir, Maartje ten Berge, Nicolaas Johannes Georgius Jansen, and Frans Berend Pltz (6 December 2002). “Risks of Ancient Practices in Modern Times” (in English) (html). Pediatrics 110 (6): e78. http://pediatrics.aappublications.org/cgi/content/full/110/6/e78. Retrieved 12/15/2009. 

^ Gerard, Claudia M.; Kathleen A. Harris and Bradley T. Thach (6 December 2002). “Spontaneous Arousals in Supine Infants While Swaddled and Unswaddled During Rapid Eye Movement and Quiet Sleep” (in English) (html). Pediatrics 110 (6): e70. http://pediatrics.aappublications.org/cgi/content/full/110/6/e70. Retrieved 12/15/2009. 

^ Franco, P; Scaillet S, Groswasser J, Kahn A. (December 2004). “Increased cardiac autonomic responses to auditory challenges in swaddled infants” (in English) (pdf). Sleep. http://www.journalsleep.org/Articles/270811.pdf. Retrieved 12/15/2009. 

^ Short MA, Brooks-Brunn JA, Reeves DS, Yeager J, Thorpe JA (June 1996). “The effects of swaddling versus standard positioning on neuromuscular development in very low birth weight infants”. Neonatal Netw 15 (4): 2531. PMID 8716525. 

^ “Fig 4. Meta-analysis of studies examining the relationship of a pacifier used during the last sleep in SIDS victims versus controls”. American Academy of Pediatrics. http://aappolicy.aappublications.org/cgi/content/full/pediatrics;116/5/1245/F4. Retrieved 2008-11-06. 

^ a b “The Changing Concept of Sudden Infant Death Syndrome: Diagnostic Coding Shifts, Controversies Regarding the Sleeping Environment, and New Variables to Consider in Reducing Risk”. American Academy of Pediatrics. http://aappolicy.aappublications.org/cgi/content/full/pediatrics;116/5/1245#SEC6. Retrieved 2008-11-06. 

^ Li DK, Willinger M, Petitti DB, Odouli R, Liu L, Hoffman HJ (2006). “Use of a dummy (pacifier) during sleep and risk of sudden infant death syndrome (SIDS): population based case-control study”. BMJ 332 (7532): 1822. doi:10.1136/bmj.38671.640475.55. PMID 16339767. 

^ Coleman-Phox K, Odouli R, Li DK (October 2008). “Use of a fan during sleep and the risk of sudden infant death syndrome”. Arch Pediatr Adolesc Med 162 (10): 9638. doi:10.1001/archpedi.162.10.963. PMID 18838649. http://archpedi.ama-assn.org/cgi/content/abstract/162/10/963. 

^ Carla K. Johnson (Associated Press writer) (2008-09-08). “Fan use linked to lower risk of sudden baby death”. Toronto Star. http://www.parentcentral.ca/parent/article/513143. Retrieved 2008-11-09. , also in Live Science
^ “Policy Statement for Bumper Pads in Cribs – Consumer Product Safety”. http://www.hc-sc.gc.ca/cps-spc/legislation/pol/bumper-bordure_e.html. Retrieved 2007-06-27. 

^ Gizela BA (2001). “Postmortem hemoglobin concentration changing in Sprague-Dawley white mouse” (in Indonesian). Berkala Ilmu Kedokteran 33: 20710. 

^ Sherburn RE, Jenkins RO (September 2004). “Cot mattresses as reservoirs of potentially harmful bacteria and the sudden infant death syndrome”. FEMS Immunol. Med. Microbiol. 42 (1): 7684. doi:10.1016/j.femsim.2004.06.011. PMID 15325400. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0928-8244&date=2004&volume=42&issue=1&spage=76. 

^ Kalokerinos A, Dettman G (July 1976). “Sudden death in infancy syndrome in Western Australia”. Med. J. Aust. 2 (1): 312. PMID 979792. 

^ Donovan J (September 1979). “Vitamin C and cot death: where is the evidence?”. Med. J. Aust. 2 (6): 311. PMID 522763. 

^ Holborow P (April 1980). “Sudden infant death syndrome”. Am. J. Clin. Nutr. 33 (4): 7301. PMID 7361687. http://www.ajcn.org/cgi/reprint/33/4/730. “There has been some controversy about the role of Vitamin C in cot death.”. 

^ Cheraskin E (October 1995). “Vitamin C, smoking and SIDS”. J R Soc Health 115 (5): 332. PMID 7473510. 

^ Dick A, Ford R (November 2009). “Cholinergic and oxidative stress mechanisms in sudden infant death syndrome”. Acta Paediatr. 98 (11): 176875. doi:10.1111/j.1651-2227.2009.01476.x. PMID 19706020. 

^ Fleming PJ, Blair PS, Mitchell EA (November 2002). “Mattresses, microenvironments, and multivariate analyses”. BMJ 325 (7371): 9812. doi:10.1136/bmj.325.7371.981. PMID 12411332. PMC 1124537. http://bmj.com/cgi/pmidlookup?view=long&pmid=12411332. 

^ “Cot Life 2000 aims to eliminate cot”. Cotlife2000.co.nz. http://www.cotlife2000.co.nz/. Retrieved 2009-10-15. 

^ See FSID Press release.

^ cotlife2000.co.nz Errors and fallacies in the UK Limerick Report: an overview, Cot Life 2000

^ Katz DM (2005). “Regulation of respiratory neuron development by neurotrophic and transcriptional signaling mechanisms”. Respiratory physiology & neurobiology 149 (1-3): 99109. doi:10.1016/j.resp.2005.02.007. PMID 16203214. 

^ ICPA – SIDS Research

^ See http://wonder.cdc.gov and http://www3.who.int/whosis/menu.cfm?path=whosis,inds,mort&language=english for data on SIDS by gender in the U.S. and throughout the world.

^ Mage DT, Donner EM (September 2004). “The fifty percent male excess of infant respiratory mortality”. Acta Paediatr. 93 (9): 12105. doi:10.1080/08035250410031305. PMID 15384886. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0803-5253&date=2004&volume=93&issue=9&spage=1210. 

^ See the data found at http://wonder.cdc.gov for 9ICD 911-912 and 10ICD W79-W80 for death rates from inhalation of food and foreign objects by sex.

^ Osmond C, Murphy M (October 1988). “Seasonality in the sudden infant death syndrome”. Paediatr Perinat Epidemiol 2 (4): 33745. PMID 3072532. 

^ Glatt, John (2000). Cradle of Death: A Shocking True Story of a Mother, Multiple Murder, and SIDS. Macmillan. ISBN 0312973020. 

^ Havill, Adrian (2002). While Innocents Slept: A Story of Revenge, Murder, and SIDS. Macmillan. ISBN 0312975171,. 

^ Spinelli, Margaret (2003). Infanticide: Psychosocial and Legal Perspectives on Mothers Who Kill. American Psychiatric Pub. p. 27. ISBN 1585620971,. 

^ Stanton J, Simpson A (December 2001). “Murder misdiagnosed as SIDS: a perpetrator’s perspective”. Arch Dis Child. 85 (6): 4549. doi:10.1136/adc.85.6.454. PMID 11719326. PMC 1719021. http://adc.bmj.com/cgi/pmidlookup?view=long&pmid=11719326. 

^ Emery JL (October 1993). “Child abuse, sudden infant death syndrome, and unexpected infant death”. Am J Dis Child. 147 (10): 1097100. PMID 8213682. 

^ “Investigation of SIDS”. N Engl J Med. 315 (26): 16757. December 1986. PMID 3785340. 

^ Carol Strickland (1997-10-19). “Investigating a Rash of SIDS Deaths, Exposing Infanticide”. The New York Times. http://query.nytimes.com/gst/fullpage.html?sec=health&res=9A06EED9163FF93AA25753C1A961958260. Retrieved 2008-04-20. 

^ “About Statistics and the Law” (Website). Royal Statistical Society. (2001-10-23) Retrieved on 2007-09-22

^ Klonoff-Cohen H, Lam PK, Lewis A (July 2005). “Outdoor carbon monoxide, nitrogen dioxide, and sudden infant death syndrome”. Arch Dis Child. 90 (7): 7503. doi:10.1136/adc.2004.057091. PMID 15970620. 

^ Sudden Infant Death Syndrome (SIDS) and Vaccines http://www.cdc.gov/vaccinesafety/Concerns/sids_faq.html

^ Thomas H. Maugh II (2007) ([dead link] Scholar search). Hearing loss may foretell SIDS risk. http://www.latimes.com/news/science/la-sci-sids28jul28,1,2214491.story?track=rss. 

^ Alastruey J, Sherwin SJ, Parker KH, Rubens DD (July 2009). “Placental transfusion insult in the predisposition for SIDS: a mathematical study”. Early Hum. Dev. 85 (7): 4559. doi:10.1016/j.earlhumdev.2009.04.001. PMID 19446412. http://linkinghub.elsevier.com/retrieve/pii/S0378-3782(09)00060-7. 

^ Pelayo R, Owens J, Mindell J, Sheldon S (March 2006). “Bed sharing with unimpaired parents is not an important risk for sudden infant death syndrome: to the editor”. Pediatrics 117 (3): 9934; author reply 9946. doi:10.1542/peds.2005-2748. PMID 16510694. http://pediatrics.aappublications.org/cgi/reprint/117/3/993.pdf. 

^ Pelligra R, Doman G, Leisman G (July 2005). “A reassessment of the SIDS Back to Sleep Campaign”. Scientific World Journal 5: 5507. doi:10.1100/tsw.2005.71. PMID 16075152. http://cgi.thescientificworld.co.uk/cgi-bin/processHtml.pl?Id=2005.03.71.html&format=Dreamweaver. 

^ a b Jones MW (2004). “Supine and Prone Infant Positioning: A Winning Combination”. J Perinat Educ 13 (1): 1020. doi:10.1624/105812404X109357. PMID 17273371. 

^ Carter H, “Flat Out” – The Guardian: Tuesday July 8, 2003.

^ Kordestani RK, Patel S, Bard DE, Gurwitch R, Panchal J (January 2006). “Neurodevelopmental delays in children with deformational plagiocephaly”. Plast Reconstr Surg. 117 (1): 20718; discussion 21920. doi:10.1097/01.prs.0000185604.15606.e5. PMID 16404269. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00006534-200601000-00032. 

^ Stevens P, “The Flip Side of Back to Sleep”, The O&P Edge.

^ von Hofsten C (June 2004). “An action perspective on motor development”. Trends Cogn. Sci. (Regul. Ed.) 8 (6): 26672. doi:10.1016/j.tics.2004.04.002. PMID 15165552. http://linkinghub.elsevier.com/retrieve/pii/S1364661304001019. 

^ Sigmundsson H, Haga M (October 2000). “[Children and motor competence]” (in Norwegian). Tidsskr. Nor. Laegeforen. 120 (25): 304850. PMID 11109395. 

^ Graham JM, Gomez M, Halberg A, et al. (February 2005). “Management of deformational plagiocephaly: repositioning versus orthotic therapy”. J. Pediatr. 146 (2): 25862. doi:10.1016/j.jpeds.2004.10.016. PMID 15689920. 

^ Lewak N. “Book Review: SIDS”. Arch Pediatr Adolesc Med 158 (4): 405. http://archpedi.highwire.org/cgi/content/full/158/4/405. 

1989 “Sleep and Arousal Synchrony of Co-Sleeping Human Mother-Infant Pairs: Implications for the Study of SIDS.” Fourth World Congress of Infant Psychiatry and Allied Disciplines (poster session). Lugano, Switzerland. Presented also at 58th Annual Meeting, American Association of P…

Sore Throat Relief, Get rid of Sore Throat

Sore throat – the most common contagious viral or bacterial infection… a tickling sensation that becomes sore, frustrating and eventually severely painful. Antibiotics can cure only bacterial sore throats but for viral based infections, antibiotics are of no use. However, natural remedies for sore throat can really do wonders with viral based infections. You will get pain relief usually within an hour or two by using these natural health remedies for sore throats, but sometimes it may take a little more time.

The belleric myrobalan, commonly known as behera in Ayurvedic parlance, is a popular Indian household remedy for coughs. The pulp of its fruit is taken. This pulp is mixed with salt, long pepper and honey. This is given for allaying the problems of sore throat. Instead of this preparation, its fried fruit can also be covered with wheat flour and then roasted on a low flame.

Cardamom is also a popular sore throat cure. You can do gargles with the infusion of the cardamom to get relief from the problem of sore throat. This is very useful especially to cure the serious throat infections. Many doctors recommend Cardamom to their patients for fast recovery. The best part of all these cures is that they do not cause any side effects to the patient.

The most amazing and effective treatment is using 5 shakes of Cayenne Pepper (Capsicum frutescens) Powder in a cup of hot water (or herbal tea or saline solution or lemon juice) and gargle every 15 minutes with the spicy elixir. May swallow each time a tiny bit. Gargling with cayenne can cause a strong burning sensation of lips and tongue. Therefore is good keeping milk or yogurt in your mouth after gargling until the burning disappears.

Excellent remedies for a sore throat is gargling with thyme tea which is a powerful antiseptic, disinfectant, antibacterial, anti this and that, or using lemon juice. If you can handle neat lemon juice, so much the better, but a lemon tea or lemonade will work well. It may sting, but it works. You can always add a little honey to it, which will also help the throat.

Usually a few gargle with a warm salt water solution will generally reduce any swelling and tends to relieve the discomfort that comes with sore throats. To be effective you should gargle at least one time every hour using one teaspoon of common table salt dissolved in approximately 8 ounces of warm water. In the event that you are bothered by postnasal drip you can safely gargle more often in order to prevent and additional throat irritation.

Go Green – conquer your sore throat with green tea. This wonderful tea is a powerful antioxidant which will fight off infection by preventing the cellular reactions that cause disease. This tea will also kill the microbes that will cause a sore throat. If you heat the tea it will also add the additional comfort.

Tonsil Stones Treatment – Is There A Tonsil Stones Cure That Works?

Tonsilloliths is the medical term for tonsil stones or tonsil rocks and they are most commonly seen during adolescence, but may come about at any time. If you have concerns, don’t worry because there is a tonsil stones treatment available that can help most of you combat this ailment and furthermore get rid of bad breath, which can so often be linked to this condition.

Tonsil stones are an uncomfortable and embarrassing condition, but one that can be treated. People with deep crypted tonsils (probably caused by tonsillitis from an early age) are more likely to get tonsil stones because of the ideal environment to trap anything that passes by. The stones are made up of a combination of food debris, saliva, bacteria, post nasal drip, white blood cells and other remains, which form small off white stones within the tonsil crypt.

Because the stones have a notably foul odor (even more so when broken open), removing them is a priority. They are a cause of bad breath (halitosis) but often people do not even know they have them, as they are not always visible. Many people see the first indication of a tonsil stone once it dislodges itself and has to be expelled through the mouth. Even the bad breath is not noticeable unless someone tells you about it, as you cannot smell your own breath.

To get rid of tonsil stones you can try and remove them yourself or you can use a readily available treatment kit. To remove them yourself you can try gently pushing against the cavity so that the stone essentially pops itself out. Be careful not to break it in your mouth: the smell will be overwhelming and may be difficult to remove for a few days.

Many people use a Q-tip to dislodge the tonsil stone. If the stones are small then this strategy can work well. It is best to try and remove the stone as soon as you notice it, rather than waiting until it grows much larger, as it will be more difficult to dislodge and to get out in one piece without breaking it.

After removing a tonsil stone, give your teeth a good brush and use a quality, gentle, alcohol free, mint mouthwash to freshen up.

However if the stones have become deeply lodged they can be rather difficult to remove and it is a good idea to purchase a product that will neutralize the bacteria. Something like aktivoxigen tablets are able to do this well. You could also try nasal sinus drops, which can help with post nasal drip, as this can also be a factor in forming the stones.

Tongue scrapers can also assist in deterring tonsil stones as the scraper is able to remove bacteria from the back of your tongue, which helps to slow down the formation of tonsil stones and get rid of bad breath problems to a certain degree.

Trying to remove tonsil stones yourself is not easy and doesn’t always work that well; ideally you would be much better off investing in a specially formulated quality tonsil stones treatment kit. A complete tonsil stones cure is what you want to leave you with a constant fresh breath feeling and eliminating those awful problems for good. The kits come with all you will need to combat the stones, bad breath and any unpleasant tastes in the mouth.

I have a website that is totally dedicated to helping and understanding this problem. It’s a great place that has lots of additional information about tonsil stones and bad breath. Feel free to check it out now.

Optimum Diabetics Supplements – Herbal Supplement To Aid Diabetes

Diabetes or diabetes mellitus is a metabolic disorder characterized by high glucose or sugar levels in blood. Our liver gives out glucose in to blood by synthesizing the carbohydrates we consume. The pancreas, an organ between liver and stomach, produce hormone insulin that regulates blood glucose level by breaking down glucose and supplying it to muscles and body cells in the form of fuel or energy required for day to day activities. When insulin fails to function properly as glucose builds up in blood, resulting in diabetes.

Diabetes is of two types: Type 1 diabetes occurs when pancreas does not produce adequate insulin to meet the body’s demand. Type 1 diabetes is common in children and adolescence, and is also known as juvenile diabetes. Type 2 diabetes occurs when the body cells are unable to respond to the insulin secreted, and as a result the glucose does not enter the cells and stays back in blood, resulting in Type 2 diabetes. This phenomenon is also termed as insulin resistance. The causes of diabetes may be heredity, viral infections, aging, sedentary lifestyle and dearth of physical activity, fat rich diet, obesity, high blood pressure, high triglyceride levels, alcoholism, tobacco dependence, disease of pancreas etc.

The major symptoms of diabetes include excessive fatigue, excessive weight loss, irritability, itching around genitals, excessive thirst, poor wound healing, blurry vision, infections, and frequent urge for urination, and increased appetite. Gestational diabetes is another type that occurs in women during pregnancy. Constant high glucose levels can damage heart, kidney, nerves and retina of eye.

Diabetes is a curse for many. It sucks in your energy leaving you incapable of participating in a full-fledged manner in the daily chores. Neither can eat at your free will; nor can you enjoy the real essence of life. This disease cripples you altogether. You have to consult doctor to treat diabetes, but the good news is that these days a number of naturally composed products are available in market to support your diabetes treatment. These products minimize the harmful side-effects of synthetic drugs. Optimum Diabetics is one such product that is naturally composed and free from side-effects. The product is an herbal supplement to aid diabetes.

It supplies the body with necessary nutrients, natural vitamins and minerals. The pills contain no preservatives and flavors, and one is to take a single pill a day. The alpha-lipoic acid contained in pill is a health restorative agent, doing away with excessive fatigue. Optimum Diabetics is an herbal supplement to aid diabetics. It keeps your diabetes under check and brings happiness back in to your life. This dietary supplement, in other words, fills the gap created when we consume lacking diets.

The ingredients of Optimum Diabetics include chromium, evening primrose oil powder, fenugreek, vanadium, bitter melon, garcinia etc. These ingredients bring back your control over your life, minimize diabetes symptoms and regulate your body. So say no to diabetes with Optimum Diabetics, the best herbal supplement to aid diabetes! This is 100% safe and effective.

Peanut Butter for the Diabetic

I am constantly surprised by the number of diabetics who are unaware that simple peanut butter is a great protein source that is beneficial in a diabetics diet.  And once I mention it they usually look at me like I am crazy and say, “but what about fat and cholesterol?”  Remember to eat everything in a reasonable amount.  I am not advocating a half jar of peanut butter per serving.  Most commercial peanut butters contain no trans fat and around 3 grams of saturated fat per a two tablespoon serving.  Two tablespoons is quite a bit of peanut butter.  Following are some easy ways to add peanut butter to your diet to help you control your blood sugar.

  • In a hurry at breakfast?  Spread a tablespoon of peanut butter on a piece of whole grain toast.
  • When eating pancakes, spread with peanut butter instead of butter or margarine.  Top off with sugar-free syrup.
  • Peanut butter, regular Jif Peanut Butter used as this example, has more protein than carbohydrates.  This is important for diabetics.
  • Need a quick snack?  Cut a slice of whole grain bread in half.  Top one of the halves with a tablespoon of peanut butter, add a tablespoon of low-sugar jelly then top with the other half of the bread.  Or you can eat it without the top piece of bread if you prefer.
  • For snacks, lunches or party platters, cut a rib of celery into three or four pieces.  Stuff the inside with some peanut butter.
  • Slice an apple into wedges.  Dip into peanut butter for snacking.  The protein in the peanut butter will help to counteract the natural sugar in the apple.
  • When eating out and tempted by dessert, eat a few bites or small slice of peanut butter pie.  This should be after eating meat or other protein during your meal.  I have done this several times at a local steakhouse and it has never caused my blood sugar to go over 120.
  • At a birthday party and want a piece of cake?  Ask the hostess for a small slice of cake and a tablespoon of peanut butter.  I always do this and it has never increased my blood sugar.

Obesity – Causes, Symptoms and Treatment – Tom Smith

Obesity is a condition in which there excessive deposits of body fat. A person with a BMI (body mass index) over 30 is characterized as being obese. Those with a BMI over 25 are considered as being overweight.

Causes of Obesity

The first cause of obesity is laziness. If you are a large person and you can honestly say that you get at least a half an hour of aerobic exercise each day, then there is something else that is causing your obesity, but if you are not getting at least that much exercise, then you need to get off your lazy butt and start exercising.

High caloric food is one of the major causes in obesity. If you are eating high caloric food, I would strongly recommend you to make up your mind and completely change your eating habits. This is the most important step in order to burn fat. You have to avoid food and drinks with a lot of simple sugar and trans fatty acids. I strongly recommend you to get used to the habit of reading the list of ingredients of food and drink packages before buying it.

Lack of exercising is the next cause of obesity. We are preoccupied with a lot of things in our lives and we keep find excuses for ourselves to stop exercising. However, when we stop working out, our body will not be able to burn away fat efficiently. This will eventually lead to obesity when there is too much fat being stored and they are not burnt by the body.

Lifestyle is the major cause of obesity in the 21st Century. In addition, it takes time for anyone to become obese and as with any illness, early intervention improves the chances of getting weight under control and avoiding the many serious and sometimes life-threatening side effects.

Symptoms of Obesity

Although most people consider a fat child cute, parents should pay more close attention to their child’s weight. There are some signs that can help you detect if your child is in danger of obesity. It can usually be determined by measuring the height and weight. A child is considered obese of his/her weight is significantly over the ideal weight for his/her age and height. The most common symptoms of child obesity include disproportionate appearance of facial features, adiposity in the breast area among boys, unusually large abdomen and exceptionally small external genitals for males. Puberty may also occur earlier in obese children.

Obesity Treatment

Give children opportunities and encourage them to be involved in physical activities such as playing sports, hiking, dancing or even martial arts. It’s also important that parents are involved on certain times while still allowing their children to accomplish tasks on their own and with a peer group. This allows interaction that children need to learn from. Remember that low physical activity is one of the causes of child obesity. So encourage exercises to at least 20 to 30 minutes a day.

Naturopathy treatment has worked miracles in treating even those chronic diseases which could not be cured by chemical medicine. This method of treatment is devoid of all side effects and results in a permanent solution in treating the ailment. It is for this reason that naturopathy treatment has been very popular among obese patients, and why not when it can achieve results similar to other methods of treatment without any harmful effects, that too on a permanent basis.

A great deal of research has been done on the guggulu plant in recent times. The guggulsterone present in it is an alkaloid that has been found to be especially effective in heart ailments. Among its myriad other benefits, one is the reduction of fat accumulation in the body, giving people a leaner physique. Guggulu is the Ayurvedic drug of choice for obesity.

If the obesity problem is obstructing your normal life, then a solution to this problem is on the way. The new anti-obesity pill in the market has become a real hope for people who are obese or overweight. Acomplia rimonabant is an anti-obesity pill that can also help you with your blood pressure, blood glucose, and cholesterol level. These conditions are usually common in obese people. You can even overcome these problems apart from losing weight, if you buy Acomplia.

How To Identify Shingles Without a Rash

Is it possible to develop shingles without a rash? Yes, but this is a rare case. Shingles is a condition which is manifested by painful rashes or blisters which show on one side of the body. It usually lasts for two weeks and can even be prolonged to a month. Most of the time, the condition shows as pain without a rash, but develop into web-like blisters after days.

The pain associated with shingles can be very mild, but it can also be severe. It can be described as burning, painful and itchy, but without something to scratch or treat on the surface. In a case where the shingles do not have manifestations on the skin, it may be difficult to diagnose and can be mistaken for other diseases. And since shingles happen more on adults aged 60 and above, it can be confused with other diseases which commonly occur among elders.

Shingles without a rash is also known as zoster sine herpete. To deal with shingles without a rash, doctors can administer a blood test to check if the virus has in fact invaded the skin. Scrapings from other wounds can also be used to see if the virus has affected the body.

If you experience pain on your chest or on your back, you could have developed shingles instead of other illnesses such as heart ailments or simple back aches. It is best to seek medical attention before the virus spreads to the body and cause extreme discomfort.

Another characteristic of the pain is that it is very sensitive and feels more like it is occurring in a band instead of on a larger area. It commonly develops on the chest, the trunk near the waist, the neck, the face, or on either the arm or the thigh. The sensitive pain is coupled by discomfort which can be caused by a burning sensation or itchiness. This is caused by the virus being in the nerves instead of only on the skin.

As soon as you develop the pains which are similar to those described above, see your doctor and ask for advice. You may be given tests which may confirm that you in fact have developed shingles. There are medicines which can prevent the virus from further spreading to your body, and so that the ain will be lessened.