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Duchenne muscular dystrophy – Wikipedia

Posted: December 4, 2016 at 11:45 am

Duchenne muscular dystrophy (DMD) is a severe type of muscular dystrophy.[1] The symptom of muscle weakness usually begin around the age of four in boys and worsens quickly.[2] Typically muscle loss occurs first in the upper legs and pelvis followed by those of the upper arms. This can result in trouble standing-up.[1] Most are unable to walk by the age of twelve.[2] Affected muscles may look larger due to increased fat content. Scoliosis is also common. Some may have intellectual disability. Females with a single copy of the defective gene may show mild symptoms.[1]

The disorder is X-linked recessive. About two thirds of cases are inherited from a person’s parents while one third of cases are due to a new mutation. It is caused by a mutation in the gene for the protein dystrophin. Dystrophin is important to maintain the muscle fiber cell membrane. Genetic testing can often make the diagnosis at birth. Those affected also have a high level of creatine kinase in their blood.[1]

There is no cure for muscular dystrophy. Physical therapy, braces, and corrective surgery may help with some symptoms.[2]Assisted ventilation may be required in those with weakness of breathing muscles.[1] Medications used include steroids to slow muscle degeneration, anticonvulsants to control seizures and some muscle activity, and immunosuppressants to delay damage to dying muscle cells.[2]

Duchenne muscular dystrophy affects about one in 5,000 males at birth. It is the most common type of muscular dystrophy.[1] The average life expectancy is 26;[3] however, with excellent care some may live into their 30s or 40s. Gene therapy, as a treatment, is in the early stages of study in humans.[1]

The main symptom of Duchenne muscular dystrophy, a progressive neuromuscular disorder, is muscle weakness associated with muscle wasting with the voluntary muscles[citation needed] being first affected, especially those of the hips, pelvic area, thighs, shoulders, and calves. Muscle weakness also occurs later, in the arms, neck, and other areas. Calves are often enlarged. Symptoms usually appear before age 6 and may appear in early infancy. Other physical symptoms are:

According to Lewis P. Rowland, in the anthology Gene Expression In Muscle, if a boy is affected with Duchenne muscular dystrophy (DMD), the condition can be observed clinically from the moment he takes his first steps. It becomes harder and harder for the boy to walk; his ability to walk usually completely disintegrates between the time the boy is 9 to 12 years of age. Most men affected with DMD become essentially paralyzed from the neck down by the age of 21.[5] Muscle wasting begins in the legs and pelvis, then progresses to the muscles of the shoulders and neck, followed by loss of arm muscles and respiratory muscles. Calf muscle enlargement (pseudohypertrophy) is quite obvious. Cardiomyopathy particularly (dilated cardiomyopathy) is common, but the development of congestive heart failure or arrhythmia (irregular heartbeat) is only occasional.

Duchenne muscular dystrophy (DMD) is caused by a mutation of the dystrophin gene at locus Xp21, located on the short arm of the X chromosome.[7]Dystrophin is responsible for connecting the cytoskeleton of each muscle fiber to the underlying basal lamina (extracellular matrix), through a protein complex containing many subunits. The absence of dystrophin permits excess calcium to penetrate the sarcolemma (the cell membrane).[8] Alterations in calcium and signalling pathways cause water to enter into the mitochondria, which then burst.

In skeletal muscle dystrophy, mitochondrial dysfunction gives rise to an amplification of stress-induced cytosolic calcium signals and an amplification of stress-induced reactive-oxygen species (ROS) production. In a complex cascading process that involves several pathways and is not clearly understood, increased oxidative stress within the cell damages the sarcolemma and eventually results in the death of the cell. Muscle fibers undergo necrosis and are ultimately replaced with adipose and connective tissue.[citation needed]

DMD is inherited in an X-linked recessive pattern. Females will typically be carriers for the disease while males will be affected. Typically, a female carrier will be unaware they carry a mutation until they have an affected son. The son of a carrier mother has a 50% chance of inheriting the defective gene from his mother. The daughter of a carrier mother has a 50% chance of being a carrier and a 50% chance of having two normal copies of the gene. In all cases, an unaffected father will either pass a normal Y to his son or a normal X to his daughter. Female carriers of an X-linked recessive condition, such as DMD, can show symptoms depending on their pattern of X-inactivation.[citation needed]Duchenne muscular dystrophy has an incidence of 1 in 3,600 male infants.[6] Mutations within the dystrophin gene can either be inherited or occur spontaneously during germline transmission.[citation needed]

Genetic counseling is advised for people with a family history of the disorder. Duchenne muscular dystrophy can be detected with about 95% accuracy by genetic studies performed during pregnancy.[6]

The muscle-specific isoform of the dystrophin gene is composed of 79 exons, and DNA testing and analysis can usually identify the specific type of mutation of the exon or exons that are affected. DNA testing confirms the diagnosis in most cases.[9]

If DNA testing fails to find the mutation, a muscle biopsy test may be performed.[10] A small sample of muscle tissue is extracted using a biopsy needle. The key tests performed on the biopsy sample for DMD are immunocytochemistry and immunoblotting for dystrophin, and should be interpreted by an experienced neuromuscular pathologist.[11] These tests provide information on the presence or absence of the protein. Where the protein is absent, this is a positive test for DMD. Where dystrophin is present, the tests will indicate the amount and molecular size of dystrophin, helping to distinguish DMD from milder dystrophinopathy phenotypes.[12] Over the past several years DNA tests have been developed that detect more of the many mutations that cause the condition, and muscle biopsy is not required as often to confirm the presence of Duchenne’s.[13]

DMD is carried by an X-linked recessive gene. Males have only one X chromosome, so one copy of the mutated gene will cause DMD. Fathers cannot pass X-linked traits on to their sons, so the mutation is transmitted by the mother.[14]

If the mother is a carrier, and therefore one of her two X chromosomes has a DMD mutation, there is a 50% chance that a female child will inherit that mutation as one of her two X chromosomes, and be a carrier. There is a 50% chance that a male child will inherit that mutation as his one X chromosome, and therefore have DMD.Prenatal tests can tell whether their unborn child has the most common mutations. There are many mutations responsible for DMD, and some have not been identified, so genetic testing only works when family members with DMD have a mutation that has been identified.[citation needed]

Prior to invasive testing, determination of the fetal sex is important; while males are sometimes affected by this X-linked disease, female DMD is extremely rare. This can be achieved by ultrasound scan at 16 weeks or more recently by free fetal DNA testing. Chorion villus sampling (CVS) can be done at 1114 weeks, and has a 1% risk of miscarriage. Amniocentesis can be done after 15 weeks, and has a 0.5% risk of miscarriage. Fetal blood sampling can be done at about 18 weeks.[citation needed] Another option in the case of unclear genetic test results is fetal muscle biopsy.

There is no cure for DMD, and an ongoing medical need has been recognized by regulatory authorities.[15] Phase 1-2a trials with exon skipping treatment for certain mutations have halted decline and produced small clinical improvements in walking.

Treatment is generally aimed at controlling the onset of symptoms to maximize the quality of life which can be measured using specific questionnaires,[16] and include the following:

Comprehensive multi-disciplinary care standards/guidelines for DMD have been developed by the Centers for Disease Control and Prevention (CDC), and were published in two parts in The Lancet Neurology in 2010. To download the two articles in PDF format, go to the TREAT-NMD website.[19]

Physical therapists are concerned with enabling patients to reach their maximum physical potential. Their aim is to:

Modern “volume ventilators/respirators,” which deliver an adjustable volume (amount) of air to the person with each breath, are valuable in the treatment of people with muscular dystrophy related respiratory problems. The ventilator may require an invasive endotracheal or tracheotomy tube through which air is directly delivered, but, for some people non-invasive delivery through a face mask or mouthpiece is sufficient. Positive airway pressure machines, particularly bi-level ones, are sometimes used in this latter way. The respiratory equipment may easily fit on a ventilator tray on the bottom or back of a power wheelchair with an external battery for portability.

Ventilator treatment may start in the mid to late teens when the respiratory muscles can begin to collapse. If the vital capacity has dropped below 40 percent of normal, a volume ventilator/respirator may be used during sleeping hours, a time when the person is most likely to be under ventilating (“hypoventilating”). Hypoventilation during sleep is determined by a thorough history of sleep disorder with an oximetry study and a capillary blood gas (See Pulmonary Function Testing).

A cough assist device can help with excess mucus in lungs by hyperinflation of the lungs with positive air pressure, then negative pressure to get the mucus up.If the vital capacity continues to decline to less than 30 percent of normal, a volume ventilator/respirator may also be needed during the day for more assistance. The person gradually will increase the amount of time using the ventilator/respirator during the day as needed.However, there are also people with the disease in their 20’s who have no need for a ventilator.[citation needed]

Duchenne muscular dystrophy is a rare progressive disease which eventually affects all voluntary muscles and involves the heart and breathing muscles in later stages. As of 2013, the life expectancy is estimated to be around 25,[6] but this varies from patient to patient. Recent advancements in medicine are extending the lives of those afflicted. The Muscular Dystrophy Campaign, which is a leading UK charity focusing on all muscle disease, states that “with high standards of medical care young men with Duchenne muscular dystrophy are often living well into their 30s”.[20]

In rare cases, persons with DMD have been seen to survive into the forties or early fifties, with the use of proper positioning in wheelchairs and beds, ventilator support (via tracheostomy or mouthpiece), airway clearance, and heart medications, if required.[citation needed] Early planning of the required supports for later-life care has shown greater longevity in people living with DMD.[citation needed]

Curiously, in the mdx mouse model of Duchenne muscular dystrophy, the lack of dystrophin is associated with increased calcium levels and skeletal muscle myonecrosis. The intrinsic laryngeal muscles (ILM) are protected and do not undergo myonecrosis.[21] ILM have a calcium regulation system profile suggestive of a better ability to handle calcium changes in comparison to outher muscles, and this may provide a mechanistic insight for their unique pathophysiological properties.[22] The ILM may facilitate the development of novel strategies for the prevention and treatment of muscle wasting in a variety of clinical scenarios.[23]

The disease was first described by the Neapolitan physician Giovanni Semmola in 1834 and Gaetano Conte in 1836.[24][25][26] However, DMD is named after the French neurologist Guillaume-Benjamin-Amand Duchenne (18061875), who, in the 1861 edition of his book “Paraplegie hypertrophique de l’enfance de cause cerebrale”, described and detailed the case of a boy who had this condition. A year later, he presented photos of his patient in his “Album de photographies pathologiques.” In 1868 he gave an account of 13 other affected children. Duchenne was the first who did a biopsy to obtain tissue from a living patient for microscopic examination.[27][28]

Alfredo Ferrari (born January, 1932 in Modena), nicknamed Alfredino or Dino, was the son of Enzo Ferrari. He designed the 1.5 L DOHC V6 engine for F2 at the end of 1955. Dino would never see the engine; he died 30 June 1956 in Modena at the age of 24, before his namesake automobiles Fiat Dino and Dino (automobile) were produced.

Rapper, Darius Weems, had the disease and used his notoriety to raise awareness and funds for treatment.[29] He passed away at the age of 27. His brother also suffered from the disease until his death at age 19. Darius Goes West is a documentary that depicts his journey of growth and acceptance of having the disease.A book entitled, The Revised Fundamentals of Caregiving, was released in 2012, written by Jonathan Evison. Netflix produced a film titled, The Fundamentals of Caring, in 2016 based on the novel. Both media depict a young man suffering from the disease.[citation needed]

Current research includes exon-skipping, stem cell replacement therapy, analog up-regulation, gene replacement and supportive care to slow disease progression.[citation needed]

Antisense oligonucleotides (oligos), structural analogs of DNA, are the basis of a potential therapy for patients afflicted with DMD. The compounds allow faulty parts of the dystrophin gene to be skipped when it is transcribed to RNA for protein production, permitting a still-truncated but more functional version of the protein to be produced.[30]

Two kinds of antisense oligos, 2′-O-methyl phosphorothioate oligos (like drisapersen) and Morpholino oligos (like eteplirsen), have been tested in early-phase clinical trials for DMD and have restored some dystrophin expression in muscles of DMD patients with a particular class of DMD-causing mutations. Clinical trials are ongoing.[31][32]

Oligo-mediated exon skipping has resulted in clinical improvement in 12 patients in a Phase 1-2a study. On a standard test, the 6-minute walk test, patients whose performance had been declining instead improved, from 385 meters to 420 meters.[33][34] DMD may result from mRNA that contains out-of-frame mutations (e.g. deletions, insertions or splice site mutations), resulting in frameshift or early termination so that in most muscle fibers no functional dystrophin is produced (though some revertant muscle fibers produce some dystrophin). In many cases an antisense oligonucleotide can be used to trigger skipping of an adjacent exon to restore the reading frame and production of partially functional dystrophin.

Patients with Becker’s muscular dystrophy, which is milder than DMD, have a form of dystrophin which is functional even though it is shorter than normal dystrophin.[35] In 1990 England et al. noticed that a patient with mild Becker muscular dystrophy was lacking 46% of his coding region for dystrophin.[35] This functional, yet truncated, form of dystrophin gave rise to the notion that shorter dystrophin can still be therapeutically beneficial. Concurrently, Kole et al. had modified splicing by targeting pre-mRNA with antisense oligonucleotides (AONs).[36] Kole demonstrated success using splice-targeted AONs to correct missplicing in cells removed from beta-thalassemia patients[37][38] Wilton’s group tested exon skipping for muscular dystrophy.[39][40] Successful preclinical research led to the current efforts to use splice-modifying oligos to change DMD dystrophin to a more functional form of dystrophin, in effect converting Duchenne MD into Becker MD.

Though AONs hold promise, one of their major pitfalls is the need for periodic redelivery into muscles. Systemic delivery on a recurring basis is being tested in humans.[41] To circumvent the requirement for periodic oligo delivery, a long-term exon-skip therapy is being explored. This therapy consists of modifying the U7 small nuclear RNA at the 5′ end of the non-translated RNA to target regions within pre-mRNA. This has been shown to work in the DMD equivalent mouse, mdx.[42]

Though stem cells isolated from the muscle (satellite cells) have the ability to differentiate into myotubes when injected directly into the muscle of animals, they lack the ability to spread systemically throughout. To effectively deliver a therapeutic dose to an isolated muscle it would require direct injections to that muscle every 2mm.[43] This problem was circumvented by using another multipotent stem cell, termed pericytes, that are located within the blood vessels of skeletal muscle. These cells have the ability to be delivered systemically and uptaken by crossing the vascular barrier. Once past the vasculature, pericytes have the ability to fuse and form myotubes.[44] This means that they can be injected arterially, crossing through arterial walls into muscle, where they can differentiate into potentially functional muscle. These findings show potential for stem cell therapy of DMD. The pericyte-derived cells would be extracted, grown in culture, and then these cells would be injected into the blood stream where the possibility exists that they might find their way into injured regions of skeletal muscle.[citation needed]

In 2014 and 2015, researchers used a new gene editing method to correct a mutation that leads to Duchenne muscular dystrophy (DMD) in a mouse model of the condition. Researchers used a technique called CRISPR/Cas9-mediated genome editing, which can precisely remove a mutation in the dystrophin gene in DNA, allowing the bodys DNA repair mechanisms to replace it with a normal copy of the gene. The benefit of this over other gene therapy techniques is that it can permanently correct the defect in a gene rather than just transiently adding a functional one.

Genome editing through the CRISPR/Cas9 system is not currently feasible in humans. However, it may be possible, through advancements in technology, to use this technique to develop therapies for DMD in the future.[45][46] In 2007, researchers did the world’s first clinical (viral-mediated) gene therapy trial for Duchenne MD.[47]

Biostrophin is a delivery vector for gene therapy in the treatment of Duchenne muscular dystrophy and Becker muscular dystrophy.[48]

While PTC124 showed promising results in mice,[49][50] the Phase II trial was suspended when participants did not show significant increases in the six-minute walk distance.[51] The Phase II trial of ACE-031 (a decoy receptor) was suspended due to safety issues.[52][53]

Safety and efficacy studies of antisense oligonucleotides for exon skipping in Duchenne muscular dystrophy with Morpholino oligos (e.g. eteplirsen)[54] and with 2′-O-methyl phosphorothioate oligos (e.g. drisapersen)[55] are in progress.

In 2011, in a study by the UK Medical Research Council and Sarepta Therapeutics (formerly known as AVI BioPharma), researchers trialled a new drug, known as Eteplirsen(AVI-4658), designed to make the body bypass genetic mutations when producing dystrophin. When given to 19 children with Duchenne muscular dystrophy, researchers found that higher doses of the drug led to an increase in dystrophin. Researchers believe that drugs which are designed to make the body skip over mutations in this way could be used to treat approximately 83% of Duchenne muscular dystrophy cases. However, the drug used in this trial only targeted mutations in a region implicated in 13% of cases. This study was conducted well and demonstrated the potential of this approach for increasing the levels of dystrophin in the short term. The trials principal aim was to work out the appropriate dosages of the drug, therefore the drugs safety profile and effects will need to be confirmed in larger, longer-term studies, particularly as patients would need to take it for the rest of their lives (or until a better treatment is available).[56]

A small study published in May 2014 in the journal Neurology showed that the erectile dysfunction drug sildenafil could improve blood flow in boys affected with Duchenne MD. A larger and longer trial of the related drug tadalafil is underway to determine if improved blood flow will translate into improved muscle function.[57]

Rimeporide, a sodiumhydrogen antiporter 1 inhibitor, is in preclinical trials as of May 2015[update].[58]

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Duchenne muscular dystrophy – Wikipedia

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Spinal cord – Wikipedia

Posted: December 3, 2016 at 5:44 am

The spinal cord is a long, thin, tubular bundle of nervous tissue and support cells that extends from the medulla oblongata in the brainstem to the lumbar region of the vertebral column. The brain and spinal cord together make up the central nervous system (CNS). The spinal cord begins at the occipital bone and extends down to the space between the first and second lumbar vertebrae; it does not extend the entire length of the vertebral column. It is around 45cm (18in) in men and around 43cm (17in) long in women. Also, the spinal cord has a varying width, ranging from 13mm (12in) thick in the cervical and lumbar regions to 6.4mm (14in) thick in the thoracic area. The enclosing bony vertebral column protects the relatively shorter spinal cord. The spinal cord functions primarily in the transmission of neural signals between the brain and the rest of the body but also contains neural circuits that can independently control numerous reflexes and central pattern generators. The spinal cord has three major functions: as a conduit for motor information, which travels down the spinal cord, as a conduit for sensory information in the reverse direction, and finally as a center for coordinating certain reflexes. [1]

The spinal cord is the main pathway for information connecting the brain and peripheral nervous system.[2] The length of the spinal cord is much shorter as compared to the length of the vertebral column. The human spinal cord extends from the foramen magnum and continues through to the conus medullaris near the second lumbar vertebra, terminating in a fibrous extension known as the filum terminale.

It is about 45cm (18in) long in men and around 43cm (17in) in women, ovoid-shaped, and is enlarged in the cervical and lumbar regions. The cervical enlargement, located from C5 to T1 spinal segments, is where sensory input comes from and motor output goes to the arms. The lumbar enlargement, located between L1 and S3 spinal segments, handles sensory input and motor output coming from and going to the legs.

The spinal cord is continuous with the caudal portion of the medulla, running from the base of the skull to the body of the first lumbar vertebra. It does not run the full length of the vertebral column in adults. It is made of 31 segments that each contain sensory nerve root and motor nerve root. The first cervical segment is usually very small and may be absent in most individuals. Nerve roots merge into 31 bilaterally symmetric pairs of spinal nerves. The peripheral nervous system is made up of these spinal roots, nerves, and ganglia.

Dorsal roots are fascicles of axons in the spinal cord that receive sensory information from the skin, muscle, and visceral organs that enter through a point of entry called the dorsal root entry zone. Dorsal root ganglia hold the cell bodies of dorsal root ganglia in the spinal ganglia (dorsal root ganglia) related with that spinal segment.

Ventral roots only have efferent fibers that arise from motor neurons (general somatic efferent neurons) whose cell bodies are found in the ventral (or anterior) gray horns of the spinal cord.

The spinal cord (and brain) are protected by three layers of tissue or membranes called meninges, that surround the canal . The dura mater is the outermost layer, and it forms a tough protective coating. Between the dura mater and the surrounding bone of the vertebrae is a space called the epidural space. The epidural space is filled with adipose tissue, and it contains a network of blood vessels. The arachnoid mater is the middle protective layer. Its name comes from the fact that the tissue has a spiderweb-like appearance. The space between the arachnoid and the underlying pia mater is called the subarachnoid space. The subarachnoid space contains cerebrospinal fluid (CSF). The medical procedure known as a lumbar puncture (or “spinal tap”) involves use of a needle to withdraw cerebrospinal fluid from the subarachnoid space, usually from the lumbar region of the spine. The pia mater is the innermost protective layer. It is very delicate and it is tightly associated with the surface of the spinal cord. The cord is stabilized within the dura mater by the connecting denticulate ligaments, which extend from the enveloping pia mater laterally between the dorsal and ventral roots. The dural sac ends at the vertebral level of the second sacral vertebra.

In cross-section, the peripheral region of the cord contains neuronal white matter tracts containing sensory and motor neurons. Internal to this peripheral region is the grey matter. The nerve cell bodies of the grey matter are contained in the three grey columns of the spinal cord that give the region its butterfly-shape. This central region surrounds the central canal, which is an extension of the fourth ventricle and contains cerebrospinal fluid.

The spinal cord has a shape that is compressed dorso-ventrally, giving it an elliptical shape. The cord has grooves in the dorsal and ventral sides. The posterior median sulcus is the groove in the dorsal side, and the anterior median fissure is the groove in the ventral side.

The human spinal cord is divided into 31 different segments. At every segment, right and left pairs of spinal nerves (mixed; sensory and motor) form. Six to eight motor nerve rootlets branch out of right and left ventro lateral sulci in a very orderly manner. Nerve rootlets combine to form nerve roots. Likewise, sensory nerve rootlets form off right and left dorsal lateral sulci and form sensory nerve roots. The ventral (motor) and dorsal (sensory) roots combine to form spinal nerves (mixed; motor and sensory), one on each side of the spinal cord. Spinal nerves, with the exception of C1 and C2, form inside intervertebral foramen (IVF). Note that at each spinal segment, the border between the central and peripheral nervous system can be observed. Rootlets are a part of the peripheral nervous system. The spinal cord is a long, slender cable of nerve tissue which extends lengthwise through the vertebrae of the spinal column. At the upper end it connects with the brain through an opening in the floor of the skull. It extends downward almost to the level of the hips. It is well protected by the vertebrae, whose bony processes join together to form a canal within which the spinal cord is located.

In the upper part of the vertebral column, spinal nerves exit directly from the spinal cord, whereas in the lower part of the vertebral column nerves pass further down the column before exiting. The terminal portion of the spinal cord is called the conus medullaris. The pia mater continues as an extension called the filum terminale, which anchors the spinal cord to the coccyx. The cauda equina (“horse’s tail”) is the name for the collection of nerves in the vertebral column that continue to travel through the vertebral column below the conus medullaris. The cauda equina forms because the spinal cord stops growing in length at about age four, even though the vertebral column continues to lengthen until adulthood. This results in sacral spinal nerves originating in the upper lumbar region.

The spinal cord can be anatomically divided into 31 spinal segments based on the origins of the spinal nerves. Each segment of the spinal cord is associated with a pair of ganglia, called dorsal root ganglia, which are situated just outside the spinal cord. These ganglia contain cell bodies of sensory neurons. Axons of these sensory neurons travel into the spinal cord via the dorsal roots.

Ventral roots consist of axons from motor neurons, which bring information to the periphery from cell bodies within the CNS. Dorsal roots and ventral roots come together and exit the intervertebral foramina as they become spinal nerves.

The grey column, (as three regions of grey columns), in the center of the cord, is shaped like a butterfly and consists of cell bodies of interneurons, motor neurons, neuroglia cells and unmyelinated axons. The anterior and posterior grey column present as projections of the grey matter and are also known as the horns of the spinal cord. Together, the grey columns and the gray commissure form the “grey H.”

The white matter is located outside of the grey matter and consists almost totally of myelinated motor and sensory axons. “Columns” of white matter carry information either up or down the spinal cord.

Within the CNS, nerve cell bodies are generally organized into functional clusters, called nuclei. Axons within the CNS are grouped into tracts.

There are 31 spinal cord nerve segments in a human spinal cord:

In the fetus, vertebral segments correspond with spinal cord segments. However, because the vertebral column grows longer than the spinal cord, spinal cord segments do not correspond to vertebral segments in the adult, particularly in the lower spinal cord. For example, lumbar and sacral spinal cord segments are found between vertebral levels T9 and L2, and the spinal cord ends around the L1/L2 vertebral level, forming a structure known as the conus medullaris.

Although the spinal cord cell bodies end around the L1/L2 vertebral level, the spinal nerves for each segment exit at the level of the corresponding vertebra. For the nerves of the lower spinal cord, this means that they exit the vertebral column much lower (more caudally) than their roots. As these nerves travel from their respective roots to their point of exit from the vertebral column, the nerves of the lower spinal segments form a bundle called the cauda equina.

There are two regions where the spinal cord enlarges:

The spinal cord is made from part of the neural tube during development. There are four stages of the spinal cord that arises from the nueral tube: The neural plate, neural fold, neural tube, and the spinal cord. Neural differentiation occurs within the spinal cord portion of the tube.[4] As the neural tube begins to develop, the notochord begins to secrete a factor known as Sonic hedgehog or SHH. As a result, the floor plate then also begins to secrete SHH, and this will induce the basal plate to develop motor neurons. During the maturation of the neural tube, its lateral walls thicken and form a longtitudinal groove called the sulcus limitans. This exends the length of the spinal cord into dorsal and ventral portions as well.[5] Meanwhile, the overlying ectoderm secretes bone morphogenetic protein (BMP). This induces the roof plate to begin to secrete BMP, which will induce the alar plate to develop sensory neurons. Dorsal root ganglion neurons differentiate from neural crest progenitors. As the dorsal and ventral column cells proliferate, the lumen of the neural tube narrows to form the small central canal of the spinal cord.[6] The alar plate and the basal plate are separated by the sulcus limitans. Additionally, the floor plate also secretes netrins. The netrins act as chemoattractants to decussation of pain and temperature sensory neurons in the alar plate across the anterior white commissure, where they then ascend towards the thalamus. Following the closure of the caudal neuropore and formation of the brain’s ventricles that contain the choroid plexus tissue, the central canal of the caudal spinal cord is filled with cerebrospinal fluid.

Earlier findings by Viktor Hamburger and Rita Levi-Montalcini in the chick embryo have been confirmed by more recent studies which have demonstrated that the elimination of neuronal cells by programmed cell death (PCD) is necessary for the correct assembly of the nervous system.

Overall, spontaneous embryonic activity has been shown to play a role in neuron and muscle development but is probably not involved in the initial formation of connections between spinal neurons.

The spinal cord is supplied with blood by three arteries that run along its length starting in the brain, and many arteries that approach it through the sides of the spinal column. The three longitudinal arteries are called the anterior spinal artery, and the right and left posterior spinal arteries.[7] These travel in the subarachnoid space and send branches into the spinal cord. They form anastamoses (connections) via the anterior and posterior segmental medullary arteries, which enter the spinal cord at various points along its length.[7] The actual blood flow caudally through these arteries, derived from the posterior cerebral circulation, is inadequate to maintain the spinal cord beyond the cervical segments.

The major contribution to the arterial blood supply of the spinal cord below the cervical region comes from the radially arranged posterior and anterior radicular arteries, which run into the spinal cord alongside the dorsal and ventral nerve roots, but with one exception do not connect directly with any of the three longitudinal arteries.[7] These intercostal and lumbar radicular arteries arise from the aorta, provide major anastomoses and supplement the blood flow to the spinal cord. In humans the largest of the anterior radicular arteries is known as the artery of Adamkiewicz, or anterior radicularis magna (ARM) artery, which usually arises between L1 and L2, but can arise anywhere from T9 to L5.[8] Impaired blood flow through these critical radicular arteries, especially during surgical procedures that involve abrupt disruption of blood flow through the aorta for example during aortic aneursym repair, can result in spinal cord infarction and paraplegia.

Somatosensory organization is divided into the dorsal column-medial lemniscus tract (the touch/proprioception/vibration sensory pathway) and the anterolateral system, or ALS (the pain/temperature sensory pathway). Both sensory pathways use three different neurons to get information from sensory receptors at the periphery to the cerebral cortex. These neurons are designated primary, secondary and tertiary sensory neurons. In both pathways, primary sensory neuron cell bodies are found in the dorsal root ganglia, and their central axons project into the spinal cord.

In the dorsal column-medial leminiscus tract, a primary neuron’s axon enters the spinal cord and then enters the dorsal column. If the primary axon enters below spinal level T6, the axon travels in the fasciculus gracilis, the medial part of the column. If the axon enters above level T6, then it travels in the fasciculus cuneatus, which is lateral to the fasciculus gracilis. Either way, the primary axon ascends to the lower medulla, where it leaves its fasciculus and synapses with a secondary neuron in one of the dorsal column nuclei: either the nucleus gracilis or the nucleus cuneatus, depending on the pathway it took. At this point, the secondary axon leaves its nucleus and passes anteriorly and medially. The collection of secondary axons that do this are known as internal arcuate fibers. The internal arcuate fibers decussate and continue ascending as the contralateral medial lemniscus. Secondary axons from the medial lemniscus finally terminate in the ventral posterolateral nucleus (VPL) of the thalamus, where they synapse with tertiary neurons. From there, tertiary neurons ascend via the posterior limb of the internal capsule and end in the primary sensory cortex.

The proprioception of the lower limbs differs from the upper limbs and upper trunk. There is a four-neuron pathway for lower limb proprioception. This pathway initially follows the dorsal spino-cerebellar pathway. It is arranged as follows: proprioceptive receptors of lower limb -> peripheral process -> dorsal root ganglion -> central process -> Clarke’s column -> 2nd order neuron -> medulla oblogata (Caudate nucleus) -> 3rd order neuron -> VPL of thalamus -> 4th order neuron -> posterior limb of internal capsule -> corona radiata -> sensory area of cerebrum.

The anterolateral system works somewhat differently. Its primary neurons axons enter the spinal cord and then ascend one to two levels before synapsing in the substantia gelatinosa. The tract that ascends before synapsing is known as Lissauer’s tract. After synapsing, secondary axons decussate and ascend in the anterior lateral portion of the spinal cord as the spinothalamic tract. This tract ascends all the way to the VPL, where it synapses on tertiary neurons. Tertiary neuronal axons then travel to the primary sensory cortex via the posterior limb of the internal capsule.

It should be noted that some of the “pain fibers” in the ALS deviate from their pathway towards the VPL. In one such deviation, axons travel towards the reticular formation in the midbrain. The reticular formation then projects to a number of places including the hippocampus (to create memories about the pain), the centromedian nucleus (to cause diffuse, non-specific pain) and various parts of the cortex. Additionally, some ALS axons project to the periaqueductal gray in the pons, and the axons forming the periaqueductal gray then project to the nucleus raphes magnus, which projects back down to where the pain signal is coming from and inhibits it. This helps control the sensation of pain to some degree.

The corticospinal tract serves as the motor pathway for upper motor neuronal signals coming from the cerebral cortex and from primitive brainstem motor nuclei.

Cortical upper motor neurons originate from Brodmann areas 1, 2, 3, 4, and 6 and then descend in the posterior limb of the internal capsule, through the crus cerebri, down through the pons, and to the medullary pyramids, where about 90% of the axons cross to the contralateral side at the decussation of the pyramids. They then descend as the lateral corticospinal tract. These axons synapse with lower motor neurons in the ventral horns of all levels of the spinal cord. The remaining 10% of axons descend on the ipsilateral side as the ventral corticospinal tract. These axons also synapse with lower motor neurons in the ventral horns. Most of them will cross to the contralateral side of the cord (via the anterior white commissure) right before synapsing.

The midbrain nuclei include four motor tracts that send upper motor neuronal axons down the spinal cord to lower motor neurons. These are the rubrospinal tract, the vestibulospinal tract, the tectospinal tract and the reticulospinal tract. The rubrospinal tract descends with the lateral corticospinal tract, and the remaining three descend with the anterior corticospinal tract.

The function of lower motor neurons can be divided into two different groups: the lateral corticospinal tract and the anterior cortical spinal tract. The lateral tract contains upper motor neuronal axons which synapse on dorsal lateral (DL) lower motor neurons. The DL neurons are involved in distal limb control. Therefore, these DL neurons are found specifically only in the cervical and lumbosacral enlargements within the spinal cord. There is no decussation in the lateral corticospinal tract after the decussation at the medullary pyramids.

The anterior corticospinal tract descends ipsilaterally in the anterior column, where the axons emerge and either synapse on lower ventromedial (VM) motor neurons in the ventral horn ipsilaterally or descussate at the anterior white commissure where they synapse on VM lower motor neurons contralaterally . The tectospinal, vestibulospinal and reticulospinal descend ipsilaterally in the anterior column but do not synapse across the anterior white commissure. Rather, they only synapse on VM lower motor neurons ipsilaterally. The VM lower motor neurons control the large, postural muscles of the axial skeleton. These lower motor neurons, unlike those of the DL, are located in the ventral horn all the way throughout the spinal cord.

Proprioceptive information in the body travels up the spinal cord via three tracks. Below L2, the proprioceptive information travels up the spinal cord in the ventral spinocerebellar tract. Also known as the anterior spinocerebellar tract, sensory receptors take in the information and travel into the spinal cord. The cell bodies of these primary neurons are located in the dorsal root ganglia. In the spinal cord, the axons synapse and the secondary neuronal axons decussates and then travel up to the superior cerebellar peduncle where they decussate again. From here, the information is brought to deep nuclei of the cerebellum including the fastigial and interposed nuclei.

From the levels of L2 to T1, proprioceptive information enters the spinal cord and ascends ipsilaterally, where it synapses in Clarke’s nucleus. The secondary neuronal axons continue to ascend ipsilaterally and then pass into the cerebellum via the inferior cerebellar peduncle. This tract is known as the dorsal spinocerebellar tract.

From above T1, proprioceptive primary axons enter the spinal cord and ascend ipsilaterally until reaching the accessory cuneate nucleus, where they synapse. The secondary axons pass into the cerebellum via the inferior cerebellar peduncle where again, these axons synapse on cerebellar deep nuclei. This tract is known as the cuneocerebellar tract.

Motor information travels from the brain down the spinal cord via descending spinal cord tracts. Descending tracts involve two neurons: the upper motor neuron (UMN) and lower motor neuron (LMN).[9] A nerve signal travels down the upper motor neuron until it synapses with the lower motor neuron in the spinal cord. Then, the lower motor neuron conducts the nerve signal to the spinal root where efferent nerve fibers carry the motor signal toward the target muscle. The descending tracts are composed of white matter. There are several descending tracts serving different functions. The corticospinal tracts (lateral and anterior) are responsible for coordinated limb movements.[9]

A congenital disorder is diastematomyelia in which part of the spinal cord is split usually at the level of the upper lumbar vertebrae. Sometimes the split can be along the length of the spinal cord.

Spinal cord injuries can be caused by trauma to the spinal column (stretching, bruising, applying pressure, severing, laceration, etc.). The vertebral bones or intervertebral disks can shatter, causing the spinal cord to be punctured by a sharp fragment of bone. Usually, victims of spinal cord injuries will suffer loss of feeling in certain parts of their body. In milder cases, a victim might only suffer loss of hand or foot function. More severe injuries may result in paraplegia, tetraplegia (also known as quadriplegia), or full body paralysis below the site of injury to the spinal cord.

Damage to upper motor neuron axons in the spinal cord results in a characteristic pattern of ipsilateral deficits. These include hyperreflexia, hypertonia and muscle weakness. Lower motor neuronal damage results in its own characteristic pattern of deficits. Rather than an entire side of deficits, there is a pattern relating to the myotome affected by the damage. Additionally, lower motor neurons are characterized by muscle weakness, hypotonia, hyporeflexia and muscle atrophy.

Spinal shock and neurogenic shock can occur from a spinal injury. Spinal shock is usually temporary, lasting only for 2448 hours, and is a temporary absence of sensory and motor functions. Neurogenic shock lasts for weeks and can lead to a loss of muscle tone due to disuse of the muscles below the injured site.

The two areas of the spinal cord most commonly injured are the cervical spine (C1-C7) and the lumbar spine (L1-L5). (The notation C1, C7, L1, L5 refer to the location of a specific vertebra in either the cervical, thoracic, or lumbar region of the spine.) Spinal cord injury can also be non-traumatic and caused by disease (transverse myelitis, polio, spina bifida, Friedreich’s ataxia, spinal cord tumor, spinal stenosis etc.)[10]

In the U.S., 10,000-12,000 people become paralyzed annually as a result of various injuries to the spinal cord.[citation needed]

Real or suspected spinal cord injuries need immediate immobilisation including that of the head. Scans will be needed to assess the injury. A steroid, methylprednisolone, can be of help as can physical therapy and possibly antioxidants.[citation needed] Treatments need to focus on limiting post-injury cell death, promoting cell regeneration, and replacing lost cells. Regeneration is facilitated by maintaining electric transmission in neural elements. Replacement of lost cells is facilitated by transplants with embryonic stem cells, stem cells from the spinal cord, and spinal cord cells from fetuses.

The spinal cord ends at the level of vertebrae L1L2, while the subarachnoid space the compartment that contains cerebrospinal fluid extends down to the lower border of S2.[10]Lumbar punctures in adults are usually performed between L3L5 (cauda equina level) in order to avoid damage to the spinal cord.[10] In the fetus, the spinal cord extends the full length of the spine and regresses as the body grows.

Spinal tumours can occur in the spinal cord and these can be either inside (intradural) or outside (extradural) the dura mater.

Spinal Cord Sectional Anatomy. Animation in the reference.

Diagrams of the spinal cord.

Cross-section through the spinal cord at the mid-thoracic level.

Cross-sections of the spinal cord at varying levels.

A portion of the spinal cord, showing its right lateral surface. The dura is opened and arranged to show the nerve roots.

The spinal cord with dura cut open, showing the exits of the spinal nerves.

The spinal cord showing how the anterior and posterior roots join in the spinal nerves.

The spinal cord showing how the anterior and posterior roots join in the spinal nerves.

A longer view of the spinal cord.

Projections of the spinal cord into the nerves (red motor, blue sensory).

Projections of the spinal cord into the nerves (red motor, blue sensory).

Cross-section of rabbit spinal cord.

Cross-section of adult mouse spinal cord: astrocytes (red) and neurons (green)

An overview of the spinal cord.

Sagittal section of pig vertebrae showing a section of the spinal cord.

The base of the brain and the top of the spinal cord

Spinal cord. Spinal membranes and nerve roots.Deep dissection. Posterior view.

Spinal cord. Spinal membranes and nerve roots.Deep dissection. Posterior view.

Spinal cord. Spinal membranes and nerve roots.Deep dissection. Posterior view.

Spinal cord. Spinal membranes and nerve roots.Deep dissection. Posterior view.

Spinal cord. Spinal membranes and nerve roots.Deep dissection. Posterior view.

Spinal cord. Spinal membranes and nerve roots.Deep dissection. Posterior view.

Spinal cord. Spinal membranes and nerve roots.Deep dissection. Posterior view.

Cerebrum.Inferior view.Deep dissection

Cerebrum.Inferior view.Deep dissection

Spinal cord. Brachial plexus. Cerebrum.Inferior view.Deep dissection.

Spinal cord. Brachial plexus. Cerebrum.Inferior view.Deep dissection.

Medulla spinalis of 8-week-old human embryo

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Spinal cord – Wikipedia

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TCM Recipe | Best Homemade Herbal Eczema Cream

Posted: December 1, 2016 at 8:43 pm

We have proof that TCM Recipe will heal your irritated skin. Countless eczema sufferers have experienced tremendous recovery by applying this all-natural nutrient extract made from traditional Chinese herbs. TCM Recipe will inspire new and healthy skin growth to help you outgrow your itchy Eczema for good!

Have you ever realized that most over-the-counter creams for your eczema need to be reapplied constantly, even when your skin appears healed, or else the irritation will return? Whats even worse is their effectiveness decreases the more often they are used. Thats why youre always forced to replace your remedy with stronger and stronger creams to maintain a clear complexion.

Believe it or not, youre suffering from a vicious cycle called the skin cream addiction and withdrawal. Are you aware that steroids are not the only creams that cause addiction? In fact, even the chemicals found in most moisturizers can lead to a serious and scary addiction too!

The more often you use them, the more dependent you become on them, and eventually you reach the point where you cant start your day without them. Do you remember the last day that you didnt need to lather moisturizer all over your skin?

Please read the following facts carefully

Its true that stronger pharmaceutical remedies may heal your Eczema initially, but they contain dangerous ingredients that will leave a long-term effect on your health. These so-called remedies can quickly turn into a fierce and potentially deadly addiction. An Ohio State University clinical study conducted by their professor of dermatology revealed numerous hazardous chemicals in many popular moisturizers:

These chemicals are not only harming your skin but they also flow into your blood stream and destroy your internal health. Your Eczema remedy will end up doing more harm than good if you cant break your addiction cycle.

Most people are careful about what they eat to avoid ingesting harmful toxins. These same health-conscious people fail to realize that they are consuming more toxic chemicals through their skin than their mouths. Our skin is the largest organ in our body and it has the greatest potential for absorbing harmful toxins.

This is especially dangerous to you as an Eczema sufferer because of your repeated exposure to hazardous chemicals. Most Eczema moisturizers contain countless of harmful chemicals and you are deliberately rubbing them into your skin each day.

If you are not worried now, think about how it will affect you 5 years from now.

What will happen 5 years down the road when your addiction reaches its maximum level? What will you do when the fiery flare-ups start taking over every inch of your skin from your scalp to your feet?

What if those toxic creams are no longer giving you any real relief?

Thats where TCM Recipe fits in.

We dont cause addiction. We beat your addiction!

TCM Recipe enables you to live independently without having to apply chemically based creams every single day for the rest of your life. And after youve established a great skin condition, you wont even need us to feel relief!

Youll experience and enjoy living a joyful life full of enthusiasm again. Youll soon forget the bad memories of Eczema like the rest of our happy customers! Thats what we at TCM Recipe called a REAL recovery.

Hows that possible?

Contrary to all those remedies youve tried, TCM recipe combines genuine herbs known by ancient skincare therapists to have superior skin healing properties. The specialized mixture of ingredients creates a remarkable formula designed to target the root cause of your Eczema and treat it.

Its very simple. TCM recipe will repair and strengthen your damaged epidermis and internal skin structure. Our effective remedy will restore your skins functionalities so it can heal by itself.

Dont you agree thats how healthy skin should be?

Plus, one of our special ingredients actually vanquishes your past addictions and leaves NO SIDE EFFECTS behind. TCM Recipe is a laboratory proven and time tested remedy thats 100% safe and natural. Weve worked hard to win our reputation and we work even harder to keep it.

Heres our official lab test approved and validated by the National Poison Centre, Malaysias most respected authority for lab testing.

We want to make this very clear. If you are looking for an instant cure that promises to solve all your Eczema symptoms overnight, this remedy is not for you. Cures that claim magical results will always have less than magical side effects.

This is for people who are serious about treating their Eczema naturally before it gets even worse. This is for sufferers who have lost hope in harmful conventional medication and want to pursue our traditional way of healing.

We have devoted our passion and time to healing your skin. Over the past 9 years, weve familiarized ourselves with every nuance of Eczema through case studies. No other authority honors the same crystal-clear understanding of this disease.

You see, Eczema is more than just a skin disease. It also indirectly affects your wellbeing, from your physical to mental health. The longer you leave it untreated, the more negative consequences you will suffer. The condition will eventually rob your health and keep you from enjoying the basic pleasures of life.

But luckily, we found the right solution to overcome your problems. Now, lets walk through how TCM Recipe can positively change your life today

Smile while you sleep!

Enjoy the luxury of a full night sleep once again. There will be no more insatiable scratching keeping you awake at night! You can now enjoy sweet dreams soundly until the sun rises without any interruptions. And once you get your sleep back, both your mental and physical health will recover.

Every expert agrees that quality sleep promotes faster healing, especially when it comes to treating your Eczema skin.Insomnia on the other hand will cause stress, stunt new skin growth, and increase your chance of developing depression.

Brings back the vitality in you

Triple your productivity and concentration. Finally! You will stay focused and perform better in your daily tasks when youre not distracted by annoying itching! The best part is that you will regain enough energy to handle your busy workload without feeling fatigued. You will never need to take histamine once you have TCM Recipe!

Stop taking those medicines that make you drowsy and start enjoying your life now! You will quickly realize how dramatic your appetite and mood can simultaneously improve once you are getting a good nights sleep.

Postpone no more, have fun!

Banish your never-ending flare-ups. TCM Recipe will stop your furious flare-ups by cooling down your skin inflammation. Once your inflammation cools down, you can just relax and allow TCM Recipe to stabilize your skin.

We created this remedy to strengthen your skins natural barrier and to prevent your Eczema from rebounding easily. By strengthening the barrier of your skin, it will become more resilient and wont breakout so easily even if you scratch it!

Thats how TCM Recipe actually works to rebuild the core foundation of your skin. It replenishes your radiant and youthful complexion one step at a time. This simply means that youll never need to put your important outings on hold because of unpredictable skin flare-up(s)!

Lets make your birthday party a memorable one!

The kind of vigorous skin youve been waiting for! What if you will never have to experience that painful sensation of water splashing on your skin during a shower again?

We know how hard simple daily tasks can be when you suffer from Eczema. Thats why we have developed this remedy to solve your external skin problems while alleviating your skins internal sensitivity.

We want you to enjoy a normal and healthy life where you can take a shower and swim in a pool without pain. You will never lose out on any precious moments with your friends and family again because of your Eczema! Sounds too good to be true? Let our customers vouch for our credibility.

Rise and shine!!

Put an End to Your Endless Oozing! Still frustrated with the pus oozing from your hives? TCM Recipe is the only remedy you will ever need to cover up your discoid wounds delicately.

Our remedy will help you to regenerate new skin tissue to seal all your wounded parts. And believe it or not, the day you wake up and realize that your pus and bloodstains have totally disappeared from your clean clothes and comfy bed is a day youll never forget.

Walk on the streets the way you are

Clearing Your Rashes Made Easy. Do you dream of you wearing short sleeve clothing confidently anytime anywhere? And just simply enjoying your social life with friends and family while feeling no embarrassment at all?

The good news is turning irritating rashes into pleasant-looking skin is what we do best. As you keep using TCM Recipe, you will witness your rashes subside into a light pinkish colour and then slowly begin to renew with a firm layer of smooth skin.

Are you ready to silence the rude remarks about your skin? Let us prove to you that we can help you to end all the gossip and weird staring youve been enduring right now!

Absorb, retain and moisturize your skin

Ensure your skins comfort and moisture all day long! We know your skin still remains rough and flaky after numerous applications of other moisturizers. Apparently theyre just making your skin wet NOT moisturized.

Consider this fact: people without Eczema dont need moisturizers and they are still comfortable with their skin. This is what we are delivering to you! TCM Recipe will gently soothe your dry skin and quench its thirst! Its the only way to retain all the moisture in your skin.

As a result, youll experience the joy of living the lifestyle everybody else is talking about. Never again you will need to bring a bag full of creams along with you every time you travel.

Everybody is born with beautiful skin

Revive your skins breathability. Getting your skin moisturized is only half the battle. Breathability is vital to keep your skin healthy long term. Without the ability to breathe, your skin cant sweat and you wont be able to excrete toxins from your body.

TCM Recipe encourages the excretion of toxins and waste materials that clog your skin pores. After the detoxification process, you will see your skin pores grow vibrantly. You CAN actually feel your skin breathing! Its that refreshing!

Dont let your scars ruin your day!

Removing your scars is our specialty! Truth be told, TCM Recipe is not perfect. We cant remove your scars instantly or even within days. Lets face it, everybodys skin condition is different and eczema scars are extremely stubborn.

Normally it takes 5-8 weeks to separate your scars from your skin so they exist just on the surface. Once there, you can simply remove them manually with your bare hands in 2 quick and easy steps. Well show you how once you buy TCM Recipe today.

Even though it has to be done by hand, there is no doubt that youre going to love this amazing experience of removing your ugly scars for good! Get your hands on our remedy today. The sooner you try TCM Recipe, the sooner you can get rid of those unwanted scars!

The key is treating your Eczema from the root

Why is removing your scars so important? Did you know that scars are a big part of the reason why your Eczema spreads like wild fire from one area to another?

Eczema scars occur after you suppress your Eczema rashes with inappropriate medication. The tricky part is that they may look benign. In reality, they are like those inconspicuous weeds that spread their roots and pollen all over the place.

Remember the last time you pulled the weeds in your garden? They grew back again in weeks, even tougher and more resilient! The same principle applies here. Your eczema lies just underneath your scars waiting to infect the next wound that you scratch.

Unlike other remedy companies, we insist on providing you with sunshine fresh herbs the way nature made them. Dont fall for those saturated advertising tactics such as Dermatological Tested or 100 % Natural. Many employees who work for these companies dont even dare to use their creams on their own skin long-term! Why should you?

Call us old fashioned but we remain dedicated to protecting you from all those commercial fragrances, artificial colours and wicked chemicals.Your skin is your asset! Why pay money to harm it?

Dont worry! Now your valuable asset is fully protected by us. We care about the longevity of our remedy and the wellbeing of your skin. We are also proud to say that you cant find any complex or weird chemical names on our active ingredient list. We searched far and wide for these rare herbs to ensure the highest quality. See for yourself:

Natural Ingredient #1: Glycyrrhiza Uralensis(Chinese Licorice)

Ancient Egyptians drank Licorice and used it as a pharmaceutical ingredient to treat skin diseases, loss of hair, stomach bleeding and even bronchitis. In TCM, Licorice act as a potent antiviral and anti-allergic agent to fight fungal infections, treat canker sores, herpes, Eczema, and psoriasis.

The book, The Way of Chinese Herbs refers to Licorice as the great detoxifier because of its ability to remove various toxins from the body and for its nature of harmonizing the qualities of other herbs. It also contains an amazing moisturizing component called Glycyrrhizinate.

The amazing anti-inflammatory actions of licorice root extend to the entire surface area of the body, both outside and inside. Not only the skin, but the mucous membranes of the gastrointestinal tract yield to the soothing and healing action of licorice root. The plant reinforces the bodys ability to withstand attack from virtually any kind of pathogen, and should therefore be considered a tonic for the musculoskeletal system. If one is looking for a broad-spectrum tonic to protect, maintain health, and heal injuries, there is no herb better than licorice root. Dr. John R. Christopher-Americas foremost herbalist, Founder of the School of Healing

Natural Ingredient #2: Ruellia Tuberosa Linn (Lu Li Hua)

This pretty lilac-colored flower originates from tropical America, but is naturalized in South East Asia (Thailand, Peninsular Malaysia, Java), as well as the tropics of India, Sri Lanka and Africa. Traditionally used to prevent stomach problems, Ruellia Tuberosa also reduces fever and alleviates pain. As a matter of fact, this plant also produces sun and salt spray that acts to reduce sensitivity, painful stimulus, and as an anti-inflammatory for skin problems. It has been scientifically proven to possess anti-microbial, anti-cancer properties as well as the ability to counteract the effect of poisons.

Natural Ingredient #3: Fritillaria Cirrhosa (Chuan Bei Mu)

In the West, Fritillaria is most commonly known as an ornamental garden plant. However, in Nepal and China, this plant has traditional value as an herbal remedy. For thousands of years, Asians have used Fritillaria to clear away heat, disperse the accumulation of pathogens and to moisten lung dryness due to Yin deficiency. Using medications prepared with Fritillaria helps counter the effects of toxic exposure. Its also very effective in treating influenza and lupus (a deadly skin disorder).

Natural Ingredient #4: Bambusa Tuldoides Munro (Zhu Qing)

The cooling nature of bamboo shavings acts as a great calming agent for dispersing constrained Qi. It calms the mind, eliminates irritability, and soothes the skin when applied directly through lotions. Modern analysis of bamboo indicates that it contains 88.8 % moisture, 3.9 % protein, 0.5 % fat, 11 % minerals, and 5.7 % carbohydrates. The minerals found in bamboo include calcium, phosphorus, iron, thiamine, riboflavin, niacin, and vitamin C, making it very valuable as a curative for your Eczema skin.

The flavone and lactone in bamboo shavings extract offer powerful anti-oxidants that help minimize wrinkles and boost youthful radiance. As you may know, a layer of natural wax lies on the green outer skin of bamboo shavings. We use this wax as the base of our ointment. Now you know why our remedy is 100% genuine. Even our wax is made from a natural herb.

Natural Ingredient #5: Angelica Dahurica (Bai Zhi)

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Hormone replacement therapy (female-to-male) – Wikipedia

Posted: November 30, 2016 at 8:44 pm

Hormone replacement therapy (HRT) of the female-to-male (FTM) type is a form of hormone therapy and sex reassignment therapy that is used to change the secondary sexual characteristics of transgender and transsexual people from feminine (or androgynous) to masculine. It is one of two types of HRT for transgender and transsexual people, the other being male-to-female, and is predominantly used to treat transgender men. Some intersex people also receive this form of HRT, either starting in childhood to confirm the assigned sex or later if the assignment proves to be incorrect.

The purpose of this form of HRT is to cause the development of the secondary sex characteristics of the desired sex, such as voice deepening and a masculine pattern of hair, fat, and muscle distribution. It cannot undo many of the changes produced by naturally occurring puberty, which may necessitate surgery and other treatments (see below). The medications used in HRT of the FTM type include, mainly, androgens (namely testosterone) and GnRH analogues.

While HRT cannot undo the effects of a person first puberty, developing secondary sex characteristics associated with a different gender can relieve some or all of the distress and discomfort associated with gender dysphoria, and can help the person to “pass” or be seen as the gender they identify with. Introducing exogenous hormones into the body impacts it at every level and many patients report changes in energy levels, mood, appetite, etc. The goal of HRT, and indeed all somatic treatments, is to provide patients with a more satisfying body that is more congruent with their true psychological gender identity.

Several contraindications to androgen therapy exist.[1] An absolute medical contraindication is pregnancy.

Relative medical contraindications are:

Testosterone is metabolized by the cytochrome P450 enzyme system (specifically CYP3A isoforms) in the liver. There are certain drugs that increase or decrease the activity of cytochrome P450 enzymes and may cause increased or decreased levels of testosterone:

Testosterone can also alter the effects of other drugs:

Because of these interactions, it is advised that trans men make their healthcare providers aware of their hormone therapy, when this is relevant to their treatment for other medical issues.

The terminal half-life of testosterone in blood is about 70 minutes, so it is necessary to have a continuous supply of the hormone for masculinization.

‘Depot’ drug formulations are created by mixing a substance with the drug that slows its release and prolongs the action of the drug. The two primarily used forms in the United States are the testosterone esters testosterone cypionate (Depo-Testosterone) and testosterone enanthate (Delatestryl) which are almost interchangeable. Testosterone enanthate is purported to be slightly better with respect to even testosterone release, but this is probably more of a concern for bodybuilders who use the drugs at higher doses (2501000mg/week) than the replacement doses used by transgender men (50100mg/week). These testosterone esters are mixed with different oils, so some individuals may tolerate one better than the other. Testosterone enanthate costs more than testosterone cypionate and is more typically the one prescribed for hypogonadal males in the United States. Testosterone cypionate is more popular in the United States than elsewhere (especially amongst bodybuilders). Other formulations exist but are more difficult to come by in the United States. A formulation of injected testosterone available in Europe and the United States, testosterone undecanoate (Nebido, Aveed)[2] provides significantly improved testosterone delivery with far less variation outside the eugonadal range than other formulations with injections required only four times yearly. However, each quarterly dose requires injection of 4mL of oil which may require multiple simultaneous injections. Testosterone undecanoate is also much more expensive as it is still under patent protection. Testosterone propionate is another testosterone ester that is widely available, including in the United States, Canada, and Europe, but it is very short-acting compared to the other testosterone ethers and must be administered once every 2 or 3 days, and for this reason, is rarely used.

The adverse side effects of injected testosterone esters are generally associated with high peak levels in the first few days after an injection. Some side effects may be ameliorated by using a shorter dosing interval (weekly or every ten days instead of twice monthly with testosterone enanthate or testosterone cypionate). 100mg weekly gives a much lower peak level of testosterone than does 200mg every two weeks, while still maintaining the same total dose of androgen. This benefit must be weighed against the discomfort and inconvenience of doubling the number of injections.

Injected testosterone esters should be started at a low dose and titrated upwards based on trough levels (blood levels drawn just before your next shot). A trough level of 500ng/dl is sought. (Normal range for a cisgender male is 290 to 900ng/dl).

Both testosterone patches, creams and gels are available. Both approximate normal physiological levels of testosterone better than the higher peaks associated with injection. Both can cause local skin irritation (more so with the patches).

Patches slowly diffuse testosterone through the skin and are replaced daily. The cost varies, as with all medication, from country to country, it is about $150/month in the US, and about 60 Euros in Germany.

Transdermal testosterone is available throughout the world under the brand names Andromen Forte, Androgel, Testogel and Testim. They are absorbed quickly when applied and produce a temporary drug depot in the skin which diffuses into the circulation, peaking at 4 hours and decreasing slowly over the rest of the day. The cost varies, as with all medication, from country to country, from as little as $50/month to about $280/month (in US Dollars).

Transdermal testosterone poses a risk of inadvertent exposure to others who come in contact with the patient’s skin. This is most important for patients whose intimate partners are pregnant or those who are parents of young children as both of these groups are more vulnerable to the masculinizing effects of androgens. Case reports of significant virilization of young children after exposure to topical androgen preparations (both prescription and ‘supplement’ products) used by their caregivers demonstrates this very real risk.

Implants, as subcutaneous pellets, can be used to deliver testosterone (brand name Testopel). 6 to 12 pellets are inserted under the skin every three months. This must be done in a physician’s office, but is a relatively minor procedure done under local anesthetic. Pellets cost about $60 each, so the cost is greater than injected testosterone when the cost of the physician visit and procedure are included. The primary advantages of Testopel are that it gives a much more constant blood level of testosterone yet requires attention only four times yearly.

Oral testosterone is provided exclusively as testosterone undecanoate. It is available in Europe and Canada, but not in the United States. Once absorbed from the gastrointestinal tract, testosterone is shunted (at very high blood levels) to the liver where it can cause liver damage (albeit very rarely) and worsens some of the adverse effects of testosterone, like lower HDL (good) cholesterol. In addition, the first pass metabolism of the liver also may result in testosterone levels too low to provide satisfactory masculinization and suppress menses. Because of the short terminal half-life of testosterone, oral testosterone undecanoate must be administered two to four times per day, preferably with food (which improves its absorption).

In 2003 the FDA approved a buccal form of testosterone (Striant). Sublingual testosterone can also be made by some compounding pharmacies. Cost for Striant is greater than other formulations ($180210/month). Testosterone is absorbed through the oral mucosa and avoids the ‘first pass metabolism’ in the liver which is cause of many of the adverse effect with oral testosterone undecanoate. The lozenges can cause gum irritation, taste changes, and headache but most side effects diminish after two weeks. The lozenge is ‘mucoadhesive’ and must be applied twice daily.

Synthetic anabolic-androgenic steroids (AAS), like nandrolone (as an ester like nandrolone decanoate or nandrolone phenylpropionate), are agonists of the androgen receptor (AR) similarly to testosterone but are not usually used in HRT for transgender men or for androgen replacement therapy (ART) in cisgender men. However, they can be used in place of testosterone with similar effects, and can have certain advantages like less or no local potentiation in so-called androgenic tissues that express 5-reductase like the skin and hair follicles (which results in a reduced rate of skin and hair-related side effects like acne, oily skin, seborrhea, excessive body hair growth, and, in particular, male-pattern baldness), although this can also be disadvantageous in a few aspects of masculinization (specifically facial hair growth, body hair growth, and clitoral enlargement). Although many AAS are not potentiated in androgenic tissues, they have similar effects to testosterone in other tissues like bone, muscle, fat, and the voice box. Also, many AAS, like nandrolone esters, are aromatized into estrogens to a greatly reduced extent relative to testosterone or not at all, and for this reason, are associated with reduced or no estrogenic effects (e.g., gynecomastia). AAS that are 17-alkylated like methyltestosterone, oxandrolone, and stanozolol are orally active but carry a high risk of liver damage, whereas AAS that are not 17-alkylated, like nandrolone esters, must be administered by intramuscular injection (via which they act as long-lasting depots similarly to testosterone esters) but have no more risk of liver damage than does testosterone.

For the sake of clarification, it should be noted that the term “anabolic-androgenic steroid” is essentially synonymous with “androgen” (or with “anabolic steroid”), and that natural androgens like testosterone are also AAS. These drugs all share the same core mechanism of action of acting as agonists of the AR and have similar effects, although their potency, pharmacokinetics, oral activity, ratio of anabolic to androgenic effects (due to differing capacities to be locally metabolized and potentiated by 5-reductase), capacity for aromatization (i.e., conversion into an estrogen), and potential for liver damage may all differ.

Dihydrotestosterone (DHT) (referred to as androstanolone or stanolone when used medically) can also be used in place of testosterone as an androgen. The availability of DHT is limited; it is not available in the United States or Canada, for instance, but it is available in certain European countries, including the United Kingdom, France, Spain, Belgium, Italy, and Luxembourg.[3] DHT is available in formulations including topical gel, buccal or sublingual tablets, and as esters in oil for intramuscular injection.[4] Relative to testosterone, and similarly to many synthetic AAS, DHT has the potential advantages of not being locally potentiated in so-called androgenic tissues that express 5-reductase (as DHT is already 5-reduced) and of not being aromatized into an estrogen (it is not a substrate for aromatase).

In all people, the hypothalamus releases GnRH (gonadotropin-releasing hormone) to stimulate the pituitary to produce LH (luteinizing hormone) and FSH (follicle-stimulating hormone) which in turn cause the gonads to produce sex steroids. In adolescents of either sex with relevant indicators, GnRH analogues, such as leuprorelin can be used to suspend the advance of sex steroid induced, inappropriate pubertal changes for a period without inducing any changes in the gender-appropriate direction. GnRH analogues work by initially over stimulating the pituitary then rapidly desensitizing it to the effects of GnRH. Over a period of weeks, gonadal androgen production is greatly reduced. There is considerable controversy over the earliest age, and for how long it is clinically, morally and legally safe to do this. The Harry Benjamin International Gender Dysphoria Association Standards of Care permit from Tanner Stage 2, but do not allow the addition of gender-appropriate hormones until 16, which could be five or more years. The sex steroids do have important other functions. The high cost of GnRH analogues is often a significant factor.

Antiestrogens (or so-called “estrogen blockers”) like aromatase inhibitors (AIs) (e.g., anastrozole) or selective estrogen receptor modulators (SERMs) (e.g., tamoxifen) can be used to reduce the effects of high levels of endogenous estrogen (e.g., breast development, feminine fat distribution) in transgender men. In addition, in those who have not yet undergone or completed epiphyseal closure (which occurs during adolescence and is mediated by estrogen), antiestrogens can prevent hip widening as well as increase final height (estrogen limits height by causing the epiphyses to fuse).

5-Reductase inhibitors like finasteride and dutasteride can be used to slow or prevent androgenic alopecia (pattern hair loss) and various other adverse androgenic symptoms (e.g., acne) in transgender men taking testosterone. However, they may also slow or reduce a few aspects of masculinization, such as facial and body hair growth and clitoral enlargement. A potential solution is to start taking a 5-reductase inhibitor after these desired aspects of masculinization have been established.

Depo-Provera (depot medroxyprogesterone acetate, or DMPA) may be injected every three months just as it is used for contraception. Generally after the first cycle, menses are greatly reduced or eliminated. This may be useful for transgender men prior to initiation of testosterone therapy.

In those who have not yet undergone or completed epiphyseal closure, growth hormone can be administered, potentially in conjunction with an aromatase inhibitor or a GnRH analogue, to increase final height.

The main effects of HRT of the FTM type are as follows:[5]

Many transgender men are unable to pass as cisgender men without hormones. The most commonly cited reason for this is that their voice may reveal them.

Facial changes develop gradually over time, and sexual dimorphism (physical difference between the sexes) tends to increase with age. Within a population of similar body size and ethnicity:

Frequently the first sign of endometrial cancer is bleeding in post-menopausal women. Transgender men who have any bleeding after the cessation of menses with androgen therapy should have an endometrial biopsy (and possibly an ultrasound) done to rule-out endometrial cancer.

A number of skeletal and cartilaginous changes take place after the onset of puberty at various rates and times. Sometime in the late teen years epiphyseal closure (in other words, the ends of bones are fused closed) takes place and the length of bones is fixed for life. Consequently, total height and the length of arms, legs, hands, and feet are not affected by HRT. However, details of bone shape change throughout life, bones becoming heavier and more deeply sculptured under the influence of testosterone. Many of these differences are described in the Desmond Morris book Manwatching.

The psychological changes are harder to define, since HRT is usually the first physical action that takes place when transitioning. This fact alone has a significant psychological impact, which is hard to distinguish from hormonally induced changes. Most trans men report an increase of energy and an increased sex drive. Many also report feeling more confident.

While a high level of testosterone is often associated with an increase in aggression, this is not a noticeable effect in most trans men. HRT doses of testosterone are much lower than the typical doses taken by steroid-using athletes, and create testosterone levels comparable to those of most cisgender men. These levels of testosterone have not been proven to cause more aggression than comparable levels of estrogen. It is assumed that the effect of the start of physical treatment is such a relief, and decreases pre-existing aggression so much, that the overall level of aggression actually decreases.

Some transgender men report mood swings, increased anger, and increased aggressiveness after starting androgen therapy. Many transgender men, however, report improved mood, decreased emotional lability, and a lessening of anger and aggression.

During HRT, especially in the early stages of treatment, blood work should be consistently done to assess hormone levels and liver function.

Israel et al. have suggested that for pre-oophorectomy trans men, therapeutic testosterone levels should optimally fall within the normal male range, whereas estrogen levels should optimally fall within the normal female range. Before oophorectomy, it is difficult and frequently impractical to fully suppress estrogen levels into the normal male range, especially with exogenous testosterone aromatizing into estrogen, hence why the female ranges are referenced instead. In post-oophorectomy trans men, Israel et al. recommend that both testosterone and estrogen levels fall exactly within the normal male ranges. See the table below for all of the precise values they suggest.[7]

The optimal ranges listed for testosterone only apply to individuals taking bioidentical hormones in the form of testosterone (including esters) and do not apply to those taking synthetic AAS (e.g., nandrolone) or dihydrotestosterone.

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Hormone replacement therapy (female-to-male) – Wikipedia

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10 Home Remedies for Eczema – eczema.net

Posted: November 29, 2016 at 11:44 am

Posted on June 29, 2012 at 5:27 pm.

Some of these triggers may originate from your home and others may not. Either way, you can find many solutions to these triggers in your home.

Here are 10 of the best home remedies for eczema that experts recommend using to stop the itch, reduce the swelling, and erase the redness.

The soap you clean your clothes with could be amplifying the burn in your skin. Avoid laundry detergents that use harsh ingredients, and instead choose those that are fragrance-free and neutral pH. You may even want to put your clothes on the double rinse cycle to ensure that all the soap gets washed out of them.

Rule #1 of eczema prevention is no scratching. When youre awake, this is something you have complete control over, but what happens when youre asleep? Wearing gloves to bed can help you avoid unconsciously scratching in your sleep.

Long hot showers dry out your skin quickly, which causes your eczema to flare up. To minimize the itching, take warm showers for no longer than 15 minutes. Thoroughly dry your skin when you get out of the shower and seal in your skins moisture with a gentle, fragrance-free lotion.

If you happen to have some hydro-cortisone or calamine lying around, these creams make great home remedies for eczema. Besides providing you with instant relief from the burn and itch of eczema, these creams can eliminate the rash.

A dry, hot climate is not a conducive environment for skin that is affected by eczema. If moving to a better climate isnt an option, use a humidifier to put some moisturize back into your surroundings. Make sure to clean the humidifier often to prevent the growth of harmful germs.

When mercury goes up, it could cause your eczema symptoms to go up too. Apply a cold compress to the areas of your skin that are affected by eczema. Stay inside air-conditioned buildings as much as you can. Wear clothes that are cool and lightweight to minimize sweating.

Unfortunately, you cant shed your scaly skin like a snake does, but you can reduce the scales by rubbing olive oil into your skin. Olive oil also has anti-inflammatory properties that could help reduce the redness and itching.

If you dont plan on eating those strawberries in your refrigerator, you can use them to make a great home remedy for eczema. Blend up the strawberries to make a paste and apply it to your eczema. This should reduce pain, redness, and inflammation.

Although the underlying cause of eczema is unknown, some experts say its caused by a weak immune system. The probiotics that are found in live culture yogurt and kefir can help boost your immune system; making you less likely to break out.

Use a quality eczema treatment. Exzaderm is full of skin-conditioning oils that moisturize, soothe, and heal eczema-afflicted skin. This leading eczema treatment is also 100% safe and natural so it should cause any reactions or skin irritation. You can visit exzaderm.com to learn more!

With these home remedies for eczema in hand, you can effectively reduce the itching, swelling, and redness that come along with this troublesome skin condition. The best news is that these remedies work quickly; theyre affordable; and most of them can already be found in your home.

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10 Home Remedies for Eczema – eczema.net

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Eczema Products 2016 – Reviewed and Ranked

Posted: at 11:44 am

Disclosure: We pay our reviewers for their reviews. We are not compensated by companies for their reviews, but we are compensated for links and advertisements on our website. Click here for details.

Although over 34 million Americans suffer from symptoms of eczema every day, scientists still don’t know what causes it. Many experts think eczema occurs through an inherited tendency for the disease, and then is “triggered” by stress or other external factors.

Eczema usually causes the affected skin area to become very dry, itchy, red, and swollen. Sometimes the skin becomes cracked, crusty, scaly, and can even start to bleed. Always, the condition is irritating, frustrating, and embarrassing.

When looking at different eczema products, you want to consider a few factors. Some of these include:

TopConsumerReviews.com has reviewed and ranked the best eczema products available today. We hope this information helps you find relief from the eczema that you’re suffering from!

2016

Skin-e-Dip is an effective topical cream used for the relief of eczema symptoms and other skin problems. The website is simple and easy to use, and the product has many satisfied customers. Read More…

Healing Natural Oils comes with strong customer feedback, BBB rating and policies but the price tag may be a turn off for some. However, for those looking for an effective eczema relief, Healing Natural Oils is worth a try. Read More…

Zenmed offers several different products for a variety of skin disorders. The DermCare system is used in the relief of eczema. It consists of a lotion and cleanser, boasting all natural ingredients. Read More…

The Biogetica Company offers a variety of products for many different aliments. Five products are used in the relief of eczema, some specializing in wet eczema and others in dry eczema. This site would appeal to customers who appreciate the all-natural aspects of homeopathic products. Read More…

Tips to prepare your skin for winter

When it’s dry, it actually makes cracks and fissures that allow germs to enter the skin and create irritations and eczema. Skin care isn’t just about skin being dry or moisturized, but rather about the skin being protected and acting as a barrier.

Published:Mon, 28 Nov 2016 11:42:00 GMT

Learn All About Eczema In This Article

Life with eczema sufferers is unpredictable. One day your skin feels great, and the next it may be raw and inflamed. Then it may take weeks and even months to get rid of it. Here are tips to control your flare-ups. To help soothe dry, itchy skin that comes …

Published:Mon, 28 Nov 2016 09:56:00 GMT

Do YOU have eczema? Revealed, the 5 top tips to manage your flare-ups

The itching and burning of eczema can be excruciating, and it is a reality that affects one in 12 British adults. Some have had it all their life – a fifth of children develop eczema, usually before their first birthday. For others, it comes on suddenly …

Published:Thu, 17 Nov 2016 23:51:00 GMT

Robbie Williams’ wife Ayda Field addresses his crippling anxiety live on Loose Women, revealing it can get so bad his skin will “break out’

ROBBIE Williams’ wife Ayda Field has admitted the sinmger’s anxiety can get so bad, his skin will “break out” with eczema and he can’t even face seeing friends. The star addressed her husband’s battle with depression and anxiety live on Loose …

Published:Mon, 28 Nov 2016 05:29:00 GMT

What Are Eczema Symptoms? Plus 5 Natural Treatments

Eczema symptoms, which commonly include skin dryness and itchiness, affect about 20 percent of children (roughly one in five) and up to 4 percent of adults. Eczema, along with related skin conditions like dermatitis and allergies, tends to develop most …

Published:Sat, 19 Nov 2016 08:39:00 GMT

The 2017 pipeline report: What to know about next year’s launches

On the autoimmune front, Sanofi and Regeneron’s dupilumab is expected to gain approval as the first prescription drug solution for patients with severe eczema. In orphan indications, Roche is hard at work on a more convenient and less burdensome solution …

Published:Mon, 28 Nov 2016 11:44:00 GMT

Home remedies for eczema

Long sleeves on summer days and pants when it’s hot outside. Eczema, it’s a condition that most people try to hide. But there is relief and it doesn’t always have to come from your pharmacist. In fact some naturopathic doctors believe prescription …

Published:Thu, 24 Nov 2016 13:48:00 GMT

Farmers advised to buy sheep sires resistant to facial eczema

The best bet for farmers to overcome the disease challenge of facial eczema (FE) is to buy resistant rams, veterinarians say. About 20 people were given the advice at a Manawatu workshop about maximising scanning percentages in ewes and lamb survival.

Published:Sun, 27 Nov 2016 18:36:00 GMT

Your health: How to naturally relieve eczema

Hi Sandra, what can you suggest to naturally help relieve eczema/dermatitis, or to at least minimise its severity? Any help would be much appreciated! Thank you for your question. There are many reasons why the skin can become irritated and itchy, such as …

Published:Sat, 26 Nov 2016 17:37:00 GMT

Baby eczema

My 6 month old has really dry patches on her elbows and checks I know they’re bothering her because she keeps scratching at them. Does anyone know any natural remedies? I put coconut oil on it as much as possible and it helps but they won’t go away.

Published:Sun, 27 Nov 2016 14:13:00 GMT

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Spinal Cord Injuries – Medscape Reference

Posted: November 28, 2016 at 12:43 pm

Spinal cord injury (SCI), as with acute stroke, is a dynamic process. In all acute cord syndromes, the full extent of injury may not be apparent initially. Incomplete cord lesions may evolve into more complete lesions. More commonly, the injury level rises 1 or 2 spinal levels during the hours to days after the initial event. A complex cascade of pathophysiologic events related to free radicals, vasogenic edema, and altered blood flow accounts for this clinical deterioration. Normal oxygenation, perfusion, and acid-base balance are required to prevent worsening of the spinal cord injury.

Spinal cord injury can be sustained through different mechanisms, with the following 3 common abnormalities leading to tissue damage:

Destruction from direct trauma

Compression by bone fragments, hematoma, or disk material

Ischemia from damage or impingement on the spinal arteries

Edema could ensue subsequent to any of these types of damage.

Neurogenic shock refers to the hemodynamic triad of hypotension, bradycardia, and peripheral vasodilation resulting from severe autonomic dysfunction and the interruption of sympathetic nervous system control in acute spinal cord injury. Hypothermia is also characteristic. This condition does not usually occur with spinal cord injury below the level of T6 but is more common in injuries above T6, secondary to the disruption of the sympathetic outflow from T1-L2 and to unopposed vagal tone, leading to a decrease in vascular resistance, with the associated vascular dilatation. Neurogenic shock needs to be differentiated from spinal and hypovolemic shock. Hypovolemic shock tends to be associated with tachycardia.

Shock associated with a spinal cord injury involving the lower thoracic cord must be considered hemorrhagic until proven otherwise. In this article, spinal shock is defined as the complete loss of all neurologic function, including reflexes and rectal tone, below a specific level that is associated with autonomic dysfunction. That is, spinal shock is a state of transient physiologic (rather than anatomic) reflex depression of cord function below the level of injury, with associated loss of all sensorimotor functions.

An initial increase in blood pressure due to the release of catecholamines, followed by hypotension, is noted. Flaccid paralysis, including of the bowel and bladder, is observed, and sometimes sustained priapism develops. These symptoms tend to last several hours to days until the reflex arcs below the level of the injury begin to function again (eg, bulbocavernosus reflex, muscle stretch reflex [MSR]).

Spinal cord injuries may be primary or secondary. Primary spinal cord injuries arise from mechanical disruption, transection, or distraction of neural elements. This injury usually occurs with fracture and/or dislocation of the spine. However, primary spinal cord injury may occur in the absence of spinal fracture or dislocation. Penetrating injuries due to bullets or weapons may also cause primary spinal cord injury. More commonly, displaced bony fragments cause penetrating spinal cord and/or segmental spinal nerve injuries.

Extradural pathology may also cause a primary spinal cord injury. Spinal epidural hematomas or abscesses cause acute cord compression and injury. Spinal cord compression from metastatic disease is a common oncologic emergency.

Longitudinal distraction with or without flexion and/or extension of the vertebral column may result in primary spinal cord injury without spinal fracture or dislocation. The spinal cord is tethered more securely than the vertebral column. Longitudinal distraction of the spinal cord with or without flexion and/or extension of the vertebral column may result in spinal cord injury without radiologic abnormality (SCIWORA).

SCIWORA was first coined in 1982 by Pang and Wilberger. Originally, it referred to spinal cord injury without radiographic or computed tomography (CT) scanning evidence of fracture or dislocation. However with the advent of magnetic resonance imaging (MRI), the term has become ambiguous. Findings on MRI such as intervertebral disk rupture, spinal epidural hematoma, cord contusion, and hematomyelia have all been recognized as causing primary or secondary spinal cord injury. SCIWORA should now be more correctly renamed as “spinal cord injury without neuroimaging abnormality” and recognize that its prognosis is actually better than patients with spinal cord injury and radiologic evidence of traumatic injury. [9, 10, 11]

Vascular injury to the spinal cord caused by arterial disruption, arterial thrombosis, or hypoperfusion due to shock are the major causes of secondary spinal cord injury. Anoxic or hypoxic effects compound the extent of spinal cord injury.

One of the goals of the physician is to classify the pattern of the neurologic deficit into one of the cord syndromes. Spinal cord syndromes may be complete or incomplete. In most clinical scenarios, physicians should use a best-fit model to classify the spinal cord injury syndrome.

A complete cord syndrome is characterized clinically as complete loss of motor and sensory function below the level of the traumatic lesion. Incomplete cord syndromes have variable neurologic findings with partial loss of sensory and/or motor function below the level of injury; these include the anterior cord syndrome, the Brown-Squard syndrome, and the central cord syndrome.

Anterior cord syndrome involves a lesion causing variable loss of motor function and pain and/or temperature sensation, with preservation of proprioception.

Brown-Squard syndrome, which is often associated with a hemisection lesion of the cord, involves a relatively greater ipsilateral loss of proprioception and motor function, with contralateral loss of pain and temperature sensation.

Central cord syndrome usually involves a cervical lesion, with greater motor weakness in the upper extremities than in the lower extremities, with sacral sensory sparing. The pattern of motor weakness shows greater distal involvement in the affected extremity than proximal muscle weakness. Sensory loss is variable, and the patient is more likely to lose pain and/or temperature sensation than proprioception and/or vibration. Dysesthesias, especially those in the upper extremities (eg, sensation of burning in the hands or arms), are common.

The conus medullaris syndrome, cauda equina syndrome, and spinal cord concussion are briefly discussed below.

Conus medullaris syndrome is a sacral cord injury, with or without involvement of the lumbar nerve roots. This syndrome is characterized by areflexia in the bladder, bowel, and to a lesser degree, lower limbs, whereas the sacral segments occasionally may show preserved reflexes (eg, bulbocavernosus and micturition reflexes). Motor and sensory loss in the lower limbs is variable.

Cauda equina syndrome involves injury to the lumbosacral nerve roots in the spinal canal and is characterized by an areflexic bowel and/or bladder, with variable motor and sensory loss in the lower limbs. Because this syndrome is a nerve root injury rather than a true spinal cord injury, the affected limbs are areflexic. Cauda equina syndrome is usually caused by a central lumbar disk herniation.

A spinal cord concussion is characterized by a transient neurologic deficit localized to the spinal cord that fully recovers without any apparent structural damage.

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MS Marijuana | Multiple Sclerosis Treatment With Marijuana

Posted: at 12:42 pm

Multiple Sclerosis Treatment With Marijuana

Can MS be treated with Marijuana?

Clinical data reported in 2006 from an extended open-label study of 167 multiple sclerosis patients found that use of whole plant cannabinoid extracts relieved symptoms of pain, spasticity and bladder incontinence for an extended period of treatment (mean duration of study participants was 434 days) without requiring subjects to increase their dose.[19] Results from a separate two-year open label extension trial in 2007 also reported that the administration of cannabis extracts was associated with long-term reductions in neuropathic pain in select MS patients. On average, patients in the study required fewer daily doses of the drug and reported lower median pain scores the longer they took it.[20] These results would be unlikely in patients suffering from a progressive disease like MS unless the cannabinoid therapy was halting its progression, investigators have suggested.

In recent years, health regulators in Canada, Denmark, Germany, Spain and the United Kingdom have approved the prescription use of plant cannabis extracts to treat symptoms of multiple sclerosis. Regulatory approval in the European Union and in the United States[21] remains pending.

Multiple Sclerosis Multiple Sclerosis is an approved Category 1 Health Canada MMAR Condition

Medical Marijuana is NOT for everyone and is often a last resort for people that have tried a variety of the pharmaceuticals below with little relief or too many side effects. Strong anecdotal evidence exists for the support of medical marijuana in treating MS symptoms but scientific research has been hampered by government legislation. We strongly suggest you discuss the potential benefit of medical marijuana with your doctor or specialist.

Condition Description Multiple Sclerosis (MS) is a painful, debilitating disorder of the central nervous system. MS is unpredictable, affecting vision, hearing, memory, balance and mobility. [1] There is no cure for MS. Symptoms vary considerably from person to person; however, one frequently noted symptom is spasticity, which causes pain, spasms, and loss of function. MS is an autoimmune disease, the exacerbations experienced with MS appear to be caused by abnormal immune activity that causes inflammation and the destruction of myelin (the protective covering of nerve fibers) in the brain or spinal cord.[2]

Commonly Prescribed Drugs Drugs commonly prescribed for muscle spasticity and tremor include Klonopin, Dantrium, Baclofen (Medtronic), Zanaflex, Klonopin (Clonazepam) and Valium (diazepam). These medications come with a list of side effects ranging from feeling lightheaded or drowsy, to slurred speech, blurred vision, changes in sexual drive and performance, gastrointestinal changes, muscle spasms and a fast or pounding heartbeat.[3]

Benefits of Marijuana Some benefits of medical marijuana that many MS patients have reported include improved:

Muscle spasms Tremors Balance Bladder control Speech Eyesight MS Patients have reported that smoking medical marijuana reduces symptoms such as muscle stiffness and tremors, and allows for greater mobility[4] Many studies of the pharmacology of marijuana have identified effects on motor systems of the central nervous system that have the potential of affecting tremor and spasticity. Moreover, marijuana has demonstrated effects on immune function that also may have the potential of reducing the autoimmune attack that is thought to be the underlying pathogenic process in MS.[3]

Cannabinoid Research Cannabinoids are chemicals that are found naturally in Marijuana. Researchers believe that these naturally found cannabinoids could create immune suppression. Much like steroids, but with fewer side effects, cannabinoids can switch off a portion of the immune response and bring down inflammation and hyperactivity of immune cells, possibly preventing or slowing some of the damage caused to the myelin by immune cells. The cannabinoids do this by interacting with the receptors on specific immune cells.[5]

Sativex Sativex is a cannabis-based pharmaceutical product developed by GW Pharmaceuticals in 2005 for treating symptoms of Multiple Sclerosis. It is composed mainly of two cannabanoids naturally found in marijuana, tetrahydrocannabinol (THC) and cannabidiol (CBD). It comes in the form of a mouth spray. It has been approved as adjunctive treatment for neuropathic pain in patients with multiple sclerosis. [6] It has also been shown to help reduce spasticity, muscle spasms and sleep disturbances in MS patients. [7][8]

Recommended Resources Please take a look at these interesting articles and books for further information on MS and the benefits of medical marijuana.

[19]Wade et al. 2006. Long-term use of a cannabis-based medicine in the treatment of spasticity and other symptoms of multiple sclerosis. Multiple Sclerosis 12: 639-645.

[20] Rog et al. 2007. Oromucosal delta-9-tetrahydrocannabinol/cannabidiol for neuropathic pain associated with multiple sclerosis: an uncontrolled, open-label, 2-year extension trial. Clinical Therapeutics 29: 2068-2079.

[21] William McGuinness. Marijuana mouth spray Sativex may hit shelves by 2013. CBS News, January 26, 2012. Articles

Marijuana Chemical May Slow Multiple Sclerosis May 2009 Cannabis truly helps multiple sclerosis sufferers September 2004 Cannabinoids and Multiple Sclerosis August 2002 Cannabis helps MS sufferers March 2000 Medical Marijuana: Reducing Spasticity in Multiple Sclerosis Patients

Which Types Of Alternative Therapies Are Recommended for MS?

Alternative therapy encompasses a variety of disciplines that range from diet and exercise to mental conditioning and lifestyle changes. Here we list acupuncture, yoga, aromatherapy, relaxation, herbal remedies, and massage.

Complementary therapies are alternative therapies used in addition to traditional treatments.

Maintain A Positive Attitude. Having a positive outlook cannot cure MS, but it can reduce your stress and help you feel better. Exercise. Exercises, such as tai chi and yoga can lower your stress, help you to be more relaxed, and increase your energy, balance, and flexibility. As with any exercise program, check with your doctor before getting started. It is important that you never exercise to the point of fatigue, as this may worsen your symptoms. Likewise, avoid getting overheated and try to exercise in the early morning on hot days. . What Are Some Other Alternative or Complementary Therapy Options for MS? Gentle Massage Therapy. Many people with MS receive regular massage therapy to help relax and reduce stress and depression, which could trigger a relapse. There is no evidence that massage changes the course of the disease. It is usually safe for people with MS to receive a massage, but if you have bone-thinning osteoporosis (usually as a result of your treatments) massage may be dangerous. Talk to your doctor first.

Be Sure Your Diet Is Healthy. It is important for people with MS to follow a healthy, well-balanced diet. Ask your doctor what diet is right for you It is important for people with MS to maintain a healthy, well-balanced diet to keep them as healthy as possible. Discuss any dietary concerns you may have with your doctor.

Marijuana Treatment Option. The use of marijuana to treat any illness remains highly controversial. Some people with MS claim that smoking marijuana helps relieve spasticity and other MS-related symptoms. However, there is little evidence to date that marijuana really works. Research is ongoing to answer this important question. Until more is known, most doctors do not recommend the use of marijuana to treat MS.

Which types of MS and MSsymptoms can be controlled with Marijuanato the point to where people can live in comfort? We need an open mind and we need Doctors willing to admit that Marijuana can work for some MS patients in controlling the terrible symptoms they endure on a daily basis.

There are various MS treatment options available today that have been shown to decrease the frequency of relapses and to delay disease progression. Some treatments use an injectioneither under the skin or into the muscle, while others are given intravenouslyor orally.

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Treatment for Autism, Cerebral Palsy, Down Syndrome, Brain …

Posted: November 27, 2016 at 12:44 am

Discovered by theGerman physician Samuel Hahnemann,homeopathy is one of the most popular alternative systems of medicine in the world.

Homeopathic medicines are consideredfree from adverse side effectsbecause of their high dilutions.

Modern advances in medical science in the area of nanotechnology help us in understanding the mechanism of action of the homeopathic remedies and biochemic tissue salts present in G Therapy (NeuroG) Medicine.

Homeopathic remedies contain nanoparticle sized ingredients of the original substance, as has been demonstrated in a recent well-cited study at the prestigious Indian Institute of Technology Bombay. This study shows the presence of nano particles of original substance in homeopathic medicines of the size of around 10 nm or nanometers (see Chikramane et al, 2010*) even beyond a dilution of C12 or D24.

New studies show that in the case of biomedicine the optimal size of the nano particle in the treatment of conditions such as cancer is in fact as small as 50nm and even lower sizes also showed enhanced effectiveness compared to larger particles as seen in Tang et al (2014*).

These findings effectively answer one of the most common question that arises on the effectiveness of homeopathic medicines, i.e. since homeopathic medicines are diluted to the extent of 10 to the power of minus 12 and even more, how can they be effective?

It can thus be understood that the biochemic mineral salts present in G Therapy (NeuroG) medicine reactivate the chemical changes for neurotransmission, while the homeopathic remedies act as catalysts to speed up the improvement, at a nanoparticle level.

Even the Indian system of medicine Ayurveda talks about the importance of giving medicine in nano doses for easy assimilation and optimum effect.

*Chikramane, P. S., Suresh, A. K., Bellare, J. R., & Kane, S. G. (2010). Extreme homeopathic dilutions retain starting materials: A nanoparticulate perspective. Homeopathy, 99(4), 231-242.

Tang, L., Yang, X., Yin, Q., Cai, K., Wang, H., Chaudhury, I., … & Dobrucki, I. T. (2014). Investigating the optimal size of anticancer nanomedicine.Proceedings of the National Academy of Sciences, 111(43), 15344-15349.

Patient with Kernicterus (Cerebral Palsy)who improved over 11 years and recently graduated in media studies

Center for Life Sciences, Health and Medicine Clover Pinnacle Ridge opp. Clover Highlands, near NIBM, Kondhwa Pune 411048, Maharashtra India

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Rehabilitative Center Treatment – TBI | Traumatic Brain Injury

Posted: at 12:44 am

The familiesof traumatic brain injury (TBI) victims often have many questions when their loved one is transferred to a rehabilitative care center.

What happens in rehabilitation?Similar tothe acute care facility, the TBI patient will be cared for by a team of professionals who specialize in the care of trauma victims.

Their goals are to:

Each day, the patient will participate in therapy. Initially, the patient may require staff assistance for even the most simple activities: brushing teeth, getting out of bed and eating. The patient also may require staff for safety because there is a risk of falling, eloping (trying to get out of the hospital to go home) or getting hurt. The patientmay be confused and forgetful.

The Rehabilitation Team

The Physiatrist is the team leader in the rehabilitation program. The physiatrist is a physician specializing in physical medicine and rehabilitation. Physiatrists treat a wide range of problems, including the changes after brain injury. The physiatristwill assess and prescribe the treatment and direct the team.

The Neuropsychologist is a key member of the rehabilitation team. The neuropsychologistwill assess the patients changesin thinking and behavior. Changes couldinclude:

Many patients areunaware of the changes in the brain and how those changesaffect their daily lives. A patient may not understand what has happened andmay bedistraughtby being away from home. Through education and counseling, the neuropsychologist can help assure the patient and the patientsfamily.

The Rehabilitation Nurse assists patients with brain injury and chronic illness in attaining maximum optimal health, and adapting to an altered lifestyle. The Rehabilitation Nurse provides care for the patient on the nursing unit. The focus of nursing care is on:

The Physical Therapistworks with people with orthopedic problems, such as low back pain, knee injuries or pain reduction. With traumatic brain injury, thePTsjob is to minimize or overcome paralyzing effects related to the brain injury.Physical therapistsare experts in the examination and treatment of musculoskeletal and neuromuscular problems that affectthe abilities to move and function indaily life.

Physical therapists help with transfers to and from the bed whena patientcannot walk alone. They train a person to begin to walk and move more normally. PTs will assess:

The Occupational Therapist assesses functions and potential complications related to the movement of upper extremities, daily living skills, cognition, vision and perception.OTS help determine, with the patient, the best ways to perform daily living skills including showering, dressing and personal hygiene.The OT willidentify equipment for eating, dressing and bathing.

The OT also will look at skills to prepare the patient for a return to the home. These skillsinclude:

The following sections explain:

Treatments for Traumatic Brain Injury Homepage Initial Treatment Rehabilitative Center Treatment Acute Treatment Surgical Treatment Supportive Care Concerns Recovery

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