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What Do Stem Cells Have to Do with a Spinal Cord Injury?

By Dr. Matthew Watson

You may have heard of stem cells in the news and that they are being used in medical research. This can be a controversial topic for many, but the fact is that the research is happening in specialties across the medical industry. Lets start with the basics to clarify how stem cells are being used in research for spinal cord injuries.

This is the bundle of nerve fibers that transmits information between the brain and rest of the body, protected by the hard vertebrae spinal column. Made up of millions of nerve cells, when connected to the brain, this forms the central nervous system. Injury to the spinal cord can cause paralysis or even death, and there is currently no effective treatment.

Following an injury, the nerve cells and motor axons, which make up the spinal cord, are crushed and torn, and the insulating sheath around the axons begins to die. Any exposed axons begin to degenerate, which means the neuron connection is disrupted, and the flow of information between thebrain and the spinal cord is subsequently blocked.

When this happens, the body is unable to replace lost cells from a spinal cord injury. As a result, their function becomes permanently impaired, leading to severe movement and sensation disability which doctors measure on various scales, including the American Spinal Injury Association Impairment Scale (AIS).

Although the research is still in its infancy, professionals believe stem cells are an ideal answer to contribute to spinal cord treatment and repair. The two main characteristics of stem cells, which make them so well-suited for this use, is

Stem cells, come from two main sources- embryonic stem cells from an embryo and somatic stem cells found throughout the body.

Studies in animals demonstrated that transplantation of stem cells contributed to the repair of spinal cord material. It did so in various ways, and these included the replacement of dead nerve cells; the generation of new cells to re-form the aforementioned insulating sheath around the axons, to stimulate the regrowth of damaged axons. It also acted to protect cells at the site of the injury from any further damage.

In prior testing situations, stem cells have been removed from brain tissue, nasal cavity lining, and tooth pulp for applications. This has only ever resulted in partial recovery of function, however, and remains in experimental stages.

There is controversy over this type of treatment at the moment; due to the fact stem cells need further research into how they behave and how they could work in a form of treatment. Stem cell behavior is directed by chemical signals, some of which are internal, and others of which are external and depend on the environment they find themselves in. These chemical signals would need to be created in the spinal cord environment in order to encourage relative growth and development.

Although stem cell treatment continues to be in testing stages, it is still a possible solution for repairing spinal cord injuries at some point in the future.

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Spinal Cord Injury Research Advances with New Stem Cells

By Dr. Matthew Watson

At Spinal Cord, were excited to share that researchers at the University of California, San Diego successfully created spinal cord neural stem cells (NSCs) that could have clinical applications in spinal cord injury and disorder treatments.

The spinal cord injury research, conducted by postdoctoral scholar Hiromi Kumamaru and Professor of Neuroscience and Director of the UCSD Translational Neuroscience Institute Mark Tuszynski, grafted the cultured cells into the spinal cords of rats with spinal cord injuries (SCIs).

Kumamaru says about the spinal cord injury research:

In grafts, these cells could be found throughout the spinal cord, dorsal to ventral. They promoted regeneration after spinal cord injury in adult rats, including corticospinal axons, which are extremely important in human voluntary motor function. In rats, they supported functional recovery.

These diverse cells are derived from immature self-replicating human stem cells known as human pluripotent stem cells (hPSCs), which morph into different types of stem cells that could disperse throughout the spinal cord. According to the researchers, these pluripotent cells could serve as a scalable source of replacement cells for individuals with spinal cord injuries.

In the Universitys press release, Tuszynski says that the new cells could serve as source cells for human clinical trials in three to five years. First, however, it first needs to be determined whether the cells are safe over long-time periods via studies on rodents and non-human primates and that the results are replicable.

According to the Universitys press release on the new stem cell research:

The achievement, described in the August 6 online issue of Nature Methods, advances not only basic research like biomedical applications of in vitro disease modeling, but may constitute an improved, clinically translatable cell source for replacement strategies in spinal cord injuries and disorders.

The hope is that the cultured spinal cord neural stem cells from this stem cell research will benefit people with other spinal cord dysfunction disorders via modeling and drug screening. According to UCSD, such disorders would include amyotrophic lateral sclerosis, progressive muscular atrophy, hereditary spastic paraplegia and spinocerebellar ataxia, a group of genetic disorders characterized by progressive discoordination of gait, hands and eye movement.

Although significant research has been done to explore the potential use of hPSC stem cells in creating new cells to repair diseased or damaged spinal cords, historically, progress has been slow and limited.

It is one of the goals of the Spinal Cord team to help keep you and your family informed about the newest medical advances in spinal cord injury research. We recently shared about exciting advances in gene therapy research that helped to restore hand function in rats with SCIs, as well as the use of olfactory ensheathing cells (cells from the bodys system that enables you to perceive smells) to trigger spinal cord nerve regeneration.

Please be sure to subscribe to our blog to get the latest updates on stem cell and other spinal cord injury research.

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Spinal Cord Injury Center – Treatments, Research …

By Dr. Matthew Watson

Spinal Cord Injuries Are Not JustCaused by Trauma

When you think of spinal cord injury (SCI), traumatic events like a serious car accident may come to mind. While its true that car accidents are the leading cause of traumatic SCI, you may be surprised that non-traumatic diseasessuch as a spinal tumorcan also cause SCI.

SCI involves damage to the spinal cord that temporarily or permanently changes how it functions. SCI is divided into 2 categories: traumatic or non-traumatic. Even if the cause of SCI is non-traumatic, that doesnt lessen its impact or severitythe aftermath of SCI can have devastating effects on a persons life.Falls are the second most common cause of traumatic spinal cord injury. Photo Source: Spinal Cord Injury

Traumatic SCI occurs more often in men than womennearly 80% of cases affect men. People of all ages may experience SCI, but certain activities tend to affect different age groups more. For example, high-impact events like car accidents and sports injuries tend to occur more often in younger people. On the other hand, traumatic SCI caused by a fall is more common in adults over age 60.

Regardless of the cause, traumatic SCI occurs most frequently in the cervical spine (about 60% of cases involve the neck), followed by thoracic spine (32% involve the mid-back). Only 9% of cases occur in the lumbosacral spine, or low back and tailbone.

Understanding the Traumatic Spinal Cord Injury CascadeA traumatic SCI doesnt simply damage your spinal cord at the point of initial impact. In traumatic SCI, the primary injury (that is, the initial traumatic event that caused the SCI) may damage cells and dislocate your spinal vertebrae, which causes spinal cord compression. The primary injury also triggers a complex secondary injury cascade, which causes a series of biological changes that may occur weeks and months after the initial injury.

During the secondary injury cascade, the following processes occur:

This cascade changes the spinal cords structure and how it normally operates. Ultimately, this secondary injury cascade may interfere with the spinal cords ability to recover itself. This means a person with traumatic SCI may experience permanent nerve pain and dysfunction because of their injury.

Non-traumatic Spinal Cord InjuryTraumatic events arent the only causes of spinal cord damageSCI can also be caused by non-traumatic diseases in the spine. Spinal tumors are the leading cause of non-traumatic SCI, but infections and degenerative disc disease can also damage your spinal cord.

Though most people connect traumatic events to SCI, non-traumatic causes of SCI are a much more likely cause. To highlight just how common non-traumatic cases are versus their traumatic counterparts, consider the incidence of traumatic SCI in North America: 39 cases per million people. On the other hand, the incidence of non-traumatic SCI is 1,227 cases per million people for Canada alone (data for the rest of North America is not available).

A Healthy Research Outlook to Improve Spinal Cord Injury OutcomesOver the past 30 years, spine researchers have made great strides in developing successful protective and regenerative therapies to improve the health of the spinal cord and the survival rate of people with SCIbut the work is far from over. Current studies and clinical trials are examining innovative medical, surgical and cell-based treatments to further the medical communitys understanding of SCI, which will improve the quality of life and preserve a brighter future for people who experience these injuries.

Suggested Additional ReadingA special issue of the Global Spine Journal set forth guidelines for the Management of Degenerative Myelopathy and Acute Spinal Cord Injury, which is summarized on SpineUniverse in Summary of the Clinical Practice Guidelines for the Management of Degenerative Cervical Myelopathy and Traumatic Spinal Cord Injury.

Sources:Ahuja CS, Wilson JR, Nori S, et al. Traumatic spinal cord injury. Nature Reviews Disease Primers. 3, 17018. Accessed January 10, 2018.

Spinal Cord Injury. Facts and figures at a glance. National SCI Statistical Center (NSCI SC). 2017. Accessed January 10, 2018.

Updated on: 01/27/19

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C3, C4, & C5 Vertebrae Spinal Cord Injury |

By Dr. Matthew Watson

The C3, C4, and C5 vertebrae form the midsection of the cervical spine, near the base of the neck. Injuries to the nerves and tissue relating to the cervical regionare the most severe of all spinal cord injuries because the higher up in the spine an injury occurs, the more damage that is caused to the central nervous system. Depending on the how severe the damage to the spinal cord is, the injury may be noted as complete or incomplete.

The C2 - C3 junction of the spinal column is important, as this is where flexion and extension occur (flexion is the movement of the chin toward the chest and extension is the backward movement of the head). Patients with spinal cord damage at the C3 level will have limited mobility in both their flexion and extension.

Symptoms of a spinal cord injury corresponding toC3 vertebrae include:

The portion of the spinal cord which relatesto the C4 vertebra directly affects the diaphragm. Patients with C4 spinal cord injuries typically need 24 hour-a-day support to breathe and maintain oxygen levels.

Symptoms of a spinal cord injury corresponding toC4 vertebrae include:

Damage to the spinal cord at the C5 vertebra affects the vocal cords, biceps, and deltoid muscles in the upper arms. Unlike some of the higher cervical injuries, a patient with a C5 spinal cord injury will likely be able to breath and speak on their own.

Symptoms of a spinal cord injury corresponding to C5 vertebrae include:

The most common causes of cervical spinal cord injuries are:

Unfortunately, there is no treatment which will completely reverse the damage frominjuries to the spinal cord at the C3 - C5 levels. Medical care is focused on preventingfurther damage to the spinal cord and utilization of remaining function.

Current treatments available for patients are:

It is an unfortunate truth that there are not many options to date to completely recover from a cervical spinal cord injury. Medical researchers are continuously looking into new drug therapies to help regain sensory and motor function. The use of stem cells is seen more and more in research as these cells are specialized enough to possibly regenerate damaged spinal cord tissues. Lab study results show greater sensory and motor function in those patients treated with stem cells for spinal cord damage.

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Overview of Spinal Cord Disorders – Brain, Spinal Cord …

By Dr. Matthew Watson

Causes of spinal cord disorders include injuries, infections, a blocked blood supply, and compression by a fractured bone or a tumor.

Typically, muscles are weak or paralyzed, sensation is abnormal or lost, and controlling bladder and bowel function may be difficult.

Doctors base the diagnosis on symptoms and results of a physical examination and imaging tests, such as magnetic resonance imaging.

The condition causing the spinal cord disorder is corrected if possible.

Often, rehabilitation is needed to recover as much function as possible.

The spinal cord is the main pathway of communication between the brain and the rest of the body. It is a long, fragile, tubelike structure that extends downward from the base of the brain. The cord is protected by the back bones (vertebrae) of the spine (spinal column). The vertebrae are separated and cushioned by disks made of cartilage.

The spine (spinal column) contains the spinal cord, which is divided into four sections:

Each section is referred to by a letter (C, T, L, or S).

The vertebrae in each section of the spine are numbered beginning at the top. For example, the first vertebra in the cervical spine is labeled C1, the second in the cervical spine is C2, the second in the thoracic spine is T2, the fourth in the lumbar spine is L4, and so forth. These labels are also used to identify specific locations (called levels) in the spinal cord.

Nerves run from a specific level of the spinal cord to a specific area of the body. By noting where a person has weakness, paralysis, sensory loss, or other loss of function, a neurologist can determine where the spinal cord is damaged.

The spine is divided into four sections, and each section is referred to by a letter.

Within each section of the spine, the vertebrae are numbered beginning at the top. These labels (letter plus a number) are used to indicate locations (levels) in the spinal cord.

Along the length of the spinal cord, 31 pairs of spinal nerves emerge through spaces between the vertebrae. Each spinal nerve runs from a specific vertebra in the spinal cord to a specific area of the body. Based on this fact, the skins surface has been divided into areas called dermatomes. A dermatome is an area of skin whose sensory nerves all come from a single spinal nerve root. Loss of sensation in a particular dermatome enables doctors to locate where the spinal cord is damaged.

The surface of the skin is divided into specific areas, called dermatomes. A dermatome is an area of skin whose sensory nerves all come from a single spinal nerve root. (Sensory nerves carry information about such things as touch, pain, temperature, and vibration from the skin to the spinal cord.)

Spinal roots come in pairsone of each pair on each side of the body. There are 31 pairs:

There are 8 pairs of sensory nerve roots for the 7 cervical vertebrae.

Each of the 12 thoracic, 5 lumbar, and 5 sacral vertebrae has one pair of spinal nerve roots.

In addition, at the end of the spinal cord, there is a pair of coccygeal nerve roots, which supply a small area of the skin around the tailbone (coccyx).

There are dermatomes for each of these nerve roots.

Sensory information from a specific dermatome is carried by sensory nerve fibers to the spinal nerve root of a specific vertebra. For example, sensory information from a strip of skin along the back of the thigh is carried by sensory nerve fibers to the 2nd sacral vertebra (S2) nerve root.

A spinal nerve has two nerve roots (a motor root and a sensory root). The only exception is the first spinal nerve, which has no sensory root.

Motor root: The root in the front (the motor or anterior root) contains nerve fibers that carry impulses (signals) from the spinal cord to muscles to stimulate muscle movement (contraction).

Sensory root: The root in the back (the sensory or posterior root) contains nerve fibers that carry sensory information about touch, position, pain, and temperature from the body to the spinal cord.

The spinal cord ends in the lower back (around L1 or L2), but the lower spinal nerve roots continue, forming a bundle that resembles a horses tail (called the cauda equina).

The spinal cord is highly organized (see figure How the Spine Is Organized). The center of the cord consists of gray matter shaped like a butterfly:

The front "wings" (anterior or motor horns) contain nerve cells that carry signals from the brain or spinal cord through the motor root to muscles.

The back (posterior or sensory) horns contain nerve cells that receive signals about pain, temperature, and other sensory information through the sensory root from nerve cells outside the spinal cord.

The outer part of the spinal cord consists of white matter that contains pathways of nerve fibers (called tracts or columns). Each tract carries a specific type of nerve signal either going to the brain (ascending tracts) or from the brain (descending tracts).

Spinal nerves carry nerve impulses to and from the spinal cord through two nerve roots:

Motor (anterior) root: Located toward the front, this root carries impulses from the spinal cord to muscles to stimulate muscle movement.

Sensory (posterior) root: Located toward the back, this root carries sensory information about touch, position, pain, and temperature from the body to the spinal cord.

In the center of the spinal cord, a butterfly-shaped area of gray matter helps relay impulses to and from spinal nerves. Its "wings" are called horns.

Motor (anterior) horns: These horns contain nerve cells that carry signals from the brain or spinal cord through the motor root to muscles.

Posterior (sensory) horns: These horns contain nerve cells that receive signals about pain, temperature, and other sensory information through the sensory root from nerve cells outside the spinal cord.

Impulses travel up (to the brain) or down (from the brain) the spinal cord through distinct pathways (tracts). Each tract carries a different type of nerve signal either going to or from the brain. The following are examples:

Lateral spinothalamic tract: Signals about pain and temperature, received by the sensory horn, travel through this tract to the brain.

Dorsal columns: Signals about the position of the arms and legs travel through the dorsal columns to the brain.

Corticospinal tracts: Signals to move a muscle travel from the brain through these tracts to the motor horn, which routes them to the muscle.

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Human nervous system – The spinal cord |

By Dr. Matthew Watson

The spinal cord is an elongated cylindrical structure, about 45 cm (18 inches) long, that extends from the medulla oblongata to a level between the first and second lumbar vertebrae of the backbone. The terminal part of the spinal cord is called the conus medullaris. The spinal cord is composed of long tracts of myelinated nerve fibres (known as white matter) arranged around the periphery of a symmetrical butterfly-shaped cellular matrix of gray matter. The gray matter contains cell bodies, unmyelinated motor neuron fibres, and interneurons connecting either the two sides of the cord or the dorsal and ventral ganglia. Many interneurons have short axons distributed locally, but some have axons that extend for several spinal segments. Some interneurons may modulate or change the character of signals, while others play key roles in transmission and in patterned reflexes. The gray matter forms three pairs of horns throughout most of the spinal cord: (1) the dorsal horns, composed of sensory neurons, (2) the lateral horns, well defined in thoracic segments and composed of visceral neurons, and (3) the ventral horns, composed of motor neurons. The white matter forming the ascending and descending spinal tracts is grouped in three paired funiculi, or sectors: the dorsal or posterior funiculi, lying between the dorsal horns; the lateral funiculi, lying on each side of the spinal cord between the dorsal-root entry zones and the emergence of the ventral nerve roots; and the ventral funiculi, lying between the ventral median sulcus and each ventral-root zone.

Associated with local regions of the spinal cord and imposing on it an external segmentation are 31 pairs of spinal nerves, each of which receives and furnishes one dorsal and one ventral root. On this basis the spinal cord is divided into the following segments: 8 cervical (C), 12 thoracic (T), 5 lumbar (L), 5 sacral (S), and 1 coccygeal (Coc). Spinal nerve roots emerge via intervertebral foramina; lumbar and sacral spinal roots, descending for some distance within the subarachnoid space before reaching the appropriate foramina, produce a group of nerve roots at the conus medullaris known as the cauda equina. Two enlargements of the spinal cord are evident: (1) a cervical enlargement (C5 through T1), which provides innervation for the upper extremities, and (2) a lumbosacral enlargement (L1 through S2), which innervates the lower extremities. (The spinal nerves and the area that they innervate are described in the section The peripheral nervous system: Spinal nerves.)

The gray matter of the spinal cord is composed of nine distinct cellular layers, or laminae, traditionally indicated by Roman numerals. Laminae I to V, forming the dorsal horns, receive sensory input. Lamina VII forms the intermediate zone at the base of all horns. Lamina IX is composed of clusters of large alpha motor neurons, which innervate striated muscle, and small gamma motor neurons, which innervate contractile elements of the muscle spindle. Axons of both alpha and gamma motor neurons emerge via the ventral roots. Laminae VII and VIII have variable configurations, and lamina VI is present only in the cervical and lumbosacral enlargements. In addition, cells surrounding the central canal of the spinal cord form an area often referred to as lamina X.

All primary sensory neurons that enter the spinal cord originate in ganglia that are located in openings in the vertebral column called the intervertebral foramina. Peripheral processes of the nerve cells in these ganglia convey sensation from various receptors, and central processes of the same cells enter the spinal cord as bundles of nerve filaments. Fibres conveying specific forms of sensation follow separate pathways. Impulses involved with pain and noxious stimuli largely end in laminae I and II, while impulses associated with tactile sense end in lamina IV or on processes of cells in that lamina. Signals from stretch receptors (i.e., muscle spindles and tendon organs) end in parts of laminae V, VI, and VII; collaterals of these fibres associated with the stretch reflex project into lamina IX.

Virtually all parts of the spinal gray matter contain interneurons, which connect various cell groups. Many interneurons have short axons distributed locally, but some have axons that extend for several spinal segments. Some interneurons may modulate or change the character of signals, while others play key roles in transmission and in patterned reflexes.

Sensory tracts ascending in the white matter of the spinal cord arise either from cells of spinal ganglia or from intrinsic neurons within the gray matter that receive primary sensory input.

The largest ascending tracts, the fasciculi gracilis and cuneatus, arise from spinal ganglion cells and ascend in the dorsal funiculus to the medulla oblongata. The fasciculus gracilis receives fibres from ganglia below thoracic 6, while spinal ganglia from higher segments of the spinal cord project fibres into the fasciculus cuneatus. The fasciculi terminate upon the nuclei gracilis and cuneatus, large nuclear masses in the medulla. Cells of these nuclei give rise to fibres that cross completely and form the medial lemniscus; the medial lemniscus in turn projects to the ventrobasal nuclear complex of the thalamus. By this pathway, the medial lemniscal system conveys signals associated with tactile, pressure, and kinesthetic (or positional) sense to sensory areas of the cerebral cortex.

Fibres concerned with pain, thermal sense, and light touch enter the lateral-root entry zone and then ascend or descend near the periphery of the spinal cord before entering superficial laminae of the dorsal hornlargely parts of laminae I, IV, and V. Cells in these laminae then give rise to fibres of the two spinothalamic tracts. Those fibres crossing in the ventral white commissure (ventral to the central canal) form the lateral spinothalamic tract, which, ascending in the ventral part of the lateral funiculus, conveys signals related to pain and thermal sense. The anterior spinothalamic tract arises from fibres that cross the midline in the same fashion but ascend more anteriorly in the spinal cord; these fibres convey impulses related to light touch. At medullary levels the two spinothalamic tracts merge and cannot be distinguished as separate entities. Many of the fibres, or collaterals, of the spinothalamic tracts terminate upon cell groups in the reticular formation, while the principal tracts convey sensory impulses to relay nuclei in the thalamus.

Impulses from stretch receptors are carried by fibres that synapse upon cells in deep laminae of the dorsal horn or in lamina VII. The posterior spinocerebellar tract arises from the dorsal nucleus of Clarke and ascends peripherally in the dorsal part of the lateral funiculus. The anterior spinocerebellar tract ascends on the ventral margin of the lateral funiculus. Both tracts transmit signals to portions of the anterior lobe of the cerebellum and are involved in mechanisms that automatically regulate muscle tone without reaching consciousness.

Tracts descending to the spinal cord are involved with voluntary motor function, muscle tone, reflexes and equilibrium, visceral innervation, and modulation of ascending sensory signals. The largest, the corticospinal tract, originates in broad regions of the cerebral cortex. Smaller descending tracts, which include the rubrospinal tract, the vestibulospinal tract, and the reticulospinal tract, originate in nuclei in the midbrain, pons, and medulla oblongata. Most of these brainstem nuclei themselves receive input from the cerebral cortex, the cerebellar cortex, deep nuclei of the cerebellum, or some combination of these.

In addition, autonomic tracts, which descend from various nuclei in the brainstem to preganglionic sympathetic and parasympathetic neurons in the spinal cord, constitute a vital link between the centres that regulate visceral functions and the nerve cells that actually effect changes.

The corticospinal tract originates from pyramid-shaped cells in the premotor, primary motor, and primary sensory cortex and is involved in skilled voluntary activity. Containing about one million fibres, it forms a significant part of the posterior limb of the internal capsule and is a major constituent of the crus cerebri in the midbrain. As the fibres emerge from the pons, they form compact bundles on the ventral surface of the medulla, known as the medullary pyramids. In the lower medulla about 90 percent of the fibres of the corticospinal tract decussate and descend in the dorsolateral funiculus of the spinal cord. Of the fibres that do not cross in the medulla, approximately 8 percent cross in cervical spinal segments. As the tract descends, fibres and collaterals branch off at all segmental levels, synapsing upon interneurons in lamina VII and upon motor neurons in lamina IX. Approximately 50 percent of the corticospinal fibres terminate within cervical segments.

At birth, few of the fibres of the corticospinal tract are myelinated; myelination takes place during the first year after birth, along with the acquisition of motor skills. Because the tract passes through, or close to, nearly every major division of the neuraxis, it is vulnerable to vascular and other kinds of lesions. A relatively small lesion in the posterior limb of the internal capsule, for example, may result in contralateral hemiparesis, which is characterized by weakness, spasticity, greatly increased deep tendon reflexes, and certain abnormal reflexes.

The rubrospinal tract arises from cells in the caudal part of the red nucleus, an encapsulated cell group in the midbrain tegmentum. Fibres of this tract decussate at midbrain levels, descend in the lateral funiculus of the spinal cord (overlapping ventral parts of the corticospinal tract), enter the spinal gray matter, and terminate on interneurons in lamina VII. Through these crossed rubrospinal projections, the red nucleus exerts a facilitating influence on flexor alpha motor neurons and a reciprocal inhibiting influence on extensor alpha motor neurons. Because cells of the red nucleus receive input from the motor cortex (via corticorubral projections) and from globose and emboliform nuclei of the cerebellum (via the superior cerebellar peduncle), the rubrospinal tract effectively brings flexor muscle tone under the control of these two regions of the brain.

The vestibulospinal tract originates from cells of the lateral vestibular nucleus, which lies in the floor of the fourth ventricle. Fibres of this tract descend the length of the spinal cord in the ventral and lateral funiculi without crossing, enter laminae VIII and IX of the anterior horn, and terminate upon both alpha and gamma motor neurons, which innervate ordinary muscle fibres and fibres of the muscle spindle (see below Functions of the human nervous system: Movement). Cells of the lateral vestibular nucleus receive facilitating impulses from labyrinthine receptors in the utricle of the inner ear and from fastigial nuclei in the cerebellum. In addition, inhibitory influences upon these cells are conveyed by direct projections from Purkinje cells in the anterior lobe of the cerebellum. Thus, the vestibulospinal tract mediates the influences of the vestibular end organ and the cerebellum upon extensor muscle tone.

A smaller number of vestibular projections, originating from the medial and inferior vestibular nuclei, descend ipsilaterally in the medial longitudinal fasciculus only to cervical levels. These fibres exert excitatory and inhibitory effects upon cervical motor neurons.

The reticulospinal tracts arise from relatively large but restricted regions of the reticular formation of the pons and medulla oblongatathe same cells that project ascending processes to intralaminar thalamic nuclei and are important in the maintenance of alertness and the conscious state. The pontine reticulospinal tract arises from groups of cells in the pontine reticular formation, descends ipsilaterally as the largest component of the medial longitudinal fasciculus, and terminates among cells in laminae VII and VIII. Fibres of this tract exert facilitating influences upon voluntary movements, muscle tone, and a variety of spinal reflexes. The medullary reticulospinal tract, originating from reticular neurons on both sides of the median raphe, descends in the ventral part of the lateral funiculus and terminates at all spinal levels upon cells in laminae VII and IX. The medullary reticulospinal tract inhibits the same motor activities that are facilitated by the pontine reticulospinal tract. Both tracts receive input from regions of the motor cortex.

Descending fibres involved with visceral and autonomic activities emanate from groups of cells at various levels of the brainstem. For example, hypothalamic nuclei project to visceral nuclei in both the medulla oblongata and the spinal cord; in the spinal cord these projections terminate upon cells of the intermediolateral cell column in thoracic, lumbar, and sacral segments. Preganglionic parasympathetic neurons originating in the oculomotor nuclear complex in the midbrain project not only to the ciliary ganglion but also directly to spinal levels. Some of these fibres reach lumbar segments of the spinal cord, most of them terminating in parts of laminae I and V. Pigmented cells in the isthmus, an area of the rostral pons, form a blackish-blue region known as the locus ceruleus; these cells distribute the neurotransmitter norepinephrine to the brain and spinal cord. Fibres from the locus ceruleus descend to spinal levels without crossing and are distributed to terminals in the anterior horn, the intermediate zone, and the dorsal horn. Other noradrenergic cell groups in the pons, near the motor nucleus of the facial nerve, project uncrossed noradrenergic fibres that terminate in the intermediolateral cell column (that is, lamina VII of the lateral horn). Postganglionic sympathetic neurons associated with this system have direct effects upon the cardiovascular system. Cells in the nucleus of the solitary tract project crossed fibres to the phrenic nerve nucleus (in cervical segments three through five), the intermediate zone, and the anterior horn at thoracic levels; these innervate respiratory muscles.

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Where Do Stem Cells Come From? | Basics Of Stem Cell …

By Dr. Matthew Watson

Where do stem cells come from? Learn the basics of master cells to better understand their therapeutic potential.

In this article:

Where do stem cells come from? You have probably heard of thewonders of stem cell therapy. Not only do stem cells make research for future scientific breakthroughs possible, but they also provide the basis for many medical treatments today. So, where exactly are they from, and how are they different from regular cells? The answer depends on the types of stem cells in question.

There are two main types of stem cells adult and embryonic:

Beyond the two broader categories, there are sub-categories. Each has its own characteristics. For researchers, the different types of stem cells serve specific purposes.

Many tissues throughout the adult human body contain stem cells. Scientists previously believed adult stem cells to be inferior to human embryonic stem cells for therapeutic purposes. Theydid not believe adult stem cells to be as versatile as embryonic stem cells (ESCs), because they are not capable of becoming all 200 cell types within the human body.

While this theoryhas notbeen entirely disproved, encouraging evidence suggests that adult stem cells can develop into a variety of new types of cells. They can also affect repair through other mechanisms.

In August 2017, the number of stem cell publications registered in PubMed, a government database, surpassed 300,000. Stem cells are also being explored in over 4,600 cell therapy clinical trials worldwide. Some of the earliest forms of adult stem cell use include bone marrow and umbilical cord blood transplantation.

It should be noted that while the term adult stem cell is used for this type of cell, it is not descriptive of age, because adult stem cells can come from children. The term simply helps to differentiate stem cells derived from living humans as opposed to embryonic stem cells.

Embryonic stem cells are controversial because they are made from embryos that are created but not used by fertility clinics.

Because adult stem cells are somewhat limited in the cell types they can become, scientists developed a way to genetically reprogram cells into what is called an inducedpluripotent stem cell or iPS cell. In creating inducedpluripotent stem cells, researchers hope to blend the usefulness of adult stem cells with the promise of embryonic stem cells.

Both embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) are known as pluripotent stem cells.

Pluripotent stem cells are a type of cell that has the capacity to divide indefinitely and create any cell found within the three germ layers of an organism: ectoderm (cells forming the skin and nervous system), endoderm (cells forming pancreas, liver, endocrine gland, and gastrointestinal and respiratory tracts), and mesoderm (cells forming connective tissues, and other related tissues, muscles, bones, most of the circulatory system, and cartilage).

Embryonic stem cells can grow into a much wider range of cell types, but they also carry the risk of immune system rejection in patients. In contrast, adult stem cells are more plentiful, easier to harvest, and less controversial.

Embryonic stem cells come from embryos harvested shortly after fertilization (within 4-5 days). These cells are made when the blastocysts inner cell mass is transferred into a culture medium, allowing them to develop.

At 5-6 days post-fertilization, the cells within the embryo start to specialize. At this time, they no longer are able to become all of the cell types within the human body. They are no longer pluripotent.

Because they are pluripotent, embryonic stem cells can be used to generate healthy cells for disease patients. For example, they can be grown into heart cells known as cardiomyocytes. These cells may have the potential to be injected into an ailing patients heart.

Harvesting stem cells from embryos is controversial, so there are guidelines created by the National Institutes of Health (NIH) that allow the public to understand what practices are not allowed.

Scientists can harvest perinatal stem cells from a variety of tissues, but the most common sources include:

The umbilical cord attaches a mother to her fetus. It is removed after birth and is a valuable source of stem cells. The blood it contains is rich in hematopoietic stem cells (HSC). It also contains smaller quantities of another cell type known as mesenchymal stem cells (MSCs).

The placenta is a large organ that acts as a connector between the mother and the fetus. Both placental blood and tissue are also rich in stem cells.

Finally, there is amniotic fluid surrounding a baby while it is in utero. It can be harvested if a pregnant woman needs a specialized kind of test known as amniocentesis. Both amniotic fluid and tissue contain stem cells, too.

Adult stem cells are usually harvested in one of three ways:

The blood draw, known as peripheral blood stem cell donation, extracts the stem cells directly from a donors bloodstream. The bone marrow stem cells come from deep within a bone often a flat bone such as the hip. Tissue fat is extracted from a fatty area, such as the waist.

Embryonic donations are harvested from fertilized human eggs that are less than five days old. The embryos are not grown within a mothers or surrogates womb, but instead, are multiplied in a laboratory. The embryos selected for harvesting stem cell are created within invitro fertilization clinics but are not selected for implantation.

Amniotic stem cells can be harvested at the same time that doctors use a needle to withdraw amniotic fluid during a pregnant womans amniocentesis. The same fluid, after being tested to ensure the babys health, can also be used to extract stem cells.

As mentioned, there is another source for stem cells the umbilical cord. Blood cells from the umbilical cord can be harvested after a babys birth. Cells can also be extracted from the postpartumhuman placenta, which is typically discarded as medical waste following childbirth.

The umbilical cord and the placenta are non-invasive sources of perinatal stem cells.

People who donate stem cells through the peripheral blood stem cell donor procedure report it to be a relativelypainless procedure. Similar to giving blood, the procedure takes about four hours. At a clinic or hospital, an able medical practitioner draws the blood from the donors vein in one of his arms using a needle injection. The technician sends the drawn blood into a machine, which extracts the stem cells. The blood is then returned to the donors body via a needle injected into the other arm. Some patients experience cramping or dizziness, but overall, its considered a painless procedure.

If a blood stem cell donor has a problem with his or her veins, a catheter may be injected in the neck or chest. The donor receives local anesthesia when a catheter-involved donation occurs.

During a bone marrow stem cell donor procedure, the donor is put under heavy sedation in an operating room. The hip is often the site chosen to harvest the bone marrow. More of the desired red marrow is found in flat bones, such as those in the pelvic region. The procedure takes up to two hours, with several extractions made while the patient is sedated. Although the procedure is painless due to sedation, recovery can take a couple of weeks.

Bone marrow stem cell donation takes a toll on the donorbecause it involves the extraction of up to 10 percent of the donors marrow. During the recovery period, the donors body gradually replenishes the marrow. Until that happens, the donor may feel fatigued and sore.

Some clinics offer regenerative and cosmetic therapies using the patients own stem cells derived from the fat tissue located on the sides of the waistline. Considered a simple procedure, clinics do this for therapeutic reasons or as a donation for research.

Stem cells differ from the trillions of other cells in your body. In fact, stem cells make up only a small fraction of the total cells in your body. Some people have a higher percentage of stem cells than others. But, stem cells are special because they are the mothers from which specialized cells grew and developed within us. When these cells divide, they become daughters. Some daughter cells simply self-replicate, while others form new kinds of cells altogether. This is the main way stem cells differ from other body cells they are the only ones capable of generating new cells.

The ways in which stem cells can directly treat patients grow each year. Regenerative medicine now relies heavily on stem cell applications. This type of treatment replaces diseased cells with new, healthy ones generated through donor stem cells. The donor can be another person or the patient themselves.

Sometimes, stem cells also exert therapeutic effects by traveling through the bloodstream to sites that need repair or by impacting their micro-environment through signaling mechanisms.

Some types of adult stem cells, like mesenchymal stem cells (MSCs), are well-known for exerting anti-inflammatory and anti-scarring effects. MSCs can also positively impact the immune system.

Conditions and diseases which stem cell regeneration therapy may help include Alzheimers disease, Parkinsons disease, and multiple sclerosis (MS). Heart disease, certain types of cancer, and stroke victims may also benefit in the future. Stem cell transplant promises advances in treatment for diabetes, spinal cord injury, severe burns, and osteoarthritis.

Researchers also utilize stem cells to test new drugs. In this case, an unhealthy tissue replicates into a larger sample. This method enables researchers to test various therapies on a diseased sample, rather than on an ailing patient.

Stem cell research also allows scientists to study how both healthy and diseased tissue grows and mutates under various conditions. They do this by harvesting stem cells from the heart, bones, and other body areas and studying them under intensive laboratory conditions. In this way, they get a better understanding of the human body, whether healthy or sick.

With the following stem cell transplant benefits, its not surprising people would like to try the therapy as another treatment option.

Physicians harvest stem cell from either the patient or a donor. For an autologous transplant, there is no risk of transferring any disease from another person. For an allogeneic transplant, the donor is meticulously screened before the therapy to make sure they are compatible with the patient and have healthy sources of stem cells.

One common and serious problem of transplants is the risk of rejecting the transplanted organs, tissues, stem cells, and others. With autologous stem cell therapy, the risk is avoided primarily because it comes from the same person.

Because stem cell transplants are typically done through infusion or injection, the complex and complicated surgical procedure is avoided. Theres no risk of accidental cuts and scarring post-surgery.

Recovery time from surgeries and other types of treatments is usually time-consuming. With stem cell therapy, it could only take about 3 months or less to get the patient back to their normal state.

As the number of stem cell treatments dramatically grew over the years, its survival rate also increased. A study published in the Journal of Clinical Oncology showed there was a significant increase in survival rate over 12 years among participants of the study. The study analyzed results from over 38,000 stem cell transplants on patients with blood cancers and other health conditions.

One hundred days following transplant, the researchers observed an improvement in the survival rate of patients with myeloid leukemia. The significant improvements we saw across all patient and disease populations should offer patients hope and, among physicians, reinforce the role of blood stem cell transplants as a curative option for life-threatening blood cancers and other diseases.

With the information above, people now have a better understanding of the answer to the question Where do stem cells come from? Stem cells are a broad topic to comprehend, and its better to go back to its basics to learn its mechanisms. This way, a person can have a piece of detailed knowledge about these master cells from a scientific perspective.

If you found this blog valuable, subscribe to BioInformants stem cell industry updates.

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Where Do Stem Cells Come From? | Basics Of Stem Cell Therapy

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Spinal Neurons Grown From Stem Cells For First Time | News …

By Dr. Matthew Watson

Modern medicine has still not managed to crack the problem of spinal cord injuries that result in significant paralysis or loss of functional status.

There are numerous factors that influence the inability to restore movement or autonomous bodily control to these patients. A prominent example of these is the inability to cultivate new neurons that make up and power the spinal cord.

However, some researchers have claimed that they have successfully induced generic human stem cells to differentiate into stem cells that apply more specifically to the spine.

Why We Cant Repair a Spine (Yet)

Strategies involving the implantation of any kind of donor cell to regenerate or recreate damaged spinal tissue have not shown much success. Furthermore, some medical researchers also believe that such forays into regenerative medicine are not feasible, in terms of costs and resources, at this point. Therefore, this area of cell-based therapy is still very much at the development stage.

The goals of many current projects in this area revolve around the restoration of the motor function in subjects (mostly rodents in animal models). This requires the full re-generation and reinstatement of the corticospinal tract (CST), an important spinal region that communicates with the relevant cortices in the brain.

A limited number of reports claim to have achieved this. However, this leaves the rest of the spine un-addressed, which may have a residual effect on movement and other functions.

New Direction in Cell-Based Therapy for Spinal Injuries

In the past, CST-based trials used grafts of multipotent cells, which were progenitor cells rather than true stem cells.

However, a newer study has documented a technique in which human pluripotent stem cells were used, which could differentiate into all the cells a spinal section needs, and not just the CST ones.

Reportedly, these neural stem cells further diversified into different types of neurons. Therefore, it can be concluded that neural stem cells may be capable of more complete regeneration of missing or damaged spinal tissue in living subjects.

The researchers behind the apparent breakthrough claimed that their cells were capable of doing this in an appropriate model. However, the research was conducted by causing the stem cells to grow a customized spinal graft, which was then transplanted using the model.

A transverse spinal section showing some functions of various spinal region. (Source: Public Domain)

The scientists claimed that these grafts integrated well with the sections of pre-existing spinal tissue upstream and downstream of the graft location. These consisted of various intra-, supra- and cortico-spinal networks of neural connections, which allowed peripheral nervous functions, including movement, under normal circumstances.

In addition, it is necessary for these networks to distinguish between the dorsal (or backward-facing) and ventral portions of the spine. This is because these regions send different signals to the brain in different directions in the average healthy spine. The researchers asserted that their spinal grafts were indeed capable of these distinctions.

The scientists behind this project reported that their models subjects gained increased functional status as a result of receiving one of these grafts. However, it can be assumed that these assertions are getting slightly ahead of their time, in terms of being approved as a real-world treatment.

The researchers also noted that their new spinal stem cells and the neurons that they differentiate into can be used as an excellent in vitro model for the neurobiology of the spine. In addition, the cells may also now be used to test other novel potential treatments for spinal disorders.


The scientists behind this project collaborated across the departments of neurosciences and psychiatry & neurology at the University of California (Los Angeles), as well as the San Diego Veterans Administrations Healthcare System. The team published their findings in an August 2018 issue of Nature Methods.

The researchers also hope that future work on this model could lead to the application of their cells to next-generation regenerative medicine that focuses on the spine and how to repair it after injury or damage.

Therefore, we may be able to look forward to a time, in which improved medicine could restore paraplegic patients to the health and autonomy that they may cherish.

Top Image: The spine is an important component of the human nervous system. (Source: Pixabay)


H. Kumamaru, et al. (2018) Generation and post-injury integration of human spinal cord neural stem cells. Nature Methods.

S. A. Goldman. (2016) Stem and Progenitor Cell-Based Therapy of the Central Nervous System: Hopes, Hype, and Wishful Thinking. Cell Stem Cell. 18:(2). pp.174-188.

K. Kadoya, et al. (2016) Spinal cord reconstitution with homologous neural grafts enables robust corticospinal regeneration. Nat Med. 22:(5). pp.479-487.

Deirdre ODonnell

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Regenerative Stem Cell Therapy | Treatment for Back Pain | VSI

By Dr. Matthew Watson


Mesenchymal stem cells are specialized cells that naturally grow in our body and can differentiate into bone, cartilage or fat cells. They are widely used in medicine as a natural healing solution to effectively treat orthopedic conditions including the spine and major joints (like the shoulder, hip, knee, ankle, etc.).

There are many benefits of stem cell therapy, including but not limited to:

The human body has multiple sites for stem cells to repair degenerated and injured structures. We have found that obtaining stem cells from the hip bone (iliac bone) is easily performed within minutes. After the stem cells are obtained, minutes later they can be used for treatment in our outpatient state-of-the-art-facility. Regenerative stem cell injections are performed using image guidance (i.e. ultrasound or fluoroscopy) to ensure accurate placement of the stem cells. Once the affected area is sterilized and numbed with a novocaine-type solution, stem cells are injected and begin regenerating and strengthening weakened joints.

Stem cell injections are most commonly used for treatment of the following conditions:

Stem cell injections are designed to heal and strengthen damaged tissue, therefore pain relief is typically noticed several weeks after the procedure. Final relief is seen approximately two to three months after the entire treatment protocol has been completed.

In most cases, patients respond very well to just one treatment. Some patients, depending on the severity of the injury, may benefit from two to three injections over the course of 12 months.

As with all procedures, there are minor risks associated with stem cell injections including infection, bleeding, or nerve damage. It is important to note that there is no risk of allergic reaction since you are using your bodys own healing factors. The physicians at Virginia Spine Institute will always recommend the safest and most efficient procedures for our patients, however, your physician will review any possible risks associated with this treatment prior to administering.

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Stem cell-filled implant restores some spinal cord …

By Dr. Matthew Watson

Stem cell-filled implants helped repair spinal cord damage in animals, according to a study led by UC San Diego scientists. If all goes well, the implants with neural stem cells could be ready for testing in human patients in a few years.

Rats with completely severed spinal cords regained some voluntary motion after getting the implants, said the study, published Monday in the journal Nature Medicine. The study is online at

They were able to move the joints of their lower legs, said study co-author Dr. Mark Tuszynski. They couldn't support their weight very well, but they could move the legs around the joints. If one were to project what this means to humans, it might mean that the legs are still weak, but that with an assist they would be able to control them.

The next step is to repeat the procedure in monkeys, said Tuszynski, director of the Translational Neuroscience Institute at UC San Diego School of Medicine.

If successful, it would fulfill one of the biggest hopes for stem cell therapy.

Repairing spinal cord injuries has long been a major goal of the states stem cell program, the California Institute for Regenerative Medicine, or CIRM. The agency was formed in 2004 with the passage of Prop. 71. The late actor Christopher Reeve figured prominently in the campaign for Prop. 71.

While there have been encouraging reports of individual spinal cord injury patients benefiting from stem cell-based therapy, no such treatment has been approved as safe and effective. So scientists at UCSD and elsewhere are trying to make a treatment that can be reliably replicated.

Another study with neural stem cells without the implant has shown benefit in monkeys after spinal cord injury, Tuszynski said. This work is closer to the clinical stage.

The rat implants were constructed by 3D bioprinting of a biologically compatible hydrogel, which is mostly made up of water. These 2-millimeter-wide implants contain tiny channels that guide growth of neural stem cells, also called neural progenitor cells. The cells matured into neurons and reconnected severed nerves, Tuszynski said.

Besides guiding growth, the implants allowed blood vessels to grow, nourishing the newly formed cells. This process, called vascularization, has been hard to achieve in growing new tissue. But with the biologically compatible implants, vascularization occurred spontaneously.

The implants also protected the neural stem cells from the inflammatory damage associated with a fresh injury.

This is a nice marriage of the technology of bioengineering and 3D printing with stem cell biology to treat a really important human disease that needs better therapy, Tuszynski said.

Implants can be quickly custom-made for human spinal cord injuries, according to the study. Researchers bioprinted implants of 4 centimeters within 10 minutes. These were made according to MRI scans of real human spinal cord injuries.

Two other UCSD study authors, Shaochen Chen and Wei Zhu, have co-founded a San Diego startup, Allegro 3D, to commercialize the rapid bioprinting technology. Allegro is doing this independently of the spinal cord injury research.

We will be talking to people to find a partner, said Chen, a founding co-director of the Biomaterials and Tissue Engineering Center at UC San Diego. It takes money, time and effort, so it won't be done in a university setting.

The neural stem cells are produced from a lineage of human embryonic stem cells. This lineage was one of the original certified while George W. Bush was president.

The researchers treat the cells with their own cocktail of growth chemicals that coax them into becoming spinal cord neural stem cells, which cant become any other kind of cell besides types of spinal cord cells.

When these cells are placed at the injury site, with or without the implant, the stem cells complete development.

Importantly, these cells grow axons, the long fibers that carry nerve signals, Tuszynski said. They extend out of the implant and into the spinal cord below the injury. They relay signals that cross synapses, the tiny gaps between nerve cells.

Because the cells arent from the patient, the body may tend to reject them. So patients receiving these cells will need immunosuppressive therapy, he said.

Newer classes of immune-suppressing drugs now available are safer and better tolerated than earlier ones, Tusyznski said.

We think patients would stay on them for awhile, he said.

The research was funded by the National Institutes of Health; the California Institute for Regenerative Medicine; and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation.

UCSD also hosts ongoing stem cell-based clinical trials for spinal cord injuries and other diseases. More information can be found at the Sanford Stem Cell Clinical Center, reachable at

Related reading

3D printed implant promotes nerve cell growth to treat spinal cord injury

Biomimetic 3D-printed scaffolds for spinal cord injury repair

Allegro 3D

Stem cell-based spinal cord therapy expanded to more patients

Stem cells have become keys to unlock how life develops

UCSD finds possible treatment for paralysis

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Stem Cell Transplantation for Spinal Cord Injuries …

By Dr. Matthew Watson

In terms of scientific advances, the discovery and use of Stem Cells to treat disease and injury, rank as critical milestones in the field of Medicine.

If any single medical advancement can be said to be revolutionary then it is Regenerative Medicine and the use of Stem Cells. Stem Cells in their most basic form are undifferentiated and have the ability to differentiate into any type of specialised cell.

Stem Cell Therapy is used as a repair system for the body that has been affected by either disease or injury. Stem Cell Transplantation for Spinal Cord Injury (SCI) patients has the potential to forever change how SCIs are viewed and how future interventions will be handled.

The greater majority of Spinal Cord Injuries are particularly harrowing since they happen without warning. Most are the result of motor vehicle accidents, physical assaults, industrial accidents and falls. It takes literally less than a second for one to move from an able-bodied state to partial or complete paralysis.

The use of walking aids such as crutches and walking frames played an important role in helping patients with incomplete SCIs to move around, however, we are already at a point where medical advancement has provided effective long term solutions where the source of treatments is within the human body itself.

Recent trials have compared the effects of Stem Cell Transplantation to those of Rehabilitation Treatment for patients with SCI. These studies involved 377 patients grouped into 10 randomised controlled trials. Some patients received only Stem Cell Therapy while others had the Stem Cell Transplantation combined with Rehabilitation Therapy. Observable developments were recorded in different areas: neurological function (sensory and locomotor functions), urination function, daily living activities and the appearance of any side effects.

The studies concluded that Stem Cell Therapy is a safe and efficient treatment for SCI. The primary action of the therapy, which was to produce measurable changes in the spinal cord, turned out positive. As a result of the Stem Cell Therapy spinal cord repair was apparent. Further,axon remyelination (or resheathing of denuded nerve cells) was observed. It was further determined that Stem Cell Therapy improved sensory and bladder functions.

Whereas a Spinal Cord Injury once meant a life sentence in a wheelchair, the advent of stem cells is bound to change this narrative. Through the use of Mesenchymal Stem Cells (MSCs), SCIs are now firmly within the scope of treatable conditions. MSCs are particularly effective in the treatment and management of SCIs as they are also able to regulate the immune systems reaction to the injury. Equally important, MSCs also have the capability to differentiate cell types including astrocytes (which are glial cells of the central nervous system) and neurons, which are responsible for transmitting nerve impulses.

A comprehensive treatment protocol that includes Stem Cell Therapy and supportive therapies such as Aquatic Therapy, Physiotherapy, Acupuncture, Occupational Therapy and others, as determined by the doctor, produces quantifiable results in various areas. Improvement is observable in balance, coordination and motor function, sensation, bowel and bladder control and sexual function. Other areas of improvement include a lessening of neuropathic pain and an increase in strength and improved muscle mass, among others.

To learn more about our Stem Cell Treatments, do get in touch and a patient representative shall guide you at your earliest convenience.

H/T:National Center for Biotechnology Information

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Spinal Cord Injury Explained – Mad Spaz Club

By Dr. Matthew Watson

Injury to the spinal cord can be caused by acute (sudden) or chronic (developing) trauma as well as medical conditions. Frequent causes of chronic compression injuries are herniated disks and primary or secondary tumors. Compromised blood perfusion, the delivery of nutritive arterial blood to capillary bed, as in anterior spinal cord syndrome can also be severely detrimental to spinal cord function. However the most damaging Spinal Cord Injury is one of acute trauma resulting in permanent paralysis.

Traumatic spinal cord injury have been classified into five categories by the American Spinal Injury Association and the International Spinal Cord Injury Classification System:

Spinal cord injury where no motor or sensory function remains in the sacral segments S4-S5.

Spinal cord injury sensory but not motor function remains below the neurological level and includes the sacral segments S4-S5. Typically a transient phase and if the person recovers any motor function below the neurological level, theyare considered motor incomplete and classified C or D.

Spinal cord injury where motor function remains below the neurological level and more than half of key muscles below the neurological level have a muscle grade of less than 3, which indicates active movement with full range of motion against gravity.

Spinal cord injury where motor function exists below the neurological level and at least half of the key muscles below the neurological level have a muscle grade of 3 or more.

Where motor and sensory scores are normal. It is possible to have spinal cord injury and neurological deficits with completely normal motor and sensory scores.

The annual incidence rate of spinal cord injury varies from country to country, ranging from 15 to 71 per million (/m). In 2008 the incidence of spinal cord injury in the United Kingdom around 13 /m, Australia 14 /m, Canadi 35 /m, China 65 /m and the United States 35 /m per year. This suggests around 40 per million or 52,000 spinal injuries occur every year globally.

Of the 12,000 new cases of paraplegia and quadriplegia that occur in the United States each year 4,000 patients die before reaching hospital. Causes of acute spinal cord injury include motor vehicle accidents, work-related accidents, recreational accidents, falls and violence (shootings and stab wounds).

Paralysis occurs our times as often in males as females where about 60% of victims are under 30 years of age and 5% under 13 years of age (the pediatric age group). Falls from a height greater than their own is the largest cause of spinal trauma amongst the pediatric age group. A long-term outcome study of patients aged 25 to 34 who had suffered acute traumatic SCI before the pediatric age showed an employment rate of 54% while the employment rate in the general population for the same age group was 84%.

Limitation or complete loss of the capability to achieve economic independence following SCI combined with additional medical costs causes severe economic hardship for many living with paralysis and their immediate family. Further limitations to living a full social life are architectural barriers, buildings only accessible by stairs and a lack of ramps on sidewalks for example.

Increased awareness through education has played a key role in resolving these barriers and those created by negative or overprotective attitudes of healthy, non-injured people toward persons with spinal cord injury. When persons with spinal cord injury cannot fully participate society suffers. Not only are ethical standards, artistic and financial contributions to society lost, huge expenses for specialised lifelong care are incurred.

80% of SCI occur in people under the age of 30. The average life-time cost of thoracic paraplegia is $1.25 million and high level cervical quadriplegia such as those on ventilators $25 million USD. In 1990 the cost for acute and long term care of surviving spinal cord injury victims was estimated at $4 billion in the United States alone.

Road traffic accidents 45%

Domestic and industrial accidents 34%

Sporting injuries 15%

Self harm and criminal assault 6%

The first known description of acute spinal cord trauma and resulting neurological deficits was in the Edwin Smith papyrus which is believed to be more than 3,500 years old. In this ancient Egyptian document Smith accurately described the clinical symptoms and traumatic effects of quadriplegia (tetraplegia) anailment not to be treated. An indication of the feelings helplessness medical practitioners suffered at the time, a doctors value measured by the extent of cure achieved.

No strategies ensuring longterm survival for patients with spinal cord injury existed. A view which prevailed well into the early 1900s. In the First World War the mortality rate for those with a spinal cord injury was 95%, mainly attributed to urinary sepsis and complications from pressure sores. Less than 1% survived for more than twenty years.

During World War II the number of casualties from spinal cord injuries both military and civilian increased dramatically in Europe. Specialized hospital units known as peripheral nerve centers developed between the wars in Germany and the United States demonstrating the advantages of concentrating special needs patients under specialized care. Great importance was placed on the unique opportunities offered by these specialized units. Gaining new insight in the natural course of the disease and further development of new therapeutic strategies.

Building on those experiences, specialized spinal cord injury units started opening throughout England in the 1940s. Mortality rates from a spinal cord injury were recorded at 35% in the 1960s. Today nearly every capital city operates an acute care spinal unit.

Dr. Ludwig Guttmann and his colleagues at the Spinal Cord Unit of Stoke Mandeville Hospital developed new treatment approaches including frequent repositioning of paralyzed patients to avoid developing bedsores, a potential source of sepsis and intermittent sterile catheterization to prevent urinary sepsis. The success in patient survival was dramatic enough to require development of completely new strategies for social reintegration of patients with spinal cord injury. Adapted workplaces and wheelchair accessible housing championed in the 1940s and 1950s by the English Red Cross has today become an integral component in the framework of social politics in most industrialized countries. Respiratory complications are now the leading cause of death in patients admitted with SCI. Secondary are heart disease, septicemia (blood poisoning), pulmonary emboli (blood clot in lungs), suicide, and unintentional injuries.

Dr. Guttmann and his colleagues viewed physical rehabilitation as the basis of social reintegration both physically and psychologically. Supporting the idea of athletic competition in disciplines adequate and adapted to the physical capacity of their patients. Starting with two teams a competition in 1948 paralleling the Olympic Games in England, the idea of competitive sports for the paralyzed developed rapidly.

In 1960 the first Paralympic Games were held in Rome. The Paralympic games were held in the same year as the Olympic Games for the able-bodied using the same facilities, a tradition that has been followed ever since. The idea of competitive sports was extended to include people with a multitude of physical handicaps other than spinal cord injury emerging as the Paralympics we know today.

In many countries initiatives have risen at communal and national levels with the intent to decrease the incidence of spinal cord trauma and offer support and advice to both those with spinal cord injuries and their families. Many generously offer financial support for scientific and clinical research.

The prevention oriented Think First initiative, Canadian-based CORD and Wheels in Motion, the Christopher Reeve Paralysis Foundation, the U.K. Spinal Cord Trust, and the Paralyzed Veterans of America all maintain informative web sites with valuable information on the subject of spinal cord injury.

Although the overall incidence of SCI has not noticeably decreased the severity of injuries has deceased overall. Fewer now suffer complete injuries and survival rates have increased. This is mostly attributed to improvements in prehospital care including widespread instruction of first aid principles as well as the introduction of spinal cord immobilization and administration of advanced medicines during rescue and transport. Increased public awareness of risk factors leading to head trauma and spinal cord injury, the introduction of mandatory use of safety belts and installation of air bags in modern vehicles has also served to decrease trauma severity.

Until recently research suggested once spinal cord trauma had occurred nothing could be done to alter the natural course of developing pathology, that damage to the central nervous system was permanent and repair impossible. At the beginning of the twenty-first century this belief came to change in the minds of scientists, clinicians, patients and their families. Research laboratories around the world adopted two new approaches:

1. Prevention of secondary injury and repair of manifest damage. The term secondary injury describes the observation that central nervous system structures that survived the primary mechanical trauma die at a later point in time due to deterioration of the milieu (nerve ending sheath) at the site of injury.

2. The amount and severity of secondary injury damage can be significantly larger than that of the primary injury. Researchers focused on identification of substances and therapeutic methods that help minimize secondary injury effects. In the field of cell biology, isolation and manipulation of specific cell types is being undertaken in effort to induce certain cell types, including stem cells and olfactory ensheathing cells to help repair damaged central nervous system structures.

Clinical research continues to improve outcomes for those with a spinal cord injury, such as stimulators for bladder control, orthopedic correctional procedures and physical mobilization. Integration of biomedical research like pattern generators, mechanics and kinetics of movement with the latest developments in computer science and engineering has given rise to neuronal networks. Neuroprostheses are being developed which enable paraplegics to move about and walk.

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Clinical trial of stem cell therapy for traumatic spinal …

By Dr. Matthew Watson

Mayo Clinic is enrolling patients in a phase 1 clinical trial of adipose stem cell treatment for spinal cord injury caused by trauma. The researchers already have approval from the Food and Drug Administration for subsequent phase 2A and 2B randomized control crossover trials.

Participants in the phase 1 clinical trial must have experienced a trauma-related spinal cord injury from two weeks to one year prior to enrollment. They will receive intrathecal injections of adipose-derived mesenchymal stem cells. No surgery or implantable medical device is required.

"That is the most encouraging part of this study," says Mohamad Bydon, M.D., a consultant in Neurosurgery specializing in spinal surgery at Mayo Clinic in Rochester, Minnesota, and the study's director. "Intrathecal injection is a well-tolerated and common procedure. Stem cells can be delivered with an implantable device, but that would require surgery for implantation and additional surgeries to maintain the device. If intrathecal treatment is successful, it could impact patients' lives without having them undergo additional surgery or maintain permanently implantable devices for the rest of their lives."

To qualify for the trial, patients must have a spinal cord injury of grade A or B on the American Spinal Injury Association (ASIA) Impairment Scale. After evaluation at Mayo Clinic, eligible patients who enroll will have adipose tissue extracted from their abdomens or thighs. The tissue will be processed in the Human Cellular Therapies Laboratories, which are co-directed by Allan B. Dietz, Ph.D., to isolate and expand stem cells.

Four to six weeks after the tissue extraction, patients will return to Mayo Clinic for intrathecal injection of the stem cells. The trial participants will then be evaluated periodically for 96 weeks.

Mayo Clinic has already demonstrated the safety of intrathecal autologous adipose-derived stem cells for neurodegenerative disease. In a previous phase 1 clinical trial, with results published in the Nov. 22, 2016, issue of Neurology, Mayo Clinic researchers found that therapy was safe for people with amyotrophic lateral sclerosis (ALS). The therapy, developed in the Regenerative Neurobiology Laboratory under the direction of Anthony J. Windebank, M.D., is moving into phase 2 clinical trials.

Dr. Windebank is also involved in the new clinical trial for people with traumatic spinal cord injuries. "We have demonstrated that stem cell therapy is safe in people with ALS. That allows us to study this novel therapy in a different population of patients," he says. "Spinal cord injury is devastating, and it generally affects people in their 20s or 30s. We hope eventually that this novel therapy will reduce inflammation and also promote some regeneration of nerve fibers in the spinal cord to improve function."

Mayo Clinic's extensive experience with stem cell research provides important guidance for the new trial. "We know from prior studies that stem cell treatment can be effective in aiding with regeneration after spinal cord injury, but many questions remain unanswered," Dr. Bydon says. "Timing of treatment, frequency of treatment, mode of delivery, and number and type of stem cells are all open questions. Our hope is that this study can help answer some of these questions."

In addition to experience, Mayo Clinic brings to this clinical trial the strength of its multidisciplinary focus. The principal investigator, Wenchun Qu, M.D., M.S., Ph.D., is a consultant in Physical Medicine and Rehabilitation at Mayo Clinic's Minnesota campus, as is another of the trial's investigators, Ronald K. Reeves, M.D. Dr. Dietz, the study's sponsor, is a transfusion medicine specialist. Also involved is Nicolas N. Madigan, M.B., B.Ch., BAO, Ph.D., a consultant in Neurology at Mayo Clinic's Minnesota campus.

The study team is in discussions with U.S. military medical centers to enroll patients, and discussing additional collaboration with international sites, potentially in Israel or Europe, for future phases of the study.

"At Mayo Clinic, we have a high-volume, patient-centered multidisciplinary practice," Dr. Bydon says. "That allows us to do the most rigorous scientific trial that is in the best interests of our patients."

Mayo Clinic. Adipose Stem Cells for Traumatic Spinal Cord Injury (CELLTOP).

Staff NP, et al. Safety of intrathecal autologous adipose-derived mesenchymal stromal cells in patients with ALS. Neurology. 2016;87:2230.

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Stem Cell Therapy for Spinal Cord Injury- Treatment for …

By Dr. Matthew Watson

Stem Cell Therapy for Spinal Cord Injury-Spinal cord injury is one of the progressively degenerating, crippling disorders attributing towards the dislocation of bones and vertebrae; which is a general result of trauma and/or injury.

The accidental injury generally damages connecting nerves internally; in order to halt the back and forth communication between brain and rest of the body parts. This communication gap is the primary cause of partial or complete loss of movement, paralysis as well as numbness. Apparently, many times it has also been evident that spinal cord may get affected not because of the injury but because of different types of nerve infection; which if ignored for a longer time, may allow unusual bleeding in between the spaces around the spinal cord. Some of the common forms of these notable infections are spinal stenosis, spina bifida, etc.

A person with a potential threat to severe spinal cord damage should be hospitalized for an intensive care unit immediately. Stabilization of blood pressure, lung function, and prevention of further damage to the spinal cord; should be emphasized with immediate effect. Other injuries are as well to be looked at; for an accidental damage.

Experts may prescribe some routine tests, in order to detect the extent of injuries. These tests can be

Classification of SCI is generally based on the extent of pain and loss of movement, associated with the damage. Moreover, when the damage is associated with neuronal loss, nerve locations and anumber of nerves that have been damaged can as well be referred to classify spinal cord injury.

The recovery period for patients suffering from spinal cord injury is dependent upon the level of injury, muscular strength and the type of injury; but in general, the notable recovery period can be anytime between 4-6 months.

Through conventionally demonstrated medicines, it is generally impossible to completely cure spinal cord damage or paralytic aftereffects of injury. In fact, the anti-inflammatory medicines that have been prescribed conventionally can affect other vital organs of the body, due to continuous hormonal modifications. Although with the advent of stem cells through the science of regenerative medicine has proven to be very helpful in offering a definite cure for SCI and other orthopedic related illnesses. The potential ability of these stem cells to be differentiated into neurons has been well studied and confirmed through different scientific literature and the same hypothesis can be applied to treat and restore back the functional attributes of damaged spinal cord.

Thus, stem cells and their regenerative powers can potentially work to solve the internal mysteries of spinal cord injury; but the extent of recovery and therapeutic outcome are still the challenges that are being faced by the medical fraternities.

For further queries regardingstem cell therapy for spinal cord injury, feel free to connect us at+91-96543 21400 or You can also connect us through Advancells Enquiry.

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Adult Stem Cells Treat Spinal Cord Injury | News | Spinal …

By Dr. Matthew Watson

Laura Dominguez-Tauer is a living, breathing example of what it takes to overcome adversity. An oil spill on a San Antonio freeway is blamed for the car crash that sent Laura and her brother directly into a retaining wall in 2001. As she lay tangled in the middle of the car, she heard a paramedic say, get a neck brace, she has a broken neck.

I didnt feel anything. I couldnt move my arms, I couldnt move my hands,

Laura was paralyzed from the neck down. I didnt feel anything. I couldnt move my arms, I couldnt move my hands, Laura said.

While others might have given up, Laura and her family started immediately searching for answers. They learned about adult stem cells and the promising results for spinal cord injury patients. In 2010, Laura joined a handful of other spinal cord patients and received an adult stem cell transplant. The transplant was a success.

Laura says, Before the stem cell procedure, I wasnt able to move very much. And then after the procedure Im able to get up. Im able to stand and walk around a little bit with help. The stem cell procedure made my upper body a lot stronger. I can feel my entire body now.

Laura went to work making herself stronger. Through physical therapy and a lot of hard work, she grew stronger and stronger. Instead of feeling sorry for herself, she opened a gym called Beyond the Chair. We opened Beyond the Chair to help people with any type of neurological disability whether its spinal cord injury, traumatic brain injury, strokes. We dont turn anybody away. Were going to help people.

In 2010, she met a young man, fell in love and was married. Then came a big surprise. I found out I was pregnant in April of 2016 and I was in disbelief, says Laura. We heard his heartbeat for the first time, and it was kind of like, oh my gosh, this is such a dream come true, its a miracle.

Young Joshau, named after his father, is what Laura is focused on now. She still helps run Beyond the Chair, but her days are mostly spent being a mom and promoting adult stem cell research.

Says Laura, a lot of people ask me about my experience with stem cells. I always tell them that at the end of the day the decision is up to them. But I promote them, I believe in them, I experienced it.

I think having the adult stem cell procedure was the best decision that Ive ever made.(Quote) I think that its been very beneficial, its helped me out so much, Laura said. My hope is that I can help other people and encourage other people. And spread the word about adult stem cells.

Disclaimer: is committed to educate about adult stem cell clinical trials and treatments which are validated by published research and approved by the U.S. FDA or similar international agencies. Clinical trials may not be effective for all patients or conditions. We are not a research or clinical facility and do not provide clinical trials or treatments.

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Stem cells for stenosis – Dr. Marc Darrow is a Stem Cell …

By Sykes24Tracey

Marc Darrow MD, JD. Thank you for reading my article. You can ask me your questions aboutthis articleusing the contact form below.

I want to begin this article with a case study from our recently published research in theBiomedical Journal of Scientific & Technical Research.

Afterphysical assessment of her lower back, we determinedher pain was generated from a lumbosacral sprain. Not the narrowing of the L1-L5,S1

She had oneBone marrow derived stem cell treatment and at first follow up two weeks after the injections,the patient experienced no pain or stiffness and reported 90% total improvement. Approximately a year after treatment, she felt evenbetter, and stated that she was able to perform aerobics and line dancing for an hour and a half a day with no pain. She reportedinfrequent stiffness, but not as severe as it was prior to treatment.

Her resting and active pain were 0/10 and functionality score was 39/40.(1)

This was one document case in the medical literature. Over the years we have helped many people avoid a stenosis surgery they did not want or possibly did not even need.

Despite the fact that many studies insist that surgical treatment is the best option for lumbar spinal stenosis, a startling study was published in the medical journal Spine. In this study, American, Canadian and Italian researchers published their evidence:

We have very little confidence to conclude whether surgicaltreatmentor a conservative approach is better forlumbarspinal stenosis, and we can provide no new recommendations to guide clinical practice. . .However, it should be noted that the rate of side effects ranged from 10% to 24% in surgical cases, and no side effects were reported for any conservativetreatment. (2)

In the above research it should be pointed out the comparison between lumbar surgery and conservative treatments did not include stem cell therapy. They included the traditional conservative treatments including physical therapy, cortisone injections, pain medications and others listed below.

One of the reasons surgery may be no better than conservative care is that the surgery tried to fix a problem that was not there: Pain.

In the medical journal Osteoarthritis and Cartilage,doctors reported that many asymptomatic individuals, those with no pain or other challenges, have radiographic lumbar spinal stenosis. In other words they only have lumbar spinal stenosis on the MRI.

The doctors noted:

A diagnosis of spinal stenosis can be frightening because of the implications that a surgery may be needed to avoid paralysis.It is important to note that in instances where stenosis is so severe that the patient has lost circulation to the legs or bladder control a surgical consult should be made immediately.

In the December 2017 edition of the medical journal Spine, doctors from the University of Pittsburgh and University Toronto reported these observations in patients seeking non-surgical treatments for lumbar spinal stenosis.

Individuals with lumbar spinal stenosis may believe misinformation and information from non-medical sources, especially when medical providers do not spend sufficient time explaining the disease process and the reasoning behind treatment strategies. Receiving individualized care focused on self-management led to fewer negative emotions toward care and the disease process. Clinicians should be prepared to address all three of these aspects when providing care to individuals with lumbar spinal stenosis.(4)

Back pain can certainly cause anxiety, depression, and catastrophizing thoughts. The people in this study wanted education and involvement in their choice of treatment. I hope I can provide some for you here in this article.

Lumbar Spinal Stenosis is a narrowing of the space between vertebrae where the spinal cord and the spinal nerves travel. It is a diagnostic term to describe lower back pain with or without weakness and loss of sensation in the legs. It is a very common condition brought on mostly by aging and the accompanying degeneration of the spine.

In the recommended surgical procedures for spinal stenosis, two choices are the most favored.

A paper published in October 2017 gives a good outline where conservative medicine is in the treatment of Lumbar stenosis. It is from doctors at the University of South Carolina

This is indeed a fair assessment of SOME of the treatment options available to patients.However, not all doctors agree. At New York University in June 2017 research, doctors wrote:

The highest levels of evidence do not support minimally invasive surgery over open surgery for cervical orlumbardisc herniation. However, minimally invasive surgery fusion demonstrates advantages along with higher revision and hospital readmission rates. These results should optimize informed decision-making regarding minimally invasive surgery versus open spine surgery, particularly in the current advertising climate greatly favoring minimally invasive surgery.(6)

Researchers at theUniversity of Sydneysay that the evidence for recommending lumbar spinal surgery as the best option to patients is lacking and it is possible that a sham or placebo surgery can deliver the same results.(7)

In the research I cited at the top of this article, doctors at the Italian Scientific Spine Institute in Milanwrote: We cannot conclude on the basis of this review whether surgical or nonsurgical treatment is better for individuals with lumbar spinal stenosis. We can however report on the high rate of effects reported in three of five surgical groups and that no side effects were reported for any of the conservative treatment options.(8)

Considering the majority of these procedures are unnecessarily being performed for degenerative disc disease alone, spine surgeons should be increasingly asked why they are offering these operations to their patients

Ateam of Japanese researchers found thatpatients with lumbar spinal stenosiswho do not improve after nonsurgical treatments are typically treated surgically using decompressive surgeryand spinal fusion surgery. Unfortunately the researchers could not determine if the surgery had any benefit either.(9)Maybe the patients problem was not the stenosis?

Now lets go to another paper that has more of an opinion: From Dr. Nancy Epstein ofWinthrop University Hospital:

Surgeons at Leiden University Medical Centre in the Netherlandsspeculate that doctors go into a diagnosis oflumbar spinal stenosis with the thought that there is osteoarthritis a bony overgrowth on the spinal nerves. Once determined, the symptoms of patients can be categorized into two groups; regional (low back pain, stiffness, and so on) or radicular (spinal stenosis mainly presenting as neurogenic claudication nerve inflammation).

In the patients who primarily complain of radiculopathy (radiating leg pain) with an stable spine, a decompression surgery may be recommendedto removebonefrom around thenerve root to give the nerve root more space.The surgeons warn of thefear that surgery to a stable spine will make it unstable.(11)

Afusion procedure to limit the movement between two vertebrae and hopefully stop the compression of nerves is another option. As mentioned by independent research above surgery for spinal stenosis should onlybe considered after conservative therapies have been exhausted.Surgical treatment of lumbar spinal disorders, including fusion, is associated with a substantial risk of intraoperative and perioperative complications,as pointed out in the research by surgeons from Catholic University in Rome.(12)

Bone growth occurs in the spine because the bone is trying to stabilize the spine from excessive movement or laxity. Fusion surgery is recommended as a means to accelerate that type of stabilization. Regenerative medicine includingPRP andStem Cell Therapy(watch the video)works in a completely different way. Theystabilize the spine by strengthening the often forgotten and underappreciated spinal ligaments and tendons.These techniques help stabilize the spine, which is imperative as unstable joints can lead to or further exacerbate the arthritis that causes spinal stenosis.

In the medical journal Insights into imaging, researchers wrote of the four factors associated with the degenerative changes of the spine that cause spinal canal stenosis:

The same research suggests that these conditions can prevent the formation of new tissue (collagen) which can initiate repair.(13)

Collagen is of course the elastic material of skin and ligaments. Here the association between collagen interruption and spinal stenosis can be made to show spinal instability can be THE problem of symptomatic stenosis.

A fascinating study on what damaged spinal ligaments can do

A fascinating study in the Asian Spine Journal investigated the relationship between ligamentum flavum thickening and lumbar segmental instability, disc degeneration, and facet joint osteoarthritis. Ligament thickening is the result of chronic inflammation. Chronic ligament inflammation is the result of a ligament injury that is not healing.

What these researchers found was a significant correlation between ligamentum flavum thickness, spinal instability and disc degeneration. More so, the worse the degenerative disc disease, the worse the ligamentum flavum thickness.(14)

PRP and stem cells address the problem of ligament damage and inflammation. Addressing these problems address the problems of spinal instability. Addressing the problems of spinal instability can address the problems of spinal and cervical stenosis.

A leading provider of bone marrow derived stem cell therapy, Platelet Rich Plasma and Prolotherapy11645 WILSHIRE BOULEVARD SUITE 120, LOS ANGELES, CA 90025

PHONE: (800) 300-9300

1 Darrow M, Shaw BS. Treatment of Lower Back Pain with Bone Marrow Concentrate. Biomed J Sci&Tech Res 7(2)-2018. BJSTR. MS.ID.001461. DOI: 10.26717/ BJSTR.2018.07.001461.

2 Zaina F, TomkinsLane C, Carragee E, Negrini S. Surgical versus nonsurgical treatment for lumbar spinal stenosis. The Cochrane Library. 2016 Jul 1.

3 Lynch AD, Bove AM, Ammendolia C, Schneider M. Individuals with lumbar spinal stenosis seek education and care focused on self-managementresults of focus groups among participants enrolled in a randomized controlled trial. The Spine Journal. 2017 Dec 12

4 Ishimoto Y, Yoshimura N, Muraki S, Yamada H, Nagata K, Hashizume H, Takiguchi N, Minamide A, Oka H, Kawaguchi H, Nakamura K. Associations between radiographic lumbar spinal stenosis and clinical symptoms in the general population: the Wakayama Spine Study. Osteoarthritis and cartilage. 2013 Jun 1;21(6):783-8.

5Patel J, Osburn I, Wanaselja A, Nobles R. Optimal treatment for lumbar spinal stenosis: an update. Current Opinion in Anesthesiology. 2017 Oct 1;30(5):598-603.

6 Vazan M, Gempt J, Meyer B, Buchmann N, Ryang YM. Minimally invasive transforaminal lumbar interbody fusion versus open transforaminal lumbar interbody fusion: a technical description and review of the literature. Acta Neurochir (Wien). 2017 Jun;159(6):1137-1146

7Machado GC, Ferreira PH, Yoo RI, et al. Surgical options for lumbar spinal stenosis. Cochrane Database Syst Rev. 2016 Nov 1;11:CD012421.

8Zaina F, Tomkins-Lane C, Carragee E, Negrini S. Surgical Versus Nonsurgical Treatment for Lumbar Spinal Stenosis. Spine (Phila Pa 1976). 2016 Jul 15;41(14):E857-68.

9 Inoue G, Miyagi M, Takaso M. Surgical and nonsurgical treatments for lumbar spinal stenosis. Eur J Orthop Surg Traumatol. 2016 Oct;26(7):695-704. doi: 10.1007/s00590-016-1818-3. Epub 2016 Jul 25.

10 Epstein NE. More nerve root injuries occur with minimally invasive lumbar surgery: Lets tell someone. Surg Neurol Int. 2016 Jan 25;7(Suppl 3):S96-S101. doi: 10.4103/2152-7806.174896. eCollection 2016.

11Overdevest GM, Moojen WA, Arts MP, Vleggeert-Lankamp CL, Jacobs WC, Peul WC.Management of lumbar spinal stenosis: a survey among Dutch spine surgeons. Acta Neurochir (Wien). 2014 Aug 7. [Epub ahead of print]

12.Proietti L, Scaramuzzo L, Schiro GR, Sessa S, Logroscino CA. Complications in lumbar spine surgery: A retrospective analysis. Indian J Orthop. 2013 Jul;47(4):340-5. doi: 10.4103/0019-5413.114909.

13 Kushchayev SV, Glushko T, Jarraya M, et al. ABCs of the degenerative spine.Insights into Imaging. 2018;9(2):253-274. doi:10.1007/s13244-017-0584-z.

14 Yoshiiwa T, Miyazaki M, Notani N, Ishihara T, Kawano M, Tsumura H. Analysis of the Relationship between Ligamentum Flavum Thickening and Lumbar Segmental Instability, Disc Degeneration, and Facet Joint Osteoarthritis in Lumbar Spinal Stenosis.Asian Spine Journal. 2016;10(6):1132-1140. doi:10.4184/asj.2016.10.6.1132.2373

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Scientists regenerate spinal cord in injured rats with …

By raymumme

With patches of stem cells on their broken spinal cords, partially paralyzed rats once againreached out and grabbed distant treats, researchers report in Nature Medicine.

While previous studies have shown progress in regenerating certain types of nerve cells in injured spinal cords, the study is the first to coax the regrowth of a specific set of nerve cells, called corticospinal axons. These bundles of biological wiring carry signals from the brain to the spinal cord and are critical for voluntary movement. In the study, researchers were able to use stem cells from rats and humans to mend the injured rodents.

The corticospinal projection is the most important motor system in humans, senior author Mark Tuszynski at the University of California, San Diego said. It has not been successfully regenerated before. Many have tried, many have failedincluding us, in previous efforts.

For the study, the researchers used rat and human neural progenitor cells, which can produce several different types of cells found in the central nervous system. The researchers coaxed the cells into forming spinal cord tissue using specific chemical signals. When injected into the damaged spinal cords of rats, the cells took root, filling lesions with new tissue and corticospinal axons. And the new nerve cells linked up with the severed connections left hanging from the injury, allowing signals to traverse the patch.

In mobility tests, injured rats that got the spinal patch could better stretch out their front legs to grab hard-to-reach treats compared with injured rats without the stem-cell grafts.

Still, the cord-patching method is far from clinical use in humans, the authors caution. Researchers will need to follow the rats to look at long-term safety and effectiveness of the patches. Then, they'll have to try out the patches in other animal models before optimizing the method for humans.

But,Tuszynski said, "now that we can regenerate the most important motor system for humans, I think that the potential for translation is more promising."

Nature Medicine, 2015. DOI: 10.1038/nm.4066 (About DOIs).

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Spinal Cord Injury Types of Injury, Diagnosis and Treatment


According to the National Spinal Cord Injury Association, as many as 450,000 people in the U.S. are living with a spinal cord injury (SCI). Other organizations conservatively estimate this figure to be about 250,000.

The spinal cord is about 18 inches long, extending from the base of the brain to near the waist. Many of the bundles of nerve fibers that make up the spinal cord itself contain upper motor neurons (UMNs). Spinal nerves that branch off the spinal cord at regular intervals in the neck and back contain lower motor neurons (LMNs).

Types and Levels of SCI

The severity of an injury depends on the part of the spinal cord that is affected. The higher the SCI on the vertebral column, or the closer it is to the brain, the more effect it has on how the body moves and what one can feel. More movement, feeling and voluntary control are generally present with injuries at lower levels.

Tetraplegia (a.k.a. quadriplegia) results from injuries to the spinal cord in the cervical (neck) region, with associated loss of muscle strength in all four extremities.

Paraplegia results from injuries to the spinal cord in the thoracic or lumbar areas, resulting in paralysis of the legs and lower part of the body.

Complete SCI

A complete SCI produces total loss of all motor and sensory function below the level of injury. Nearly 50 percent of all SCIs are complete. Both sides of the body are equally affected. Even with a complete SCI, the spinal cord is rarely cut or transected. More commonly, loss of function is caused by a contusion or bruise to the spinal cord or by compromise of blood flow to the injured part of the spinal cord.

Incomplete SCI

In an incomplete SCI, some function remains below the primary level of the injury. A person with an incomplete injury may be able to move one arm or leg more than the other or may have more functioning on one side of the body than the other. An incomplete SCI often falls into one of several patterns.

Anterior cord syndrome results from injury to the motor and sensory pathways in the anterior parts of the spinal cord. These patients can feel some types of crude sensation via the intact pathways in the posterior part of the spinal cord, but movement and more detailed sensation are lost.

Central cord syndrome usually results from trauma and is associated with damage to the large nerve fibers that carry information directly from the cerebral cortex to the spinal cord. Symptoms may include paralysis and/or loss of fine control of movements in the arms and hands, with far less impairment of leg movements. Sensory loss below the site of the SCI and loss of bladder control may also occur, with the overall amount and type of functional loss related to the severity of damage to the nerves of the spinal cord.

Brown-Sequard syndrome is a rare spinal disorder that results from an injury to one side of the spinal cord. It is usually caused by an injury to the spine in the region of the neck or back. In many cases, some type of puncture wound in the neck or in the back that damages the spine may be the cause. Movement and some types of sensation are lost below the level of injury on the injured side. Pain and temperature sensation are lost on the side of the body opposite the injury because these pathways cross to the opposite side shortly after they enter the spinal cord.

Injuries to a specific nerve root may occur either by themselves or together with a SCI. Because each nerve root supplies motor and sensory function to a different part of the body, the symptoms produced by this injury depend upon the pattern of distribution of the specific nerve root involved.

"Spinal concussions" can also occur. These can be complete or incomplete, but spinal cord dysfunction is transient, generally resolving within one or two days. Football players are especially susceptible to spinal concussions and spinal cord contusions. The latter may produce neurological symptoms including numbness, tingling, electric shock-like sensations and burning in the extremities. Fracture-dislocations with ligamentous tears may be present in this syndrome.

Penetrating SCI

"Open" or penetrating injuries to the spine and spinal cord, especially those caused by firearms, may present somewhat different challenges. Most gunshot wounds to the spine are stable; i.e., they do not carry as much risk of excessive and potentially dangerous motion of the injured parts of the spine. Depending upon the anatomy of the injury, the patient may need to be immobilized with a collar or brace for several weeks or months so that the parts of the spine that were fractured by the bullet may heal. In most cases, surgery to remove the bullet does not yield much benefit and may create additional risks, including infection, cerebrospinal fluid leak and bleeding. However, occasional cases of gunshot wounds to the spine may require surgical decompression and/or fusion in an attempt to optimize patient outcome.


When SCI is suspected, immediate medical attention is required. SCI is usually first diagnosed when the patient presents with loss of function below the level of injury.

Signs and Symptoms of Possible SCI:

Clinical Evaluation

A physician may decide that significant SCI does not exist simply by examining a patient who does not have any of the above symptoms, as long as the patient meets the following criteria: unaltered mental status, no neurological deficits, no intoxication from alcohol, drugs or medications and no other painful injuries that may divert his or her attention away from a SCI.

In other cases, such as when patients complain of neck pain, when they are not fully awake, or when they have obvious weakness or other signs of neurological injury, the cervical spine is kept in a rigid collar until appropriate radiological studies are completed.

Radiological Evaluation

The radiological diagnosis of SCI has traditionally begun with X-rays. In many cases, the entire spine may be X-rayed. Patients with a SCI may also receive both computerized tomography (CT or CAT scan) and magnetic resonance imaging (MRI) of the spine. In some patients, centers may proceed directly to CT scanning as the initial radiological test. For patients with known or suspected injuries, MRI is helpful for looking at the actual spinal cord itself, as well as for detecting any blood clots, herniated discs or other masses that may be compressing the spinal cord. CT scans may be helpful in visualizing the bony anatomy, including any fractures.

Even after all radiological tests have been performed, it may be advisable for a patient to wear a collar for a variable period of time. If patients are awake and alert, but still complaining of neck pain, a physician may send them home in a collar, with plans to repeat X-rays in the near future, such as in one to two weeks. The concern in these cases is that muscle spasm caused by pain might be masking an abnormal alignment of the bones in the spinal column. Once this period of spasm passes, repeat X-rays may reveal abnormal alignment or excessive motion that was not visible immediately after the injury. In patients who are comatose, confused or not fully cooperative for some other reason, adequate radiographic visualization of parts of the spine may be difficult. This is especially true of the bones at the very top of the cervical spine. In such cases, the physician may keep the patient in a collar until the patient is more cooperative. Alternatively, the physician may obtain other imaging studies to look for a radiologically-evident injury.


Treatment of SCI begins before the patient is admitted to the hospital. Paramedics or other emergency medical services personnel carefully immobilize the entire spine at the scene of the accident. In the emergency department, this immobilization is continued while more immediate life-threatening problems are identified and addressed. If the patient must undergo emergency surgery because of trauma to the abdomen, chest or another area, immobilization and alignment of the spine are maintained during the operation.

Intensive Care Unit Treatment

If a patient has a SCI, he or she will usually be admitted to an intensive care unit (ICU). For many injuries of the cervical spine, traction may be indicated to help bring the spine into proper alignment. Standard ICU care, including maintaining a stable blood pressure, monitoring cardiovascular function, ensuring adequate ventilation and lung function and preventing and promptly treating infection and other complications, is essential so that SCI patients can achieve the best possible outcome.


Occasionally, a surgeon may wish to take a patient to the operating room immediately if the spinal cord appears to be compressed by a herniated disc, blood clot or other lesion. This is most commonly done for patients with an incomplete SCI or with progressive neurological deterioration.

Even if surgery cannot reverse damage to the spinal cord, surgery may be needed to stabilize the spine to prevent future pain or deformity. The surgeon will decide which procedure will provide the greatest benefit to the patient.


Persons with neurologically complete tetraplegia are at high risk for secondary medical complications. The percentages of complications for individuals with neurologically complete tetraplegia have been reported as follows:

Pressure ulcers are the most frequently observed complications, beginning at 15 percent during the first year post-injury and steadily increasing thereafter. The most common pressure ulcer location is the sacrum, the site of one third of all reported ulcers.

Source: National Spinal Cord Injury Statistical Center, University of Alabama at Birmingham, Annual Statistical Report, June 2004

Neurological Improvement

Recovery of function depends upon the severity of the initial injury. Unfortunately, those who sustain a complete SCI are unlikely to regain function below the level of injury. However, if there is some degree of improvement, it usually evidences itself within the first few days after the accident.

Incomplete injuries usually show some degree of improvement over time, but this varies with the type of injury. Although full recovery may be unlikely in most cases, some patients may be able to improve at least enough to ambulate and to control bowel and bladder function. Patients with anterior cord syndrome tend to do poorly, but many of those with Brown-Sequard syndrome can expect to reach these goals. Patients with central cord syndrome often recover to the point of being ambulatory and controlling bowel and bladder function, but they often are not able to perform detailed or intricate work with their hands.

Once a patient is stabilized, care and treatment focuses on supportive care and rehabilitation. Family members, nurses or specially trained aides all may provide supportive care. This care might include helping the patient bathe, dress, change positions to prevent bedsores and other assistance.

Rehabilitation often includes physical therapy, occupational therapy and counseling for emotional support. The services may initially be provided while the patient is hospitalized. Following hospitalization, some patients are admitted to a rehabilitation facility. Other patients can continue rehab on an outpatient basis and/or at home.


Mortality associated with SCI is influenced by several factors. Perhaps the most important of these is the severity of associated injuries. Because of the force that is required to fracture the spine, it is not uncommon for a SCI patient to suffer significant damage to the chest and/or abdomen. Many of these associated injuries can be fatal. In general, younger patients and those with incomplete injuries have a better prognosis than older patients and those with complete injuries.

Respiratory diseases are the leading cause of death in people with SCI, pneumonia accounting for 71.2 percent of these deaths. The second and third leading causes of death, respectively, are heart disease and infections.

The cumulative 20-year survival rate for SCI patients is 70.65 percent, but due to underreporting and cases that are lost in follow-up, the mortality rates may be higher.

Source: National Spinal Cord Injury Statistical Center, University of Alabama at Birmingham, Annual Statistical Report, June 2004

SCI Prevention

While recent advances in emergency care and rehabilitation allow many SCI patients to survive, methods for reducing the extent of injury and for restoring function are still limited. Currently, there is no cure for SCI. However, ongoing research to test surgical and drug therapies continues to make progress. Drug treatments,decompression surgery,nerve cell transplantation,nerve regeneration, stem cells and complex drug therapies are all being examined in clinical trials as ways to overcome the effects of SCI. However, SCI prevention is crucial to decreasing the impact of these injuries on individual patients and on society.

Motor Vehicle Safety Tips:

Tips to Prevent Falls in the Home:

Water and Sports Safety Tips:

Firearms Safety:

SCI Resources

The AANS does not endorse any treatments, procedures, products or physicians referenced in these patient fact sheets. This information is provided as an educational service and is not intended to serve as medical advice. Anyone seeking specific neurosurgical advice or assistance should consult his or her neurosurgeon, or locate one in your area through the AANS Find a Board-certified Neurosurgeon online tool.

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Spinal Cord Injury Types of Injury, Diagnosis and Treatment

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Repairing the Damaged Spinal Cord – Scientific American

By Dr. Matthew Watson

Editor's Note: This story, originally printed in the September 1999 issue of Scientific American, is being posted due to a new study showing that nerve cells can be regenerated by knocking out genes that typically inhibit their growth.

For Chinese gymnast Sang Lan, the cause was a highly publicized headfirst fall during warm-ups for the 1998 Goodwill Games. For Richard Castaldo of Littleton, Colo., it was bullets; for onetime football player Dennis Byrd, a 1992 collision on the field; and for a child named Samantha Jennifer Reed, a fall during infancy. Whatever the cause, the outcome of severe damage to the spinal cord is too often the same: full or partial paralysis and loss of sensation below the level of the injury.

Ten years ago doctors had no way of limiting such disability, aside from stabilizing the cord to prevent added destruction, treating infections and prescribing rehabilitative therapy to maximize any remaining capabilities. Nor could they rely on the cord to heal itself. Unlike tissue in the peripheral nervous system, that in the central nervous system (the spinal cord and brain) does not repair itself effectively. Few scientists held out hope that the situation would ever change.

Then, in 1990, a human trial involving multiple research centers revealed that a steroid called methylprednisolone could preserve some motor and sensory function if it was administered at high doses within eight hours after injury. For the first time, a therapy had been proved to reduce dysfunction caused by spinal cord trauma. The improvements were modest, but the success galvanized a search for additional therapies. Since then, many investigatorsincluding us have sought new ideas for treatment in studies of why an initial injury triggers further damage to the spinal cord and why the disrupted tissue fails to reconstruct itself.

In this article we will explain how the rapidly burgeoning knowledge might be harnessed to help people with spinal cord injuries. We should note, however, that workers have also been devising strategies that compensate for cord damage instead of repairing it. In the past two years, for example, the U.S. Food and Drug Administration has approved two electronic systems that regulate muscles by sending electrical signals through implanted wires. One returns certain hand movements (such as grasping a cup or a pen) to patients who have shoulder mobility; another restores a measure of control over the bladder and bowel.

A different approach can also provide grasping ability to certain patients. Surgeons identify tendons that link paralyzed forearm muscles to the bones of the hand, disconnect them from those muscles and connect them to arm muscles regulated by parts of the spine above the injury (and thus still under voluntary control). Further, many clinicians suspect that initiating rehabilitative therapy earlyexercising the limbs almost as soon as the spine is stabilizedmay enhance motor and sensory function in limbs. Those perceptions have not been tested rigorously in people, but animal studies lend credence to them.

The Cord at Work The organ receiving all this attention is no thicker than an inch but is the critical highway of communication between the brain and the rest of the body. The units of communication are the nerve cells (neurons), which consist of a bulbous cell body (home to the nucleus), trees of signal-detecting dendrites, and an axon that extends from the cell body and carries signals to other cells. Axons branch toward their ends and can maintain connections, or synapses, with many cells at once. Some traverse the entire length of the cord.

The soft, jellylike cord has two major systems of neurons. Of these, the descending, motor pathways control both smooth muscles of internal organs and striated muscles; they also help to modulate the actions of the autonomic nervous system, which regulates blood pressure, temperature and the bodys circulatory response to stress. The descending pathways begin with neurons in the brain, which send electrical signals to specific levels, or segments, of the cord. Neurons in those segments then convey the impulses outward beyond the cord.

The other main system of neurons the ascending, sensory pathwaystransmit sensory signals received from the extremities and organs to specific segments of the cord and then up to the brain. Those signals originate with specialized, transducer cells, such as sensors in the skin that detect changes in the environment or cells that monitor the state of internal organs. The cord also contains neuronal circuits (such as those involved in reflexes and certain aspects of walking) that can be activated by incoming sensory signals without input from the brain, although they can be influenced by messages from the brain.

The cell bodies in the trunk of the cord reside in a gray, butterfly-shaped core that spans the length of the spinal cord. The ascending and descending axonal fibers travel in a surrounding area known as the white matter, so called because the axons are wrapped in myelin, a white insulating material. Both regions also house glial cells, which help neurons to survive and work properly. The glia include star-shaped astrocytes, microglia (small cells that resemble components of the immune system) and oligodendrocytes, the myelin producers. Each oligodendrocyte myelinates as many as 40 different axons simultaneously.

The precise nature of a spinal cord injury can vary from person to person. Nevertheless, certain commonalities can be discerned.

When Injury Strikes When a fall or some other force fractures or dislocates the spinal column, the vertebral bones that normally enclose and protect the cord can crush it, mechanically killing and damaging axons. Occasionally, only the gray matter in the damaged area is significantly disrupted. If the injury ended there, muscular and sensory disturbances would be confined to tissues that send input to or receive it from neurons in the affected level of the cord, without much disturbing function below that level.

For instance, if only the gray matter were affected, a cervical 8 (C8) lesion involving the cord segment where the nerves labeled C8 originatewould paralyze the hands without impeding walking or control over the bowel and bladder. No signals would go out to, or be received from, the tissues connected to the C8 nerves, but the axons conveying signals up and down the surrounding white matter would keep working.

In contrast, if all the white matter in the same cord segment were destroyed, the injury would now interrupt the vertical signals, stopping messages that originated in the brain from traveling below the damaged area and blocking the flow to the brain of sensory signals coming from below the wound. The person would become paralyzed in the hands and lower limbs and would lose control over urination and defecation.

Sadly, the initial insult is only the beginning of the trouble. The early mechanical injury triggers a second wave of damageone that, over the subsequent minutes, hours and days, progressively enlarges the lesion and thus the extent of functional impairment. This secondary spread tends to occur longitudinally through the gray matter at first before expanding into the white matter (roughly resembling the inflation of a footballshaped balloon). Eventually the destruction can encompass several spinal segments above and below the original wound.

The end result is a complex state of disrepair. Axons that have been damaged become useless stumps, connected to nothing, and their severed terminals disintegrate. Often many axons remain intact but are rendered useless by loss of their insulating myelin. A fluid-filled cavity, or cyst, sits where neurons, other cells and axons used to be. And glial cells proliferate abnormally, creating clusters termed glial scars. Together the cyst and scars pose a formidable barrier to any cut axons that might somehow try to regrow and connect to cells they once innervated. A few axons may remain whole, myelinated and able to carry signals up or down the spine, but often their numbers are too small to convey useful directives to the brain or muscles.

First, Contain the Damage If all these changes had to be fully reversed to help patients, the prospects for new treatments would be grim. Fortunately, it appears that salvaging normal activity in as little as 10 percent of the standard axon complement would sometimes make walking possible for people who would otherwise lack that capacity. In addition, lowering the level of injury by just a single segment (about half an inch) can make an important difference to a persons quality of life. People with a C6 injury have no power over their arms, save some ability to move their shoulders and flex their elbows. But individuals with a lower, C7 injury can move the shoulders and elbow joints and extend the wrists; with training and sometimes a tendon transfer, they can make some use of their arms and hands.

Because so much damage arises after the initial injury, clarifying how that secondary destruction occurs and blocking those processes are critical. The added wreckage has been found to result from many interacting mechanisms.

Within minutes of the trauma, small hemorrhages from broken blood vessels appear, and the spinal cord swells. The blood vessel damage and swelling prevent the normal delivery of nutrients and oxygen to cells, causing many of them to starve to death.

Meanwhile damaged cells, axons and blood vessels release toxic chemicals that go to work on intact neighboring cells. One of these chemicals in particular triggers a highly disruptive process known as excitotoxicity. In the healthy cord the end tips of many axons secrete minute amounts of glutamate. When this chemical binds to receptors on target neurons, it stimulates those cells to fire impulses. But when spinal neurons, axons or astrocytes are injured, they release a flood of glutamate. The high levels overexcite neighboring neurons, inducing them to admit waves of ions that then trigger a series of destructive events in the cellsincluding production of free radicals. These highly reactive molecules can attack membranes and other components of formerly healthy neurons and kill them.

Until about a year ago, such excitotoxicity, also seen after a stroke, was thought to be lethal to neurons alone, but new results suggest it kills oligodendrocytes (the myelin producers) as well. This effect may help explain why even unsevered axons become demyelinated, and thus unable to conduct impulses, after spinal cord trauma.

Prolonged inflammation, marked by an influx of certain immune system cells, can exacerbate these effects and last for days. Normally, immune cells stay in the blood, unable to enter tissues of the central nervous system. But they can flow in readily where blood vessels are damaged. As they and microglia become activated in response to an injury, the activated cells release still more free radicals and other toxic substances.

Methylprednisolone, the first drug found to limit spinal cord damage in humans, may act in part by reducing swelling, inflammation, the release of glutamate and the accumulation of free radicals. The precise details of how it helps patients remain unclear, however.

Studies of laboratory animals with damaged spinal cords indicate that drugs able to stop cells from responding to excess glutamate could minimize destruction as well. Agents that selectively block glutamate receptors of the so-called AMPA class, a kind abundant on oligodendrocytes and neurons, seem to be particularly effective at limiting the final extent of a lesion and the related disability. Certain AMPA receptor antagonists have already been tested in early human trials as a therapy for stroke, and related compounds could enter safety studies in patients with spinal cord injury within several years.

Much of the early cell loss in the injured spinal cord occurs by necrosis, a process in which cells essentially become passive victims of murder. In the past few years, neurobiologists have also documented a more active form of cell death, somewhat akin to suicide, in the cord. Days or weeks after the initial trauma, a wave of this cell suicide, or apoptosis, frequently sweeps through oligodendrocytes as many as four segments from the trauma site. This discovery, too, has opened new doors for protective therapy. Rats given apoptosisinhibiting drugs retained more ambulatory ability after a traumatic spinal cord injury than did untreated rats.

In the past few years, biologists have identified many substances, called neurotrophic factors, that also promote neuronal and glial cell survival. A related substance, GM-1 ganglioside (Sygen), is now being evaluated for limiting cord injury in humans. Ultimately, interventions for reducing secondary damage in the spinal cord will probably enlist a variety of drugs given at different times to thwart specific mechanisms of death in distinct cell populations.

The best therapy would not only reduce the extent of an injury but also repair damage. A key component of that repair would be stimulating the regeneration of damaged axonsthat is, inducing their elongation and reconnection with appropriate target cells.

Although neurons in the central nervous system of adult mammals generally fail to regenerate damaged axons, this lapse does not stem from an intrinsic property of those cells. Rather the fault lies with shortcomings in their environment. After all, neurons elsewhere in the body and in the immature spinal cord and brain regrow axons readily, and animal experiments have shown that the right environment can induce axons of the spinal cord to extend quite far.

Then, Induce Regeneration One shortcoming of the cord environment turns out to be an overabundance of molecules that actively inhibit axonal regenerationsome of them in myelin. The scientists who discovered these myelin-related inhibitors have produced a molecule named IN-1 (inhibitorneutralizing antibody) that blocks the action of those inhibitors. They have also demonstrated that infusion of mouse-derived IN-1 into the injured rat spinal cord can lead to long-distance regrowth of some interrupted axons. And when pathways controlling front paw activity are severed, treated animals regain some paw motion, whereas untreated animals do not. The rodent antibody would be destroyed by the human immune system, but workers are developing a humanized version for testing in people.

Many other inhibitory molecules have now been found as well, including some produced by astrocytes and a number that reside in the extracellular matrix (the scaffolding between cells). Given this array, it seems likely that combination therapies will be needed to counteract or shut down the production of multiple inhibitors at once.

Beyond removing the brakes on axonal regrowth, a powerful tactic would supply substances that actively promote axonal extension. The search for such factors began with studies of nervous system development. Decades ago scientists isolated nerve growth factor (NGF), a neurotrophic factor that supports the survival and development of the peripheral nervous system. Subsequently, this factor turned out to be part of a family of proteins that both enhance neuronal survival and favor the outgrowth of axons. Many other families of neurotrophic factors with similar talents have been identified as well. For instance, the molecule neurotrophin- 3 (NT-3) selectively encourages the growth of axons that descend into the spinal cord from the brain.

Luckily, adult neurons remain able to respond to axon-regenerating signals from such factors. Obviously, however, natural production of these substances falls far short of the amount needed for spinal cord repair. Indeed, manufacture of some of the compounds apparently declines, instead of rising, for weeks after a spinal trauma occurs. According to a host of animal studies, artificially raising those levels after an injury can enhance regeneration. Some regeneration- promoting neurotrophic factors, such as basic fibroblast growth factor, have been tested in stroke patients. None has been evaluated as an aid to regeneration in people with spinal cord damage, but many are being assessed in animals as a prelude to such studies.

Those considering neurotrophic factors for therapy will have to be sure that the agents do not increase pain, a common long-term complication of spinal cord injury. This pain has many causes, but one is the sprouting of nascent axons where they do not belong (perhaps in a failed attempt to address the injury) and their inappropriate connection to other cells. The brain sometimes misinterprets impulses traveling through those axons as pain signals. Neurotrophic factors can theoretically exacerbate that problem and can also cause pain circuits in the spiral cord and pain-sensing cells in the skin to become oversensitive.

After axons start growing, they will have to be guided to their proper targets, the cells to which they were originally wired. But how? In this case, too, studies of embryonic development have offered clues.

During development, growing axons are led to their eventual targets by molecules that act on the leading tip, or growth cone. In the past five years especially, a startling number of substances that participate in this process have been uncovered. Some, such as a group called netrins, are released or displayed by neurons or glial cells. They beckon axons to grow in some directions and repel growth in others. Additional guidance molecules are fixed components of the extracellular matrix. Certain of the matrix molecules bind well to specific molecules (cell adhesion molecules) on the growth cones and thus provide anchors for growing axons. During development, the required directional molecules are presented to the growth cones in specific sequences.

Establish Proper Connections At the moment, no one knows how to supply all the needed chemical road signs in the right places. But some findings suggest that regeneration may be aided by supplying just a subset of those targeting moleculessay, a selection of netrins and components from the extracellular matrix. Substances already in the spinal cord may well be capable of supplying the rest of the needed guidance.

A different targeting approach aims to bridge the gap created by cord damage. It directs injured axons toward their proper destinations by supplying a conduit through which they can travel or by providing another friendly scaffolding able to give physical support to the fibers as they try to traverse the normally impenetrable cyst. The scaffolding can also serve as a source of growth-promoting chemicals.

For instance, researchers have implanted tubes packed with Schwann cells into the gap where part of the spinal cord was removed in rodents. Schwann cells, which are glia of the peripheral nervous system, were chosen because they have many attributes that favor axonal regeneration. In animal experiments, such grafts spurred some axonal growth into the tubes.

A second bridging material consists of olfactory-ensheathing glial cells, which are found only in the tracts leading from the nose to the olfactory bulbs of the brain. When those cells were put into the rat spinal cord where descending tracts had been cut, the implants spurred partial regrowth of the axons over the implant. Transplanting the olfactory-ensheathing glia with Schwann cells led to still more extensive growth.

In theory, a biopsy could be performed to obtain the needed olfactory ensheathing glia from a patient. But once the properties that enable them (or other cells) to be competent escorts for growing axons are determined, researchers may instead be able to genetically alter other cell types if desired, giving them the required combinations of growthpromoting properties.

Fibroblasts (cells common in connective tissue and the skin) are among those already being engineered to serve as bridges. They have been altered to produce the neurotrophic molecule NT-3 and then transplanted into the cut spinal cord of rodents. The altered fibroblasts have resulted in partial regrowth of axons. Along with encouraging axonal regrowth, NT-3 stimulates remyelination. In these studies the genetically altered fibroblasts have enhanced myelination of regenerated axons and improved hind limb activity.

Replace Lost Cells Other transplantation schemes would implant cells that normally occur in the central nervous system. In addition to serving as bridges and potentially releasing proteins helpful for axonal regeneration, certain of these grafts might be able to replace cells that have died.

Transplantation of tissue from the fetal central nervous system has produced a number of exciting results in animals treated soon after a trauma. This immature tissue can give rise to new neurons, complete with axons that travel long distances into the recipients tissues (up and down several segments in the spinal cord or out to the periphery). It can also prompt host neurons to send regenerating axons into the implanted tissue. In addition, transplant recipients, unlike untreated animals, may recover some limb function, such as the ability to move the paw in useful ways. What is more, studies of fetal tissue implants suggest that axons can at times find appropriate targets even in the absence of externally supplied guidance molecules. The transplants, however, are far more effective in the immature spinal cord than in the injured adult cordan indication that young children would probably respond to such therapy much better than adolescents or adults would.

Some patients with long-term spinal cord injuries have received human fetal tissue transplants, but too little information is available so far for drawing any conclusions. In any case, application of fetal tissue technology in humans will almost surely be limited by ethical dilemmas and a lack of donor tissue. Therefore, other ways of achieving the same results will have to be devised. Among the alternatives is transplanting stem cells: immature cells that are capable of dividing endlessly, of making exact replicas of themselves and also of spawning a range of more specialized cell types.

Various kinds of stem cells have been identified, including ones that generate all the cell types in the blood system, the skin, or the spinal cord and brain. Stem cells found in the human adult central nervous system have, moreover, been shown capable of producing neurons and all their accompanying glia, although these so-called neural stem cells seem to be quiescent in most regions of the system. In 1998 a few laboratories also obtained much more versatile stem cells from human tissue. These human embryonic stem cells (in common with embryonic stem cells obtained previously from other vertebrates) can be grown in culture and, in theory, can yield almost all the cell types in the body, including those of the spinal cord.

Stem Cell Strategies How might stem cells aid in spinal cord repair? A great deal will be possible once biologists learn how to obtain those cells readily from a patient and how to control the cells differentiation. Notably, physicians might be able to withdraw neural stem cells from a patients brain or spinal cord, expand the numbers of the still undifferentiated cells in the laboratory and place the enlarged population in the same persons cord with no fear that the immune system will reject the implant as foreign. Or they might begin with frozen human embryonic stem cells, coax those cells to become precursors, or progenitors, of spinal cells and implant a large population of the precursors. Studies proposing to examine the effects on patients with spinal cord injuries of transplanting neural stem cells (isolated from the patients brains by biopsy) are being considered.

Simply implanting progenitor cells into the cord may be enough to prod them to multiply and differentiate into the needed lineages and thus to replace useful numbers of lost neurons and glial cells and establish the proper synaptic connections between neurons. Stem cells transplanted into the normal and injured nervous systems of animals can form neurons and glia appropriate for the region of transplantation. Combined with the fetal tissue results, this outcome signifies that many important cues for differentiation and targeting preexist in the injured nervous system. But if extra help is needed, scientists might be able to deliver it through genetic engineering. As a rule, to be genetically altered easily, cells have to be able to divide. Stem cells, unlike mature neurons, fit that bill.

Scenarios involving stem cell transplants are admittedly futuristic, but one day they themselves may become unnecessary, replaced by gene therapy alone. Delivery of genes into surviving cells in the spinal cord could enable those cells to manufacture and release a steady supply of proteins able to induce stem cell proliferation, to enhance cell differentiation and survival, and to promote axonal regeneration, guidance and remyelination. For now, though, technology for delivering genes to the central nervous system and for ensuring that the genes survive and work properly is still being refined.

Until, and even after, cell transplants and gene therapies become commonplace for coping with spinal cord injury, patients might gain help through a different avenuedrugs that restore signal conduction in axons quieted by demyelination. Ongoing clinical tests are evaluating the ability of a drug called 4-aminopyridine to compensate for demyelination. This agent temporarily blocks potassium ion channels in axonal membranes and, in so doing, allows axons to transmit electrical signals past zones of demyelination. Some patients receiving the drug have demonstrated modest improvement in sensory or motor function.

At first glance, this therapy might seem like a good way to treat multiple sclerosis, which destroys the myelin around axons of neurons in the central nervous system. Patients with this disease are prone to seizures, however, and 4-aminopyridine can exacerbate that tendency.

Neurotrophic factors, such as NT-3, that can stimulate remyelination of axons in animals could be considered for therapy as well. NT-3 is already entering extensive (phase III) trials in humans with spinal cord injury, though not to restore myelin. It will be administered by injection in amounts capable of acting on nerves in the gut and of enhancing bowel function, but the doses will be too low to yield high concentrations in the central nervous system. If the drug proves to be safe in this trial, though, that success could pave the way for human tests of doses large enough to enhance myelination or regeneration.

The Years Ahead Clearly, the 1990s have seen impressive advances in understanding of spinal cord injury and the controls on neuronal growth. Like axons inching toward their targets, a growing number of investigators are pushing their way through the envelope of discovery and generating a rational game plan for treating such damage. That approach will involve delivery of multiple therapies in an orderly sequence. Some treatments will combat secondary injury, some will encourage axonal regrowth or remyelination, and some will replace lost cells.

When will the new ideas become real treatments? We wish we had an answer. Drugs that work well in animals do not always prove useful in people, and those that show promise in small human trials do not always pan out when examined more extensively. It is nonetheless encouraging that at least two human trials are now under way and that others could start in the next several years.

Limiting an injury will be easier than reversing it, and so treatments for ameliorating the secondary damage that follows acute trauma can be expected to enter human testing most quickly. Of the repair strategies, promoting remyelination will be the simplest to accomplish, because all it demands is the recoating of intact axons. Remyelination strategies have the potential to produce meaningful recovery of function, such as returning control over the bladder or bowel abilities that uninjured people take for granted but that would mean the world to those with spinal cord injuries.

Of course, tendon-transfer surgery and advanced electrical devices can already restore important functions in some patients. Yet for many people, a return of independence in daily activities will depend on reconstruction of damaged tissue through the regrowth of injured axons and the reconnection of disrupted pathways.

So far, few interventions in animals with well-established spinal cord injuries have achieved the magnitude of regrowth and synapse formation that would be needed to provide a hand grasp or the ability to stand and walk in human adults with long-term damage. Because of the great complexities and difficulties involved in those aspects of cord repair, we cannot guess when reconstructive therapies might begin to become available. But we anticipate continued progress toward that end.

Traditionally, medical care for patients with spinal cord injury has emphasized compensatory strategies that maximize use of any residual cord function. That focus is now expanding, as treatments designed to repair the damaged cord and restore lost functionscience fiction only a decade agoare becoming increasingly plausible.

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Repairing the Damaged Spinal Cord - Scientific American

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Spinal Surgery Stem Cell Treatment | ProMedSPINE

By daniellenierenberg

Stem cells have the incredible ability to develop into a variety of different cell types within the body. In addition, stem cells can play a crucial role in internally repairing many types of tissues. During this process, stem cells divide, replenishing other cells without limit.

While stem cells have been used by medical professionals for a wide variety of reasons in order to treat injuries, ailments, and diseases affecting every part of the body, the use of stem cells in the treatment of spinal damage may be the most exciting and potent use yet. Through the application of these spinal treatments, patients have the ability to recover not only more completely, but also in a more natural and therefore more complete manner than ever before. When paired with the insight of a skilled spinal surgeon, the results can be astonishing.

If you or a loved one is suffering from spine damage and are looking to learn more about how stem cell treatments can help you, get in touch with the expert back team at ProMed SPINE today by filling out ouronline contact form. Schedule a consultation with us and begin the path to recovery today!

Stem cells differ from other cell types because they are unspecialized and therefore capable of renewing themselves through cell division. Under certain physiologic or experimental conditions, they have the ability to become tissue or even organ-specific cells with special functions. Given these unique regenerative abilities, stem cells offer new potential in the enhancement of every surgery.

Rather then undergoing an invasive surgery that wont actually repair damage from degenerative disc disease, stem cell spinal treatments are short, minimally invasive and capable of healing the damage that has been done to the disc. Stem cell therapy produces new disc cells inside the disc itself, allowing it to rebuild to a like-new condition. When treating degenerative disc disease, bone marrow is extracted from the patients hipbone and stem cells are filtered out using a centrifuge. Then stem cells are injected into the disc with the help of an x-ray. After this step, the patient is free to go home and begin the recovery process. Over the next few months to a year, patients will experience a lessening of back pain as the disc begins to restore itself. It is quite common for patients who have undergone stem cell injections to experience complete relief from back pain and a vast improvement in their overall quality of life.

Stem cells can also be used to enhance the effects of a spinal fusion surgery. A lack of useful new bone growth after this type of surgery can be a significant problem. This new technology helps patients grow new bone and avoid harvesting a bone graft from the patients own hip or using bone from a deceased donor. By avoiding these steps, patients are able to recover faster and prevent painful procedures.

A major component of stem cells is their ability to reinforce stronger, healthier healing in patients. Oftentimes, the body is in a weakened state following a surgical procedure and therefore more susceptible to developing infection. Stem cells unique ability to replenish themselves offers the body fresh, healthy cells that are not nearly as vulnerable to incurring infection so that the body can heal more quickly and effectively.

After undergoing a surgery and the rehabilitation process that follows, many patients are left with unsightly scars. These scars are often painful reminders of a traumatic event and, in some cases, cause self-consciousness or outright embarrassment due to their appearance. Stem cells have become an increasingly useful aid in ridding patients of unattractive scars so that they can fully recover from their injuries. Stem cells are useful in the treatment of scarring in three major ways: they carry anti-inflammatory properties that prevent excessive scarring, are capable of replenishing normal cells in the tissue through differentiation, and finally, stem cells dissolve the excess collagen in scar tissue by emitting large amounts of enzymes whose specific function is to dissolve scar tissue.

Click here to learnmore about stem cell therapy from

The potential medical benefits of stem cell research are unparalleled in the healing and rejuvenating processes following a spinal procedure. Whether you are facing a major surgery or are considering your options concerning continued pain and physical limitations, knowing what options may be best for you is vital in the search for skilled medical care. Schedule an appointment with a laser spine surgeonto find out how stem cell therapy can be used to help you find a healthier and happier life.

Next, please read about disc replacement surgery.

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Spinal Surgery Stem Cell Treatment | ProMedSPINE

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