Last updated:
August 14, 2019
Years published: 1988, 1990, 2000, 2013, 2019
NORD gratefully acknowledges Forest Tennant, MD, MPH, DrPH, Ingrid Hollis, and Lynn Ashcraft, Arachnoiditis Research Project of the Tennant Foundation, and Donna Corley, Arachnoiditis Society for Awareness and Prevention, for the preparation of this report.
Summary
Arachnoiditis is an inflammation of the middle layer (arachnoid) of the meninges, which is the protective covering that surrounds the brain, spinal cord and cauda equina nerve roots. The meninges (spinal canal covering) are connective tissue composed mainly of collagen and elastin. Injury, trauma, tumor, or infection can cause inflammation of the arachnoid layer at any location. Genetic and autoimmune disorders are now known to cause dissolution and degeneration of the arachnoid layer.
Arachnoiditis has been known since the 19th century when its major cause was infections, mainly tuberculosis and syphilis. The notorious and fearful label of arachnoiditis stems from the inability to treat or improve the condition once it is established. In the past and with no treatment available, this disorder caused excruciating pain, paralysis, immobility, incontinence, adrenal failure, and early death. Hence, its reputation as both “hopeless and untreatable”. During the 20th century the major cause of arachnoiditis was the use of insoluble oil-based dyes that were injected into spinal fluid to enhance x-ray vision, called myelograms, for diagnostic purposes. In this century adhesive arachnoiditis (AA) is the condition of most concern. It is caused by the adherence or “gluing” of the cauda equina nerve roots to the arachnoid spinal canal lining by adhesions. The major causes of AA are anatomic abnormalities, and genetic, autoimmune, and traumatic injuries.
Most recently, the scientific understandings of both neuroinflammation and neuroregeneration has led to the development of treatment protocols for AA. While formerly viewed as an untreatable disease, this reputation is no longer true. Thanks to multiple recent scientific discoveries, a medical treatment process or protocol has been developed consisting of 3 basic components: (1) suppression of neuroinflammation; (2) promotion of neuroregeneration; and (3) pain control. Although it is in its first generation, this process is spreading in medical practice and has been receiving a most positive, albeit anecdotal, response. The process will undoubtedly improve with controlled studies and more widespread clinical experience.
Introduction
Arachnoiditis is simply defined as inflammation of the arachnoid membrane which is the middle layer of the meninges, the protective covering tissue that envelopes and encases the brain and spinal cord.1 The outer layer of this covering is the dura mater and the inner most layer is called the pia mater. Since the arachnoid layer covers the entire brain and spinal cord, inflammation of the arachnoid can occur in many locations from a variety of causes. Trauma, infection, hemorrhage, or a cancerous growth involving the arachnoid layer may cause inflammation and be labeled according to its cause and/or anatomic location.2 Terms such as cerebral, neoplastic, or thoracic arachnoiditis have been used. Although the arachnoid layer is the one layer most involved with the inflammatory process, the other two layers, the pia mater and dura, may also become inflamed.3 The most prevalent forms of arachnoiditis occur in the lumbar-sacral (lower back) and cervical (neck) regions of the spinal cord.
Thanks to modern diagnostic technology of contrast magnetic resonance imaging (MRI), the term lumbar-sacral adhesive arachnoiditis (AA) has come into usage, and this form of arachnoiditis is the major concern of these modern times.6-8 This term is applied when a lumbar-sacral MRI shows that some cauda equina nerve roots have clumped together and formed adhesions to the arachnoid layer of the spinal canal covering (meninges). This condition entraps, inflames, and renders the affected lumbar-sacral nerve roots impaired and dysfunctional. Neurologic impairments and severe, devastating pain may result, since the nerve roots connect to and regulate the nerves of the gastrointestinal tract, urinary system, sex organs, and lower extremities. All or some may become impaired and dysfunctional when nerve conduction is blocked by inflammatory damage to the nerves. Besides direct neurologic impairments and pain from trapped and damaged nerves, AA may produce spinal fluid flow impairment and chronic leakage or “seepage” through the dural layer into the soft tissue that surrounds the spinal column. Since lumbar-sacral AA is the most prevalent form of arachnoiditis that produces severe disability, suffering, and pain, this report only refers to (AA) unless specifically noted.
History
The word “arachnoid” derives from the arachnoid membrane’s fragile spider web like appearance.2 Arachnoiditis as a distinct disease was first recognized in the mid 1800’s. The common causes of arachnoiditis then were the infections of tuberculosis and syphilis. The famous French neurologist, Jean Martin Charcot, recorded a description of the disorder in 1869.9 Dr. Thomas Addison, the British physician who discovered adrenal failure, published his findings on 11 autopsied patients in 1855.10 Two of these cases had severe pain and atrophied adrenals with calcium deposits and fluid around the arachnoid layer. This suggested that long-standing, end stage arachnoiditis was the likely cause of severe pain and consequent adrenal failure. The exact year the disorder was named and credited is uncertain, but the 1873 “Comprehensive Medical Dictionary” published by J.B. Lippincott & Co. included this definition of arachnitis: “A faulty term, denoting inflammation of the arachnoid membrane”.1 The same dictionary simply defined arachnoiditis as, “inflammation of the arachnoid membrane”.1
The first recorded attempt to treat arachnoiditis was probably in 1781 when Dr. John Fothergill, a famous British physician, treated a patient with severe back and sciatic pain along with other symptoms compatible with arachnoiditis.11 Opioids failed to relieve the pain, but a mercury concoction resulted in a positive result. In 1899 the first edition of the Merck Manual listed drugs and measures for spinal meningitis with notations that the recommendations were for chronic and tubercular meningitis.12 No less than 30 recommendations were made including opium and water baths which are still used today. In 1909 the neurosurgeon, Sir Victor Horsley, recognized inflammation of the meninges to be from infection or hemorrhage, and he coined the term “chronic spinal meningitis” which established the notion that inflammation involved all layers of the meninges.3 Harvey, in 1926, determined that adhesion formation that connects nerve roots, spinal cord, or brain to the meninges to be a major cause of pain and disability.13 He established the concept of a serious pathological partnership involving the nerve roots and the arachnoid layer.
The major cause of arachnoiditis changed as infectious disease treatment agents were developed in the 1900’s for syphilis and tuberculosis. A new cause, however, originated in about 1930, when poorly soluble oil dyes were infused into the spinal canal to enhance x-ray visualization for diagnostic purposes.2,3,13 These x-rays were called myelograms. A small percentage of patients who received these dyes developed arachnoiditis. Magnetic Resonance Imaging (MRI) technology was developed about 1987. MRI’s progressively replaced oil-based dyes and consequently, for a time, arachnoiditis seemed to almost totally disappear. New developments, however, have caused this disorder to reappear in these modern times.6-8
Beginning around the year 2000, an increasing lifespan, obesity, and sedentary lifestyle, have all helped produce degenerative disorders of the spine. Accidental traumas such as whiplash due to an auto accident or repetitive stress injuries due to motions from performing a job or playing sports can cause progressive spinal deterioration, over time, as well. These factors along with highly technical medical and surgical interventions have all contributed to the emergence of AA in today’s world.
Natural Course of the Disorder
Without treatment, arachnoiditis has a somewhat unpredictable natural course. Some cases may resolve naturally and do so completely with no evidence that they existed.2,4,5 Once AA is established, however, it may be classified as mild, modest, severe, or catastrophic. A mild case, for example, is one in which pain is intermittent and there is no impairment of bladder function or extremity range of motion. A moderate case is one with constant, but easily controlled pain and accompanied by some impairment of bladder function and weakness of the lower extremities. A severe case will require daily pain control medication as the pain is severe, constant, and intractable. There is impairment of bladder function, inability to sit or stand in one position for more than a few minutes, and weakness and paraparesis (partial paralysis) of the lower extremities. A catastrophic case will have all the elements of a severe case plus paraparesis (partial paralysis) of the lower extremities, cognitive impairment, severe fatigue, a largely bed or couch bound existence, and a need for assistance to carry out activities of daily living. When untreated, catastrophic cases of AA will leave the patient with shortened life span, autoimmunity, and terminal events are usually related to overwhelming infections or cardiac-adrenal failure.33 A major goal of modern treatment is to prevent the disease from progressing from a mild or moderate case to a catastrophic state.
The seriousness of AA is directly related to the intensity of glial cell activation and neuroinflammation in the nerve roots of the cauda equina.28-31 Serum testing of neuroinflammatory markers reveals that neuroinflammation fluctuates from high intensity to being relatively innocuous or inactive.32 The natural, untreated course is, therefore, unpredictable. In addition to spontaneous resolution, some cases appear, for unknown reasons, to have active neuroinflammation that stops or “dies off” but leaves behind permanent neurologic impairments and pain. Most cases that come to the attention of today’s physicians tend to be progressive with intermittent periods of remission and activity.
The catastrophic stage of AA may be disappearing likely due to medical and physical measures that do not cure or eliminate the disorder but do seem to prevent its most catastrophic and devastating complications such as lower extremity paralysis, adrenal failure, severe autoimmunity, immune deficiency, and early, life-ending infection and sepsis.33 To support this possibility, MRI’s of today’s patients rarely show calcification (arachnoiditis ossificans) which was typical and well-recorded in the last century2. In summary, modern day treatment measures, whether specifically directed at AA or other spine disorders, seems to have reduced the occurrence and severity of complications and the progression to a catastrophic state.
Symptoms
The typical symptom profile of AA is constant pain with a variety of neurologic manifestations.7,8 Pain intensity may change with movement between sitting, reclining, or standing positions. Persons with AA may achieve comfort while standing or lying down or the situation may be just the opposite, either sitting or lying down may increase pain. In addition to positional pain relief, other symptoms experienced by the majority of AA patients include the sensations of water dripping and/or bugs crawling on the legs. Burning sensation on the bottom of the feet is also common. Some urination difficulty symptoms are usually present. It may involve hesitancy in starting or difficulty stopping (neurogenic bladder). Dribbling between urinations is also common. Many patients complain of blurred vision, headache and dizziness, which are believed to be due to spinal fluid flow obstruction. Spinal canal narrowing as well as clumps and scar tissue present within the spinal canal act as a “dam” obstructing constant fluid flow. Spinal fluid may leak, or more appropriately “seep”, through the arachnoid and dura layers of the spinal canal covering into the soft tissues surrounding the spinal canal. Cerebral spinal fluid is extremely toxic to soft tissue, so considerable pain may develop, and soft tissues including muscles, nerves, and fascia may degenerate, scar and contract after coming in contact with the leaking fluid.
Arachnoiditis, like other brain and spinal cord diseases, can create a systemic or generalized autoimmune disorder with immunodeficiency.21-23 This is believed to occur when inflammatory by-products and/or brain or spinal cord tissue reach the general circulation.22,23 Auto-immune manifestations include arthritis of joints, muscle pain, thyroiditis, and small fiber neuropathies. Some arachnoiditis patients are first diagnosed with an autoimmune disorder such as systemic lupus erythematosus or Hashimoto’s. Some are diagnosed with fibromyalgia.
Since nerve roots of the cauda equina have multiple connections to various internal organs, a variety of symptoms may occur depending upon the anatomical location of the inflamed and entrapped nerve roots.These may include the stomach and intestine including the rectum and anus. Food sensitivity, nausea, vomiting, constipation, diarrhea, urinary and fecal incontinence, may all occur in different patients. Sex organ, bladder and bowel function may be adversely affected. In severe cases incontinence and impotence may occur. Breathing symptoms, including shortness of breath may occur. Leg and feet impairments are extremely common including foot drops, unsteady gait, and weakness in the legs and feet. Paraparesis is relatively common and even total paralysis from the waist down is known to occur.7,8
Physical Signs
The major physical signs in an AA patient are to be found in the lower extremities and back. Physical signs in the legs include weakness, instability, poor balance, and abnormal reflexes. Pain may occur with extension or stretching of the legs. Paraparesis of the lower legs may occur. AA patients usually have more pain on one side of the body than the other. Consequently, the patient will often tend to favor one side, constantly leaning in a position that lowers their pain. Over time, this attempt to find comfort and relief produces asymmetrical muscle groups in the back with observable areas of muscle hypertrophy and atrophy.8
If paraspinal muscles and soft tissues have been bathed in chronic cerebral spinal fluid seepage, they may scar and contract. Consequently, patients may not be able to fully extend their arms and legs. Chronic cerebral spinal fluid seepage may also cause considerable contraction of the soft tissues between the skin and spine resulting in an indentation of midline, tissue along the lower spine and occasionally discoloration.
In the 21st century there are 4 basic causes of AA: (1) anatomic disorders of spinal structure; (2) genetic connective tissue disorders; (3) trauma, and (4) autoimmune disorders.6,7,8 AA may be initiated with damage to the arachnoid lining or to the nerve roots in the cauda equina. Regardless of which site the damage starts, eventually, adhesions will adhere or glue nerve roots and arachnoid lining together which causes severe pain and impairment. The spinal cord ends at about the top of the lumbar spine and turns into about a dozen, nerve roots. They free float in the spinal fluid canal (“pipe”) and are collectively known as the cauda equina. At some point along the lumbar and sacral spine, nerve roots individually exit to connect and energize the feet, legs, bladder, sex organs, intestine, and stomach.
Any anatomic alteration that causes the spinal canal to narrow, bend, or otherwise distort the spinal canal in the lumbar-sacral region of the spine has the potential to eventually cause AA. The spinal canal which contains the cerebral spinal fluid must always remain open and free from obstruction of blockage. Spinal fluid is made in the brain and it recreates itself about 4 times a day. It leaves the brain to enter the spinal canal.14 The cerebral spinal fluid function is to carry nutrients, remove contaminants such as inflammatory byproducts, and lubricate and constantly bathe the nerve roots of the cauda equina so they don’t rub on each other. To do so will cause irritation, neuroinflammation, scarring, and adhesion formation.14-16 The spinal canal which carries the spinal fluid must constantly remain open and clear so there is no fluid flow obstruction or compression of nerve roots.16 It is for this reason that the human body is designed to stand and walk every few minutes and turn often during sleep. There are several spinal conditions that can interfere with spinal fluid flow and cause compression which irritates nerve roots in the cauda equina. Spine/vertebral arthritis, osteoporosis, vertebral collapse, and intervertebral disc herniation may be age or accident related. Kyphoscoliosis, spondylolisthesis, and rheumatoid spondylitis are genetically caused. The most common anatomical structural condition which causes AA is chronic intervertebral disc protrusions (herniations). The protruding discs narrow the spinal canal (“stenosis”) and force nerve roots in the cauda equina to compress together into clumps. These clumps subsequently produce irritation and neuroinflammation, which eventually develops into adhesions that adhere or glue them to the arachnoid lining. Any trauma, including medical interventions, that may irritate the arachnoid lining or nerve roots or toxic substances, including medicinal agents, may enter the spinal canal and accelerate the underlying neuroinflammation process initiated by intervertebral disc protrusions or any other anatomic abnormalities of the spine.
Another recognized pathologic process in this century that may cause AA is genetic, autoimmune, or viral disorders that directly cause degeneration and deterioration of the arachnoid and other layers of the meninges. The genetic conditions are called “connective tissue disorders” of which the best known are of the Ehlers-Danlos/Marfan types.17-20 Collagen dissolution is the pathologic mechanism, and the very fragile tissues of the spinal cord and canal such as the pia mater and arachnoid linings are particularly susceptible to deterioration from genetic collagen disorders and inflammation development as they are composed mainly of collagen and elastin.17-20 Besides AA, other spinal conditions may result from this process and include perineural (Tarlov) cysts, syringomyelia, tethered cord, and Chiari disorders.17-20 Patients with genetic connective tissue disorders are at high risk and more prone to experience injuries and AA from intrathecal, epidural, and surgical procedures due to softer, inherently fragile connective tissues. Autoimmune disorders can also attack spinal tissue and cause inflammation in the arachnoid layer.21-23 Autoimmune disorders that are associated with AA include systemic lupus erythematosus, rheumatoid arthritis, and psoriasis. Once the arachnoid layer is damaged and inflamed by a genetic or autoimmune disorder, it may “capture” and “glue” nerve roots to itself by adhesion formation.
Trauma, both from accidents and from medical interventions in the form of medical injections and surgery, may cause AA.24-27 Severe, acute trauma from accidents that affects the lumbar-sacral spine for any reason, including motor vehicle, work-related, or falls may incite the development of inflammation in either the arachnoid layer or nerve roots. Once initiated the inflammation may proceed to involve the other “partner” by adhesion formation. Unfortunately, there are now well-documented cases where a single spinal tap or epidural injection for therapeutic or anesthetic purposes has caused AA. In some cases, there was no known underlying anatomic structural, genetic, or autoimmune condition to predispose to the development of AA.
At this time, the precise mechanism for the rare development of AA after a medically justified spinal tap or epidural injection is unclear. A spinal tap is clearly a traumatic procedure and it is possible that a toxic contaminant could enter spinal fluid in the spinal canal through the needle track. Epidural injections of anesthetics, corticosteroids, or other medications are almost always safe when administered under fluoroscopy. Rarely is there trauma to the dural and arachnoid linings. The epidural space is, however, not totally separate from the subdural and/or subarachnoid space.24-27 Many thousands of villi or granules are present on the arachnoid layer that form connecting channels between the epidural veins and spinal fluid.25 These channels, therefore, allow any chemical, such as an anesthetic, corticosteroid, or solvent injected into the epidural space to potentially enter the spinal fluid.
Although the majority of diagnosed, clinical arachnoiditis cases are in the lumbar-sacral region, some arachnoiditis cases occur in the cervical (neck) region. The diagnosis in these cases is almost entirely clinical as there is no equivalent to the cauda equina nerve root complex to be observed on MRI. Cervical neck arachnoiditis is almost entirely in patients with degenerative spine conditions and stenosis who have also had surgery and/or multiple epidural injections. Cervical arachnoiditis is manifested by severe pain on backward extension of the neck. There may be arm and hand neurological deficiency signs. MRI images suggest a thickened arachnoid layer with clearly visible spinal fluid flow obstruction.
Arachnoiditis is a rare disorder affecting more females than males, possibly because two thirds of the pregnant women in the USA, Latin America and most other countries receive spinal or epidural anesthesia for the delivery. (It is estimated that about 4% of them develop arachnoiditis due to complications of anesthesia).
Individuals who have had spinal surgery, intrathecal injection of toxic fluids (i.e. hyaluronidase, blood, dyes, steroids and local anesthetics with preservatives) into the spinal dural sac, or have had injuries to the spine or head, may be at greater risk to develop this disorder. However, the precise prevalence and incidence of arachnoiditis is unknown. According to one estimate, approximately 11,000 new cases occur each year in the USA; however, the cause varies, ranging from back surgery, pain relief procedures and diagnostic interventions mostly performed in North and South America, Europe and Asia, with an undetermined number in Africa. Obviously, the greater number of surgical and anesthetic spinal interventions has increased the number of cases considerably. For different reasons, some cases of arachnoiditis may go misdiagnosed or undiagnosed, making it difficult to determine its real frequency in the general population. Diagnosis of arachnoiditis by MRI with intravenous contrast is preferred.
Laboratory Tests
At this time there is no specific laboratory test that identifies an AA patient. Since AA is a neuroinflammatory disease, some by-products of inflammation known as “markers”, are often elevated. These include the erythrocyte sedimentation rate (ESR); C-reactive protein (CRP) myeloperoxidase, and cytokines.32 If any of these markers are elevated, treatment goals should include suppressing neuroinflammation and lowering the affected marker(s) into its normal serum range. It is emphasized that an absence of elevated inflammatory markers does not necessarily mean that neuroinflammation is either controlled or absent.
Some adrenal and gonadal hormones such as cortisol, testosterone, and pregnenolone may drop in the serum due to the severe stress and pain of AA.34 Serum hormone levels that are low are regarded as indicators that the disease process is not well-controlled.
Diagnosis of Adhesive Arachnoiditis (AA)
The diagnosis of AA requires 4 elements: (1) history of an inciting event or disease; (2) typical symptoms; (3) abnormal physical signs; and (4) MRI findings. Specific evidence of AA is usually recognized on a contrast MRI which is one that uses injected dye or high-resolution (3) Tesla imaging to contrast the spinal fluid from the spinal cord, nerve roots and arachnoid covering. The necessary evidence to make a diagnosis of AA is considered to be the presence of nerve root clumping and adhesions which attach the clumps to the arachnoid layer of the spinal cord covering. While other indicators such as nerve root displacement, enlargement, and asymmetry may be present on MRI imaging, these findings, by themselves, are insufficient to warrant a diagnosis of AA.4-6
A major issue is that the classic appearance of nerve root clumping and adhesion formation may not be visible for several months after an inciting event such as a spinal tap or epidural injection. Also, patients may have symptoms, physical signs, and laboratory test abnormalities that indicate AA is present but not show MRI evidence of AA. In these cases, therapeutic trials with medications used to treat AA are warranted.
Treatment
Until recently, AA has often been called “untreatable” and “hopeless”.2,5 Two major scientific discoveries, however, have made it possible to develop a “first generation” medical process or protocol to treat it. The first discovery is that neuroinflammation is caused by activation of cells in the brain and spinal cord called “glia”.28-31 Pain, injury, infection, or exposure to foreign chemicals or metals (such as those that may enter the spinal fluid with medical interventions and surgical procedures) may activate glia cells producing neuroinflammation. Since these discoveries, some medicinal agents and hormones have been identified that will suppress glial cell activation and neuroinflammation.29,31
The second discovery is that the brain and spinal cord make certain hormones called neurohormones whose primary functions are to suppress neuroinflammation and/or regenerate damaged nerve cells.35-41 Some are called “neurosteroids” since they contain the steroidal, chemical structure.35,36 Included are: pregnenolone, allopregnanolone, progesterone, dehydroepiandrosterone, and estradiol. External administration of some of these intrinsic hormones has been well-demonstrated to control neuroinflammation and promote neuroregeneration in laboratory animals.38,40,41 The administration of some of these hormones and their chemical analogues are now being used to treat AA.8
The treatment process of AA consists of two basic elements: (1) medication; and (2) physical measures. Medications consist of 3 therapeutic classes: (1) suppressors of neuroinflammation (examples: ketorolac, methylprednisolone); (2) neuroregeneration agents (examples: pregnenolone, nandrolone); and (3) pain control agents (examples: low dose naltrexone, gabapentin, opioids).
Physical measures are targeted at maximizing spinal fluid flow and the prevention of scarring and contraction of nerve roots, muscles, and other potentially affected cells that may cause neurologic impairments and pain.15,16 The basic physical measures include daily walks, gentle stretching of the extremities, water soaking, deep breathing, and light weightlifting.
Pain control for AA is symptomatic and basically follows that of standard pain care. Unfortunately, the pain of AA may rival or exceed that of metastatic bone cancer and of necessity require last-resort, symptomatic measures such as implanted electrical stimulators and high dose opioids including those administered by injection, suppository and implanted intrathecal pumps. Many new pain treatments are being investigated for severe intractable pain similar to that caused by AA. Some, such as intravenous infusions of lidocaine, vitamin C, and ketamine are reportedly providing extended periods of pain relief. While pain control is purely symptomatic, the physical measures and medical agents to suppress neuroinflammation and promote neuroregeneration are implemented to permanently bring about some disease resolution and diminution of symptoms and impairments.
Readers of this review need to be clearly advised that the treatment process for AA is new, a “first generation” effort at effective treatment and must be considered elementary. The current protocol will undoubtedly be changing as new discoveries are made. While the three components of medical treatment, (1) suppression of neuroinflammation; (2) promotion of neuroregeneration; and (3) pain control, are enduring concepts, specific treatment agents, including the examples listed here, should all be considered a “first generation effort” with improvements to come when additional clinical studies, including controlled drug trials, are forthcoming.
Prevention
The finding that many cases of AA are preceded by degenerative or structural abnormalities of the spine suggest that primary prevention of AA is possible. Chronic spine degenerative conditions are well known to be associated with sedentary lifestyles, obesity, and lack of exercise. It is also well known that back pain and injuries are too often quickly subjected to high technology, invasive medical procedures before non-invasive measures are fully exploited. While AA is seldom or rarely the result of a single spinal tap or epidural injection, persons who have a degenerative, structural, or genetic spine condition should be well-aware of the risk of AA with these procedures.24-27 Consequently, anyone considering these procedures is well-advised to consider non-invasive measures for back and spine conditions and seek second opinions before embarking on invasive medical procedures including surgery.
Persons who develop lumbar pain with leg and bladder dysfunction immediately following a medical procedure including spinal tap, epidural anesthesia, or surgery are at high risk to develop AA. In suspected cases, and to prevent AA, it is recommended that the most potent anti-neuroinflammatory agents such as ketorolac and methylprednisolone be administered on an emergency basis to possibly prevent AA.
Information on current clinical trials for multiple myeloma is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government website.
For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:
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Email: [email protected]
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https://rarediseases.org/living-with-a-rare-disease/find-clinical-trials/
For information about clinical trials sponsored by private sources, contact:
www.centerwatch.com
For information about clinical trials conducted in Europe, contact:
https://www.clinicaltrialsregister.eu/
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