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Posted 13 April 2016 - 01:26 PM
This article aims to give an overview of this complex and relatively uncommon condition, so that patients and their physicians have a clearer understanding, and can work together to combat the devastating effect it can have on people's lives.
Arachnoiditis is a chronic, insidious condition that causes debilitating, intractable pain and a range of other neurological problems. It has been regarded as rare by the medical community, but Burton reported as early as 1978(i) that it is "common in patients with severe back and/or leg pain and functional impairment due to the failed back surgery syndrome." Arachnoiditis is the third most common cause of Failed Back Surgery Syndrome (FBSS), after stenosis and recurrent disc problems. Arachnoiditis was previously the second most common cause. This was largely due to the adverse effects of oil-based myelography. The incidence has decreased, but a high proportion of cases of clinically significant adhesive arachnoiditis is now found to be due to the adverse effects of epidural steroids such as Depo-Medrol (Depo-Medrone).
THE SCALE OF THE PROBLEM
Adhesive arachnoiditis is not a notifiable disease and is significantly under-diagnosed. During the Proceedings of the British House of Commons, March 25th, 1998, the issue of arachnoiditis due to Myodil was raised. In answer to the question of the number of cases within the last 20 years, the Under-Secretary of State for Health replied "the information requested is not available" (ii). Burton (iii)has attempted to suggest an estimated figure for cases in the U.S., using results of an international study that showed lumbo-sacral adhesive arachnoiditis to be responsible for about 11% of all Failed Back Surgery Syndrome cases. Tying this in with the number of surgeries performed in the last 50 years, and an average rate of 25% FBSS, he estimates "at least 1,000,000 FBSS cases in the U.S. would then have been causally and primarily due to the production of lumbo-sacral adhesive arachnoiditis. If one brings in the rest of the world the case estimate would have to be doubled."
ARACHNOIDITIS OR EPIDURAL FIBROSIS?
A frequent question arises about the difference between these two terms. Arachnoiditis is chronic inflammation inside the dura, in the arachnoid layer of the meninges (see below) whereas epidural (peridural, extradural) fibrosis is scarring outside the dural sac. It may also be referred to as "adhesions" or "scar tissue". Many doctors appear to regard epidural fibrosis as less clinically significant than arachnoiditis, but in essence the nerve root compression arising from epidural fibrosis may cause similar clinical problems in terms of lower limb pain, sensory disturbance and weakness. Epidural fibrosis differs from arachnoiditis in that it is more likely to be a localised problem and is generally a post-surgical phenomenon, although it may also be a sequela to invasive procedures such as chemonucleolysis. In cases of arachnoiditis, there is often associated epidural fibrosis, but the reverse is not generally acknowledged, so that patients may be left with a diagnosis of epidural fibrosis and are unable to get a diagnosis of arachnoiditis even when the clinical picture fits. Arachnoiditis is an underdiagnosed condition.
Arachnoiditis is chronic inflammation of the arachnoid layer of the meninges. (The spinal meninges are in 3 layers, dura, arachnoid and pia.) The arachnoid layer of the meninges is part of the leptomeninges, the pia being the other. It may therefore also be known as chronic leptomeningitis. Other terms include arachnoiditis adhesiva circumscripta, and arachnitis. Arachnoiditis may be present in anyone who has had spinal injury, surgery or introduction of foreign substances, but in most people it causes no problems. The most common form is arachnoid adhesions. The second type is local arachnoiditis, which generally results from some local insult to the subarachnoid space, such as injury or surgery. Again, it may not cause symptoms. The most severe type, which may be progressive and more likely to cause symptoms, is adhesive arachnoiditis. It may be mild, moderate or severe, and either focal (localised) or diffuse. The latter type tends to result from insults involving introduction of foreign substances into the subarachnoid space. (See causes)
THE INFLAMMATORY NATURE OF ADHESIVE ARACHNOIDITIS
Arachnoiditis is chronic inflammation of the arachnoid layer of the meninges which consists of trabeculae, a mesh of interwoven collagen fibrils resembling tissue paper. These secrete spinal fluid, which circulates through the cerebrospinal axis and is absorbed through the arachnoid villi in the brain. The initial phase of the inflammatory process involves influx of white blood cells in response to an insult to the subarachnoid space, such as blood (trauma, surgery), foreign substance (dye, etc) or infectious agent (e.g. meningitis). This is initiated via the action of cytokines, (proteins that act as immune modulators). There is infiltration by macrophages and mesenchymal cells; the latter transform into fibroblasts, which make collagen (scar tissue). Usually the fibrinolytic process, which breaks down excess scar tissue, limits this, but in arachnoiditis the scar tissue continues to form. Authors such as Jayson (iv)have suggested that there may be a defect in the fibrinolytic pathway.
The neurosurgeon Mayfield, through his research in the 1980s, felt that there might be an immune response that is responsible for the degree of reaction, especially to chemical insult. Frank et al cultured arachnoidal cells in vitro and demonstrated their immune capabilities. (v) A further interesting point to note is that some features of arachnoiditis are suggestive of Chemically Induced Immune System Disorder, as described by The National Foundation For the Chemically Hypersensitive in 1989. This disorder is a complex, multisystem condition that results from toxic exposure. This causes chemical poisoning, that provokes an immune response, which in turn may lead to development of autoantibodies.
Furthermore, there may be a "spreading phenomenon" which leads to multiple sensitivity, to a variety of substances e.g. petroleum products, phenol, pesticides, detergent enzymes and synthetic fragrances. This scenario might explain why some patients with arachnoiditis after myelogram or epidural steroid exhibit signs of multiple chemical hypersensitivity. (See under Symptomatology and Iatrogenesis). Indeed, there is an argument for hypothesising that the cases with diffuse arachnoiditis and widespread symptoms outside the CNS are due to a form of Chemically Induced Immune System Disorder i.e. a toxic phenomenon.
Anecdotal evidence suggests that a number of patients with arachnoiditis also have autoimmune type symptoms (See below) and/or a diagnosed coexisting autoimmune disorder such as Sjogren's syndrome, Rheumatoid Arthritis, Systemic Lupus Erythematosus. These conditions are known to be associated with vasculitic neuropathies. Also, Rheumatoid arthritis and various other connective tissue diseases show features of fibrosis (see Appendix I). It therefore seems reasonable to hypothesise that arachnoiditis may be an autoimmune condition, possibly involving antibodies that affect the fibrinolytic pathway, such as antiplasminogen antibodies (seen in Rheumatoid Arthritis), in response to an insult to the arachnoid meninges, especially when that insult is chemical in nature.
There have been several papers recently discussing the possible role of previous viral infections, particularly Epstein-Barr virus (EBV) in the aetiology of autoimmune disorders such as Sjogren's syndrome, and Systemic Lupus Erythomatosus (vi).Many patients with arachnoiditis have had previous viral infections, including EBV and Cytomegalovirus (CMV). It is possible that this has some significance in the development of an autoimmune component to arachnoiditis, which could account for the degree of severity of the condition in that group of patients.
MacDonald (vii)noted that 18% of the general population carry a factor in the blood (Histamine Release Factor HRF) which causes a dramatically potentiated, sustained autoimmune reaction to foreign substance in the people who carry this factor. As this factor may be implicated in autoimmune responses, this may be relevant in explaining why there is only a minority of patients with arachnoiditis who develop the condition to a clinically significant degree.
In the first stage of arachnoiditis, the spinal nerves are swollen and the adjacent blood vessels distended (hyperaemia). The subarachnoid space disappears. In thesecond stage, the scar tissue increases, and the nerves become adherent to each other and the dura. The third stage, (adhesive arachnoiditis), involves complete encapsulation of the nerve roots. The scarring prevents the arachnoid from producing spinal fluid in that area. In some cases, the scar tissue calcifies (arachnoiditis ossificans). Benini and Blanco (viii) described arachnoiditis as "cystic and adhesive in nature". The cysts are collections of spinal fluid walled off by the meningeal adhesions. Arachnoid cysts are seen in some cases. An animal study (ix) showed that there was proliferation of fibrous tissue, lymphocyte infiltration and that the pial blood vessels were obliterated. In the spinal cord adjacent, there were multiple small areas of demyelination. Cavitation of the cord was observed in areas where there was ischaemia (poor blood supply). Syringomyelia (cavity) is a complication of arachnoiditis, probably arising due to the pressure dissociation between the subarachnoid space and the central canal. It must be stressed that it does not occur in all cases of arachnoiditis.
A further, uncommon, complication is communicating hydrocephalus. This is thought to be due to alterations in the cerebrospinal fluid dynamics, due to the effects of the scarring in the subarachnoid space. Arachnoiditis may, in a minority of cases, involve the brain as well as the spinal cord. There are also subdivisions of the condition called rhinosinugenic arachnoiditis and optochiasmic arachnoiditis, which are rare forms principally affecting the brain.
Brenner classification of arachnoiditis (1978):
The radiologists classify arachnoiditis according to Delamarter's MRI classification:
Type I: central clumping of nerve roots
Type II: peripheral adhesion of nerve roots to the theca ("empty sac")
Type III: complete opacification of the thecal sac, extending over at least one vertebral level.
THE IATROGENIC ASPECT OF ADHESIVE ARACHNOIDITIS
It is recognised that arachnoiditis most commonly arises from medical procedures such as surgery, myelograms and epidural injections. Clinically significant adhesive arachnoiditis is, however, a relatively rare adverse effect. When it was originally described over 100 years ago, it was predominantly a disease of the thoracic spine, due to infections such as tuberculosis. However, nowadays, it is most common in the lumbar region, and also seen in the cervical region, whereas thoracic arachnoiditis is now uncommon. This trend is the result of the influence of iatrogenic causes. Surgery tends to cause localised arachnoiditis, whereas chemical insults such as myelograms and epidural injections give rise to a more diffuse picture, due to their spread in the cerebrospinal axis. The introduction of myelograms earlier this century heralded an upsurge in severe diffuse adhesive arachnoiditis. Air myelograms were the first, and these led on to Thorotrast, which was highly toxic due to its radioactive nature. No- one knows how many people were damaged by it, but the numbers were undoubtedly in the thousands. Oil-based contrast agents such as Myodil (Pantopaque) were introduced after very cursory pre-clinical trials. They were highly toxic and caused incidence of serious adverse effects as frequent as 74%(x). These have been well documented by many authors (xi). Water-soluble agents such as Omnipaque (Iohexol) have since replaced Pantopaque. These are less toxic, but still capable of serious and lasting side-effects, of which arachnoiditis is one (xii). Metrizamide (Amipaque) is particularly linked with risk of seizures and neuropsychiatric disturbance. (xii) In 1997, H.R. 738 was introduced as a Bill in the House of Representatives, concerning "Myelogram-Related Arachnoiditis Amendments" calling for discontinuance of the use of Pantopaque, Amipaque, Omnipaque and Isovue. (See under Diagnostic Tests.)
Since the withdrawal of oil-based myelography, Depo-Medrol is the principal cause of adhesive arachnoiditis in the Western world. Dr. Burton maintains that almost all cases of clinically significant adhesive arachnoiditis are caused by Depo-Medrol. Depo-Medrol (Depomedrone) is a steroid preparation administered epidurally or intrathecally in the treatment of Failed Back Surgery Syndrome (FBSS). The rationale for its use is that the steroid (methylprednisolone) is an anti-inflammatory agent. Although in itself beneficial, the drug is in a solution that contains preservatives such as polyethylene glycol (also used in antifreeze). Other preparations such as Kenalog use benzyl alcohol. It should be noted that alcohol is a recognised cause of toxic neuropathy, so adverse reactions are unsurprising. Wood (xiv) studied the effects of injections of methylprednisolone acetate into rat sciatic nerves. Nerves treated with either the steroid or its vehicle showed damage, including collagen (scar) formation and demyelination. The manufacturers, Upjohn, stated in 1981 that "we would advise against the epidural/extradural routes of administration because of possible adverse reactions". However, this specific recommendation was withdrawn from the data sheet in 1997.
However, Kenalog, another steroid drug used in epidural injections, has "not recommended for administration via the epidural route" on the data sheet from the manufacturers, Bristol Myers Squibb. The drug remains unlicensed for use around the spine, the use being left to the individual doctor's discretion and clinical judgement. Its use in UK is extensive and epidural steroid injection (ESI) is practised by a variety of clinicians including GPs and specially trained physiotherapists. Currently, literature on Depo-medrol states that it is contraindicated for intrathecal administration and that it contains benzyl alcohol, which is potentially toxic when administered locally to neural tissue. Most patients who have had adverse effects from the drug say they would NOT have had the injection if they had known it was not licensed for use around the spine. Many of them say that they are significantly worse since receiving the drug.
Nelson (xv) maintains that "the epidural space is not wholly separate from the subdural and/or subarachnoid space" and that the spaces are "not only contiguous, but continuous". He therefore concludes that epidural delivery of drugs may not guarantee that the substance will remain isolated in the epidural space. Moreover, he cites a 2.5% risk of inadvertent injection directly into the subarachnoid space. The Mackinnon studies on rats (xvi) showed that a variety of injectable steroids may damage peripheral nerves if injected intraneurally. Furthermore, the NHMRC report (xvii) from 1994 shows that the risk of dural puncture is, on average, "at least 5%". The authors also warn, "particular care must be taken if attempting an epidural injection in patients previously treated by spinal surgery. Complete obliteration of the epidural space occurs following decompressive laminectomy and in such cases an attempted epidural injection carries a very high risk of dural tap."
Byrod and Olmarker (xviii) found evidence that the potential barrier properties of the dura/arachnoid "seem less than effective" for preventing substances in the epidural space from reaching the endoneural space of nerve roots.
It is also important to note that several authors have questioned the efficacy of epidural steroid injections (ESI) in treating disc prolapse, lumbar stenosis or FBSS. Rosen et al (xix) concluded in 1988, "overall results were poor", with only approximately 50% of patients receive temporary relief, whilst long-term relief occurs in less than 25% of patients. Anderson and Mosdal (xx) found that epidural steroid injection was "useless" in patients with long-lasting complaints and previous disc operations. This finding was also seen in the study by Cuckler et al (xxi), which failed to demonstrate ESI efficacy, with the authors also raising the issue of published reports of "serious complications". More recently, in 1997, Carette et al (xxii) studied patients with prolapsed nucleus pulposus and found that epidural steroid "offers no significant functional benefit, nor does it reduce the need for surgery," although there may be short-term improvement in pain and sensory deficit. Ringsdal et al (xxiii) proposed that "future correctly designed studies are necessary to clarify whether the injection should be a supplement to the established treatment of low back pain and sciatica," as they found that previous studies showed conflicting results. The NHMRC report suggests that ESI are of greater use in sciatica when there is a substantial inflammatory component (especially if acute) but are less useful if there is a predominantly compressive radiculopathy .The AHCPR Clinical Practice Guideline (xxiv) clearly states that "Epidural injections are invasive and pose rare but serious potential risks. There was no evidence that epidural steroids are effective in treating acute radiculopathy." These papers demonstrate that there remains a question about the benefit of ESI, which at best tends to be temporary (less than 6 months) and thus the risks seem to outweigh the benefits and call into question the advisability of continuing use of this form of treatment.
Epidural anaesthetics are another group of drugs implicated in causing arachnoiditis. (See below). Vandermeulen (xxv) includes arachnoiditis as a "mishap"… "solely due to … epidural anaesthesia". Haisa et al (xxvi) state that lumbar adhesive arachnoiditis should be considered for differential diagnosis of back and leg pain after epidural anaesthesia. Furthermore, epidural anaesthesia may cause subarachnoid cysts or cavities, which are also recognised complications of arachnoiditis. (See below) If the epidural space is already compromised by disc herniation, stenosis or epidural fibrosis, the risk is greater. Yuen et al (xxvii) state that neurological complications " may be more severe in the presence of spinal stenosis".
Rocco et al (xxviii) in a study of pressure gradients in the epidural space, concluded that as resistance to inflow of fluid was significantly higher in the diseased epidural space, "spread of anesthetics might be difficult to predict".
In 1955, Hurst conducted studies on monkeys (xxix), which demonstrated that a wide range of chemicals, when introduced into the CSF, produced an immediate pathological
response, which "proceeds steadily to its termination". The early stages are asymptomatic, but after a latent period, the clinical picture is then one of "severe and progressive signs and symptoms". This is similar to the picture in arachnoiditis, and therefore all short-term studies (which make up the majority of the evidence concerning safety of ESI) will fail to address the issue of arachnoiditis, which tends to occur after an indeterminate interval following exposure. Chymopapain, an enzyme that has been used for chemonucleosis in treatment of prolapsed discs, also has been implicated in causing epidural fibrosis (xxx) and animal Studies show severe nerve damage if injected into the nerve sheath (xxxi). In fact, one paper suggests use of intrathecal chymopapain for use as a model for chemically induced spinal cord injury. (xxxii)
PRESERVATIVES IN SPINAL INJECTIONS In 1975, Kelly et al (xxxiii) wrote a paper describing the neuropathological effects of intrathecal water. They concluded that infusion of distilled water intrathecally could cause distinctive lesions of spinal roots and cord. It follows therefore, that if a substance as inert as water can cause damage, that more complex preparations are likely to carry some risk also. As early as 1954, Moore (xxxiv) advised that local anaesthetic administered epidurally should be free of preservatives. Malinovsky (xxxv) suggests that "neurotoxicity can result from decrease in neuronal blood supply, elicited by high concentrations of the solutions, long duration exposure to local anaesthetics, and the use of adjuvants." Some authors suggest that arachnoiditis occurs as a result of the vasoconstrictive component of the anaesthetic, whilst others say that contaminants (xxxvi) or preservative agents are responsible. It must be stressed that ANY drug preparation injected in to the spine, may contain preservatives such as benzyl alcohol, polyethylene glycol, and chlorobutanol (a derivative of chloroform) and that these carry a risk of neurotoxic effects. Another preservative that can cause reaction is sodium bisulfate, which may trigger a severe allergic reaction if the patient is susceptible (and it is unclear how many of the general population may be susceptible). Burm (xxxvii) states that epidural anaesthesia results from the interactions of local anaesthetics with nerve structure within the subarachnoid space, which they reach by uptake into the epidural fat and via systemic absorption, and that consequently, epidural doses need to be much higher than spinal doses. Bearing this in mind, it is unsurprising that there is evidence that epidural anaesthetic agents such as those used in childbirth also carry a risk of neurological damage.
It is vital that patients be FULLY informed of the risks for these procedures outlined above, so that they can give an informed consent. Unfortunately, it is commonplace for this not to be the case. Many doctors feel that it would be confusing to the patient to be given a detailed breakdown of the relative risk of each adverse effect. In addition, arachnoiditis continues to be viewed by the medical profession as a RARE complication and as such, does not warrant mentioning. As regards therapeutic techniques, it is essential that the potential benefit be weighed against the risk of the procedure causing serious adverse effects. Regrettably there is an under-reporting of adverse effects, so that clinicians may not have access to accurate information to pass on to the patient.
Arachnoiditis has been described as an insidious disease that is incurable. Guyer's paper on the prognosis of arachnoiditis (xxxviii) suggests that there tends to be a spectrum of the course of the disease, which varies from mild and non-progressive, to a fulminating progression that may cause paralysis and even death. Wilkinson (xxxix) believes that progression after the first 24 months is unlikely to be due to the disease process alone. Most authors state that its onset may be years after the precipitating cause. In general, arachnoiditis presents a highly variable clinical picture, with a fluctuating course. Some patients seem to reach a "plateau" and stabilise without further deterioration, whereas there is a group of patients who develop a relatively rapid progressive deterioration (within a matter of months) during which they tend to lose function in the affected limb(s). This tends to happen after a seemingly trivial event such as a minor fall or car accident.
THE SYNDROMIC NATURE OF SYMPTOMS IN ADHESIVE ARACHNOIDITIS
Adhesive arachnoiditis presents with diverse symptoms, which may relate to problems outside the CNS, and could therefore be described as a syndromic picture. However, bearing in mind that the treatments used for the neurological symptoms may cause a variety of side-effects, it is difficult to say exactly which symptoms can be directly and solely ascribed to arachnoiditis and which are more complex in origin.
The medical literature mostly describes symptoms in the lower back and or legs, with pain, weakness and sensory loss. Some authors also discuss bladder and sexual dysfunction. Jenik et al (xi) described the symptoms as "predominantly syringomyelic sensory deficits" (see below). A recent symptom survey amongst the support group COFWA (Circle of friends with Arachnoiditis) involving 66 members, has shown that there are a wide variety of symptoms. (xli)
One of the principal problems arachnoiditis sufferers experience is the dismissal of their symptoms as psychosomatic.
This section of the article will attempt to clarify the range of symptoms that may be experienced in arachnoiditis. It must, however, be stressed that many people with arachnoiditis will not have some of these symptoms, especially the uncommon ones.
The predominant and most distressing symptom of arachnoiditis is chronic, persistent pain which is primarily neurogenic (nerve generated) and thus difficult to treat. This pain is transmitted from the dorsal root ganglia (DRG) in the spinal cord. In contrast with normal DRG, inflamed DRGs produce sustained pain impulse from any mild stimulus such as body movements or even breathing. Pain tends to increase with activity. There is may be a delay after onset of activity, with a slow summation, to a point where the pain suddenly becomes unbearable and then persists once the activity has ceased. This can make it difficult for patients and physicians or physiotherapists to assess what is the tolerable level of exercise. Pain may be due to other factors besides nerve damage. These include musculoskeletal secondary to disuse, overuse or compensatory use of muscle groups, due to alteration of spine dynamics. There may also be muscle tension due to being in pain, or increased muscle tone (spasticity) caused by nerve damage. Joint pain may be due to similar factors, or may be part of the autoimmune picture (see below). Pain is generally described as burning, but often people are unable to describe it. This type of pain is termed dysesthesia (by definition indescribable, bizarre pain). It is not felt in normal people and is specifically a feature of incomplete nerve damage. It may sometimes be called deafferentation pain, or causalgia. Many patients suffer from burning feet, in particular. The majority of patients also have transient shooting pains that may vary in intensity from an insect bite to an electric shock. Some of the sensory problems may be generated from centres higher than the spinal cord. This is called central pain, and is due to hypersensitivity of the central nervous system. This type of pain may include feeling pain from normally painless stimuli especially from light touch such as clothing (this is termed allodynia). Changes in temperature commonly trigger this type of pain, so that sufferers have a very narrow window of comfort as regards temperature. (See also under autonomic effects). Another problem may be an enhanced response to painful stimuli. This is called hyperpathia and may lead doctors to conclude that the patient has a low pain threshold. In fact, there is not a lowered threshold, rather a raised one, but once it is reached the response is magnified. This is called "delay with overshoot". This is particularly noticeable in "visceral hyperpathia" in which normal bladder and bowel sensation is diminished, but once the signals of fullness are perceived, there is burning pain and urgency. This can lead to embarrassing accidents, especially if there is also nerve damage to bladder or bowel causing overactivity or sphincter dysfunction. The areas commonly affected by pain are: In most cases: lumbar, buttocks, legs (often both), feet, perineum, hip, abdomen. In some cases: arms and hands, neck, head and face, chest.
However, it is important to remember that one of the aspects of central pain is that pain may be experienced over large areas of the body, rather than just in the lower part. This may lead to fear that the disease has spread or may cause doctors to dismiss symptoms as psychological. Therapeutically speaking, central (non-nociceptive) pain is generally acknowledged as being poorly responsive to opiate treatment. (See below). For this reason, it is important that evaluation of pain of central origin is undertaken. Tingling and numbness are common features. Other sensory symptoms include loss of proprioception (sense of limb position up or down in relation to ground). This can result in tripping and falls. Temperature perception is sometimes diminished. There may also be bizarre sensations such as feeling as if you are walking on broken glass, water running down the legs, or insects crawling over the skin. These can be very distressing and many patients are reluctant to admit them to their doctor. A minority of patients may suffer from tinnitus and/or vertigo. Vertigo of cervical origin has been described in one paper (xlii), with features of ataxia (unsteady gait).
Motor nerve damage may cause loss of muscle strength, especially in the lower back and legs, in some patients. In most cases with weakness, it is mild, but it may progress sufficiently in some patients to necessitate use of walking aids or even a wheelchair. Also, many patients report that they fatigue quickly. There may be compensatory overuse of some muscle groups to allow the patient to walk, but this leads to the muscle fatiguing more rapidly than normal. This is similar to the picture seen in PostPolio Syndrome (PPS). Increase in muscle tone is quite a common feature and makes the legs stiff, which may have an effect on mobility. Muscle spasms and cramps may be violent and painful. Muscle twitches (fasciculations) are usually painless and transient. A number of patients complain of symptoms suggestive of Restless Legs Syndrome, with nocturnal unpleasant sensations in the legs, accompanied by motor restlessness. Less commonly there may be trouble swallowing, sometimes due to oesophageal muscle spasms. (See also under autonomic problems).
A common component of the arachnoiditis syndrome is the effect on the autonomic nervous system. (responsible for regulating involuntary processes such as blood pressure and temperature, bladder and bowel function etc.) Disturbance of this system occurs because the nerves involved run along the spinal cord in the "sympathetic and parasympathetic chains"(thoraco-lumbar and cranio-sacral respectively). Bowsher's paper (xliii) on central pain describes how most patients with central pain develop "autonomic instability", referring to increase of pain by physical and emotional stress, with cutaneous blood flow and sweating also being affected.
Ziegler et al (xliv) describe how systemic diseases such as diabetes can cause peripheral sympathetic neuropathy, giving rise to postural hypotension, heat intolerance etc. They also maintain that patients with diseases of the sympathetic nervous system demonstrate marked abnormal stress responses to minor stresses such as change of posture or ambient temperature.
Principal symptoms of autonomic dysfunction include: Bladder, bowel and sexual dysfunction. These are often very distressing to patients. Neurogenic bladder dysfunction may cause difficulty initiating urination and emptying the bladder, or hyperactive detrusor with sphincter disturbance causing incontinence. If the bladder is incompletely emptied (leaving a residual volume) there is a risk of recurrent urine infection. Detrusor hyperactivity can give rise to high bladder pressures and possible reflux of urine to the kidneys, with a risk of hydronephrosis. Either problem may be exacerbated by decreased bladder sensation, which may lead to overflow incontinence, especially if there is an element of visceral hyperpathia (see above). There may also be nocturia. Drugs such as antidepressants (e.g. amitriptyline) may worsen bladder dysfunction, causing difficulty in initiating micturition and emptying the bladder. Bowel function may also be affected. Constipation due to drug treatment (especially opiates) and decreased mobility may complicate the picture. Dyspepsia and intermittent vomiting are relatively uncommon problems. They may be due to gastroparesis (delayed gastric emptying) similar to that seen in diabetic autonomic neuropathy. Symptoms of gastroparesis include postprandial nausea, epigastric pain/burning, bloating, anorexia and vomiting. There may be vomiting of undigested food in the middle of the night or in the morning prior to eating breakfast. (See treatment options) Sexual dysfunction may affect potency and ejaculation in men, as well as causing problems with orgasm in both sexes.
Blood pressure disturbance (high, low or fluctuating); this may cause dizziness, syncope, or headaches. Orthostatic (postural) hypotension may occur. Mathias (xlv) describes how in chronic autonomic dysfunction, pressor stimuli such as mental arithmetic, isometric exercise and cold, do not result in the normal increase in blood pressure. Also, stimuli such as food ingestion, which would normally activate the sympathetic system to maintain blood pressure, tend to actually cause marked hypotension. Khurana discussed cases with chronic cervical myelopathy who responded to orthostatic challenge with hypotension, followed by hyperhidrosis (excess sweating), hypertension and chills. (xlvi) Very rarely, there may be autonomic dysreflexia as seen in spinal cord injuries, with paroxysmal hypertension due to excess sympathetic activity reflexly activated by bladder or bowel distension, as described by various authors. (xlvii) Other cardiovascular symptoms include palpitations.
Cold extremities (Raynaud type phenomenon) are a common vasomotor problem. (Note: Raynaud's is also seen in autoimmune disorders such as lupus: see below)
Sudomotor effects of hyperhidrosis or anhydrosis (increased or absent sweating) may impact on temperature regulation, which is a common problem. Hyperhidrosis may be compensatory for loss of sweating in another area, or may be the initial phase before progression to anhydrosis. An uncommon problem may be facial pain, loss of sweating on one side of the face and change in size of one pupil (Horner's syndrome). There are also isolated reports of Adie's tonic pupil.
Swelling (oedema) of the limbs (c.f. reflex sympathetic dystrophy RSD) is seen in some patients. However, it is difficult to assess whether this is a direct effect of arachnoiditis or a side effect of treatments such as intraspinal opiates. (See below) A number of patients seem to be diagnosed with Reflex Sympathetic Dystrophy (RSD), which is also known as Complex Regional Pain Syndrome Type I. This is characterised by severe burning pain in a limb, after trauma or surgery. There is usually an element of allodynia and hyperpathia. Autonomic effects include sudomotor (sweating) and vasomotor (vascular) abnormalities. There are changes in limb temperature, discolouration and oedema. Later stages may involve joint stiffness, loss of mobility and osteopaenia or osteoporosis (loss of bone density), as well as skin texture and hair growth changes. The similarities between this condition and arachnoiditis suggest that the RSD type symptoms are in fact a part of the arachnoiditis syndrome, rather than a separate disease entity.
The following group of symptoms is reflective of the inflammatory nature of the condition and may point to an autoimmune component: Most arachnoiditis sufferers experience a fluctuating course of symptoms, with intermittent "flare-ups" and periods of relative remission. Some sufferers have intermittent low-grade fevers, malaise and raised ESR (SED) and/or white cell count. These laboratory indices are both indicative of a non-specific inflammatory process. Auld (xlviii) mentions fever and chills as part of the syndrome of chronic spinal arachnoiditis. They may also have lymphadenopathy (enlarged lymph glands). A common feature is skin rash, often unexplained. Often this is urticarial (hives) or there may be angio-oedema , both suggestive of an allergic-type reaction. A few patients develop photosensitivity, but this may be related to medication. Joint pains are also common, not just in weight bearing joints, but also small joints. Rarely, there may be neurogenic arthropathy (Charcot joint), due to loss of sensation around the joint. (This is also seen in peripheral neuropathies such as diabetic neuropathy.)
A number of patients complain of dry eyes and mouth (as seen in Sjogren's syndrome) but this is likely to be due to side effects of medication in most cases. Other eye problems include iritis and uveitis, both inflammatory conditions seen also in association with autoimmune diseases. (See below) Patients may have a dual diagnosis of arachnoiditis and fibromyalgia (or chronic fatigue). It is likely that the features of myofascial pain and malaise are part of the arachnoiditis syndrome itself rather than a separate condition.
A minority of patients also has a diagnosis of an autoimmune disease in conjunction with their diagnosis of arachnoiditis. These include Systemic Lupus Erythematosus, Sjogren's syndrome, Thyroiditis, Sweet's syndrome, Rheumatoid Arthritis, Primary Biliary Cirrhosis and Crohn's disease. This is an area for further investigation.
It is also apparent that a small number of sufferers develop multiple drug allergies, which is also seen in autoimmune conditions such as lupus.
Miscellaneous problems such as osteoporosis (c.f. in RSD, or due to decreased mobility) low potassium (possibly due to medication), chest pain mimicking angina, recurrent sinusitis, dyspnoea (shortness of breath) are seen in a few patients. Eye problems (see autoimmune symptoms) seem to be quite common, with patients who have undergone myelography complaining of photoaversion (intolerance of bright light). Some patients describe stabbing pains or tingling and seeing "stars". There is an increased incidence of migrainous type headaches, often with auras. It should be noted that there is an association between photoaversion and anticonvulsant treatment, particularly phenytoin and carbamazepine. (xlix) Recurrent dental problems are quite common. Many patients undergo repeated root canal procedures but continue to suffer from facial pain and odontalgia (tooth pain) without attributable dental pathology. A number of patients also suffer from bleeding gums (periodontal disease) and a few have "burning mouth syndrome". It is possible that some of these problems are related to medications that cause dry mouth, the lack of saliva contributing to reduced protection against infection and caries. The burning mouth symptoms could have a neuropathic component. Dysphagia (difficulty swallowing) may affect some patients, especially those who have cervical pathology. In particular, this may occur if there is arachnoiditis accompanied by degenerative changes such as anterior osteophytes (bony outgrowths). However, it may also be experienced by those with only lumbar pathology, though the reasons are unclear. Pharyngeal symptoms may include feeling as if a lump is stuck in the throat, and this may be dismissed by some clinicians as "globus hystericus", a psychosomatic complaint.
Fatigue is a very common complaint, and can be due to a variety of factors.
Weight gain is a common problem. This is largely to do with decreased mobility and possibly to fluid retention secondary to medication (from drugs such as: Amitriptyline, Gabapentin, Ibuprofen, Morphine and other opiates, prednisolone/methylprednisolone). Alternatively, some patients may suffer weight loss, due to general debility and often, poor appetite.
The cognitive effects of arachnoiditis are anxiety and reduced ability to think clearly, with some short-term memory impairment. These are usually in direct proportion to the pain level being experienced. (l) Sleep disturbance is common, and usually directly related to pain. It may contribute to depression, which is an understandable reaction to intractable pain, loss of function, loss of role and job, financial and relationship problems as seen in other chronic, debilitating conditions. Fear for the future (prognosis cannot be predicted) and uncertainty about the diagnosis substantially increase this problem. Many sufferers are reluctant to admit to depression, as they fear that their more unusual symptoms may be more readily dismissed by doctors as a product of their mental state.
Side effects of medication. These occur, to some extent, in most arachnoiditis patients, largely because of the potent drugs involved, which are often in combinations. Opiates alone can cause a wide variety of side effects, but when taken in combination with adjuncts such as antidepressants, anticonvulsants or muscle relaxants, there may be a cumulative effect. The most common side effects are dry mouth, constipation, drowsiness, nausea, dizziness, urinary retention and blurred vision. Some drugs, such as opiates, NSAIDS and certain antidepressants may cause fluid retention, and thus weight gain. There are a few patients who develop liver and kidney problems, but it is difficult to distinguish adverse effects from medication (more probable) from effects of arachnoiditis on these organs, (which is unproven, but possible if it is an autoimmune syndrome).
IT MUST BE STRESSED THAT ANY PERSISTENT NEW SYMPTOM OR SUSTAINED INCREASE IN PAIN SHOULD BE CHECKED OUT BY A DOCTOR AND NOT ASSUMED TO BE PART OF THE ARACHNOIDITIS SYNDROME.16.
COMPLICATIONS OF ADHESIVE ARACHNOIDITIS
1. Subarachnoid cysts: These are a recognised complication of arachnoiditis, in particular that caused by myelographic dyes or epidural anaesthesia. (li) They tend to be more common in the thoracic region than cervical or lumbar. Kendall et al (lii) stated that incidence of cysts at myelography, as incidental findings, is relatively common, but rarely of clinical significance. In symptomatic cases, clinical presentation is generally non-specific, although there may be a sensory level, unlike in uncomplicated arachnoiditis. Surgical excision or drainage is often successful, provided that there is early intervention.
2.Whilst an uncommon sequela to arachnoiditis, syringomyelia should nevertheless be considered as a possible complication. Indeed, Kamada et al (liii) recommend follow-up serial MRI imaging for patients with adhesive arachnoiditis in order to detect syringomyelia as early as possible. In 1990, Caplan et al (liv) proposed that arachnoiditis causes syrinx formation by obliterating spinal blood vessels, thereby causing ischaemia. Small cystic areas may form, and these tend to coalesce to form cavities. Alteration of spinal fluid dynamics due to scar tissue creating spinal block contributes to this process. This was borne out by an animal study in 1992(lv), which concluded from the data that "cavitation within the cord would be induced by the ischemia, and hydromyelia would be produced by the pressure dislocation between the spinal subarachnoid space and the central canal." Syrinx formation tends to occur in the segment of spinal cord adjacent to the area affected by arachnoiditis. It then starts to expand, due to pressure differences along the spine causing the fluid to move within the cavity. This is sometimes referred to as noncommunicating syringomyelia. The primary symptom of syringomyelia is pain, which may spread upward from the site of original pathology (arachnoiditis lesion). Neurological deficit tends to be in a "cape-like" distribution in the upper part of the body. Increased levels of pain, increased spasticity and decreased physical function are often early indicators of syrinx development. See Appendix II for clinical features, diagnosis and treatment.
3.Hydrocephalus: This is a rare complication, details of which are beyond the scope of this article. It is of the communicating type. Medical literature on hydrocephalus secondary to arachnoiditis is scant, but there are isolated reports. One of these(lvi)describes a case in which a combination of aseptic meningitis, arachnoiditis, communicating hydrocephalus and Guillain-Barre syndrome followed metrizamide myelography.
Essentially, this involves excluding other causes of FBSS, such as recurrent disc herniation, disc fragments, stenosis, spondylosis or epidural fibrosis. However, other causes of polyneuropathy should also be considered, especially those of an autoimmune origin. (See above). It is interesting to note that a number of patients have a dual diagnosis of arachnoiditis and Multiple Sclerosis (MS). This is presumably due to some similarities between the two conditions. Fibromyalgic symptoms are likely to be part of the arachnoiditis syndrome, as opposed to being due to a separate disease entity. Limb symptoms may be diagnosed as RSD.
It is vital for the assessing physician to take into account that adhesive arachnoiditis does not present with a discrete clinical picture and that there may be symptoms that at first glance appear unrelated to any proven pathology. Sadly, a significant proportion of patients may have had difficult previous experiences with the medical profession. Many have been labelled as having psychosomatic problems, although as the Mensana study in 1993(lvii) found, chronic pain patients do tend to have underlying organic pathology. There is, moreover, a physician bias against patients involved in litigation and also women with chronic pain conditions (xli). These factors may cause distrust from the patient. This can be compounded by feelings of anger about iatrogenic causes for the condition (if the patient is aware of this) and thus the patient may be either over-assertive or excessively anxious. It may therefore be unproductive to assess the patient's personality and coping abilities within the first interview, and this may be best postponed until a good rapport has been established. Historical information may be convoluted and patients are often poorly able to communicate the sequence of events and the current, usually diverse symptoms. Examination may or may not reveal significant neurological deficit. However, the possibility of pain of central origin should be borne in mind even if there is no obvious clinically observable abnormality.
One point that may be relevant is that the conventional measurement of muscle strength may be insufficiently sensitive in detecting weakness and fatigability. Perry has published two papers (lviii) about the limitations of manual testing for weakness and also discussing compensatory overuse of muscle groups in Postpolio Syndrome, which shares some of the features of arachnoiditis. Perry states that "muscles with grade 5,4 or even 3+ strength allow a person to move normally; the greater intensity of effort is unrecognised," and that studies show that "the mean strength of grade-4 muscles was approximately 40% of normal." This is likely to also be the case in arachnoiditis patients.
It should also be remembered that occasionally there might be denervation hypertrophy of muscles instead of atrophy. The Mensana authors stated that "Unfortunately, the psychiatric abnormalities that are the normal response to chronic pains tend to bias many physicians, resulting in less than extensive evaluations". They go on to recommend a multidisciplinary approach, which they believe leads to improved diagnostic accuracy. Although the study does not refer specifically to arachnoiditis, as it is a chronic neurogenic pain syndrome, it would seem beneficial to adopt this approach. Clearly, it is vital to exclude treatable causes of the presenting symptoms, but, this done, the onus is on the clinician to maintain an active programme and doctor-patient relationship to ensure that the unfortunate sufferers of arachnoiditis do not feel they have been "just left to get on with it."
As arachnoiditis does not present with a discrete clinical picture of specific motor, sensory and reflex abnormalities, diagnosis tends to rest on tests such as MRI or CT scans. There are, however, still some centres which perform myelograms as diagnostic procedures for arachnoiditis. Taking into consideration the fact that any foreign agent introduced into the spine has the potential to cause arachnoiditis, the rationale behind this type of testing seems questionable. Burton (lix) points out that whilst the incidence of arachnoiditis following non-ionic water-soluble myelographic agents is "quite small", if the "wrong water-soluble agents, or the wrong concentrations of agents, are administered there can be serious consequences such as permanent neurological injury or death." Moreover, he goes on to state that "It is important to understand that myelography has never really been a great diagnostic study…a poor means of demonstrating many important entities such as pathology in the foraminal zone of the vertebral canal." The current investigation of choice is a T2 weighted, fat suppressed, gadolinium enhanced, high resolution MRI scan. Ideally, this should be read by a neuroradiologist experienced with the appearance of arachnoiditis. It is important that treatable causes of Failed Back Surgery Syndrome (FBSS) such as recurrent disc herniation, disc fragments or stenosis be excluded. Further tests which demonstrate nerve damage include electromyography (EMG) and nerve conduction studies (NCS). For bladder dysfunction, urodynamic studies may be required.
Generally speaking, this complex neurogenic pain syndrome is best treated at a specialist pain clinic, with a multidisciplinary approach.
Of the well-established treatment regimes, opiates are frequently used. However, these may be ineffective in combating any central component of the pain.
The issue of dependency concerns most practitioners and may lead to reluctance to prescribe. It is likely that there will be a risk of physical dependence, and thus of withdrawal symptoms if the opiate medication is discontinued. Also, there is an element of tolerance that may develop in long- term use, with the need for increasing doses for effective pain relief. However, psychological dependence and abuse are less likely in chronic pain patients than in those who use opiate drugs recreationally.
It is best to start with short-acting morphine four hourly, until adequate analgesia is established. Breakthrough pain may require top-up doses. Once control has been established, it is advisable to change to a slow release preparation such as MS Continus, which has a predictable duration of action for 8-12 hours, and can thus be given twice daily. Oromorph and Oromorph SR have similar pharmacokinetics to MS Contin. Fluctuations in dose requirement may occur, and in this case, the slow-release preparation should be replaced with a shorter acting one for the period of increased dose requirement.
There are new preparations such as Kapanol and Reliadol, which are modified-release formulations, which may be given once daily. There are a variety of opioid drugs. Morphine remains the drug of choice. However, occasionally it may induce a paradoxical hyperpathia, which is resolved by substitution with an alternative opiate medication. (lx) Other opiates include: Methadone: which can be beneficial for neuropathic pain, but may have an unpredictable duration of action; Pethidine has unwanted central effects and is too short acting; Codeine is too weak and has constipating side effects. Oxycodone: too short acting but suppositories may overcome this; Dextropropoxyphene: a weak agonist, possibly metabolised to a cardiotoxic metabolite. (but a recent paper (lxi) has described it as an NMDA antagonist: see below) Fentanyl: short-acting
There are also partial opiate agonists such as buprenorphine (Temgesic) which has a maximum analgesic dose equivalent to moderate doses of narcotics, but tend to cause less dependency. Alternatively, Tramadol (Tramal/Ultram) is a synthetic centrally acting analgesic, which is unrelated to opiates and carries less risk of dependence. It is useful for moderate to severe pain and has few serious side effects. However, it should be used with caution in patients who are also taking CNS depressants.
McQuay (lxii) describes "Incident pain", which may be brought on by activity, and is a major problem, as adequate background analgesia may be insufficient to control it. There may also be another type of incident pain, which is intermittent, and can occur at rest, without obvious trigger factors. It is very difficult to control.
Adjunctive treatment may be necessary to combat this type of pain: Antidepressants are useful for the background burning neuropathic pain, but are used in far lower doses than for depression (e.g. amitriptyline 25mg at night). It should be noted that the more selective antidepressants such as Prozac have been found to be poorly effective against neuropathic pain, first generation tricyclics being much more useful.
Anticonvulsants such as carbamazepine are particularly useful for the sharp, lancinating type of neuropathic pain. A relatively new drug, Neurontin (Gabapentin) is useful for pain relief and muscle spasms. A recent study in rats has shown that low-dose combinations of morphine, desipramine and serotonin can achieve good pain control. (lxiii) The clinical application of this finding will only be possible after further studies have been undertaken. Antiarrythmic drugs such as mexiletine (which is a local anaesthetic) may also be used for neuropathic pain. Muscle relaxants may be needed, including benzodiazepines such as diazepam. For increased muscle tone (spasticity) baclofen is a useful drug. However, it should be noted that paradoxical increase in spasticity may occur. Also the Committee for Safety of Medecines(CSM) has advised that serious side-effects such as autonomic dysreflexia may be seen on withdrawal and a gradual dose reduction over at least 1-2 weeks should be undertaken to avoid these. (lxiv)
Ketamine, an NMDA receptor antagonist, has been used successfully for neuropathic pain, especially in conjunction with opiates, when it may reduce the dose of opiate required.
Non-steroidal anti-inflammatory drugs (NSAIDs) e.g. ibuprofen are not generally effective for pain relief and may cause significant gastrointestinal side effects and occasionally kidney problems after prolonged use. Some patients have found that the troublesome nocturnal muscle cramps may be relieved by quinine.
Invasive treatments These are not recommended by the Arachnoiditis Trust who believe that ANY invasive procedure carries a significant risk of exacerbating the inflammation of arachnoiditis, thereby worsening the patient's condition. However, as always, it must be a question of weighing up possible benefits against possible risks, and individual needs must be assessed.
INA (Intraspinal narcotic analgesia): the "pump". This was originally developed for use in terminally ill cancer patients and thus was not being used long term. Of the studies of long term pump use, there are varying opinions as to its safety and efficacy. One recent paper states: "About one third of the patients get good long-term pain relief without complications or side effects, many require the addition of local anesthetics, and some never get effective relief. There are major questions to be answered before this form of therapy becomes widely disseminated."(lxv) Opiates are often supplemented with either local anaesthetics such as bupivicaine, or antispasmodics such as baclofen.
Principal problems with perispinal drug therapy include system failure, infection and neurotoxicity. System malfunction varies according to manufacturer, but tends to run at about 20%(lxvi). There are a number of papers documenting cases in which intrathecal granulomatous tissue has formed at the pump site. (lxvii) Bearing in mind that this is a form of scar tissue, this has special relevance to arachnoiditis patients who already have scarring problems. A further paper (lxviii) describes evidence of focal subdural fibrosis and discrete injuries to nerve roots in patients with intrathecal infusions of morphine and bupivicaine. The neurotoxicity of intrathecal drugs is mostly related to the preservatives used in the solutions. Baclofen for intrathecal injection is preservative free, but anaesthetic agents are usually in solutions containing preservatives. The FDA has cleared the use of preservative free morphine sulfate and baclofen, for pump use. Usually the injectable form of morphine sulfate contains 0.5% chlorobutanol (a derivative of chloroform) and not more than 1% sodium bisulfate in every ml of morphine sulfate injection USP. An animal study in 1993 showed that 0.05% chlorobutanol injected intrathecally "induced significant severe spinal cord lesions" (lxix) It is therefore vital to ensure that preservative free solution is used. Chlorobutanol toxicity may cause increased somnolence, alterations in speech patterns, dysarthria and haemodynamic changes. (lxx) A study on the neurotoxicity of intrathecal agents (lxxi) suggests that complications may occur in patients after high doses of morphine. These were related to one of its metabolites, morphine-3-glucuronide. Adverse effects of INA such as constipation, nausea, vomiting and itching tend to be short-term, whereas loss of libido and potency may persist for several months. The most persistent side-effects are sweating and oedema (swelling), the latter of which may necessitate INA being discontinued. The most serious adverse effect is respiratory depression.
Spinal Cord Electrostimulation (SCS) involves electrical stimulation by implanted electrodes around the spinal cord. (in the epidural space), in the area that is most involved in causing pain. The very low energy current shuts down the input of pain fibres. Success rates seem to vary in different studies but are overall approximately 50% when all types of chronic pain are considered, and the benefits may decrease with time. However, there is little literature on its efficacy in the specific case of arachnoiditis. Kumar (lxxii) suggests that there is a favourable response to treatment of postsurgical arachnoiditis or perineural fibrosis if the pain is predominantly confined to one lower extremity. Meilman et al (lxxiii) also state that SCS is of greater efficacy for unilateral lower limb pain than for more widespread nerve root involvement. It is best for controlling the dull, constant pain and poor for the sharp, lancinating pain. SCS may also be useful for neurogenic bladder problems. (lxxiv)
Complications include wound infection, electrode displacement and fibrosis at the tip of the stimulating electrode. (lxxv) The latter is, of course, of concern as regards the potential problems specific to arachnoiditis patients.
Surgical treatment is generally regarded to have a low success rate. Resection of scar tissue is often followed by recurrence. Some specialists are now using laser techniques, but data on the outcomes is limited.
Epidural steroid and local anaesthetic injections: as previously detailed, these are of questionable (and temporary) benefit and carry a risk of causing the very problem they are being used to treat. O'Connor et al (lxxvi) sum up the situation by stating that the "abnormalities of the epidural and subarachnoid spaces in such patients"(i.e. with chronic spinal arachnoiditis)… gives rise to "unpredictable and potentially dangerous results" following drug injection into these spaces.
Local nerve blocks For those patients who have been diagnosed with RSD, sympathetic blockade may be offered. However, the literature is divided as to the efficacy of these techniques. Whilst they may be of use in the initial phases of the condition, when sympathetically maintained pain (SMP) is predominant, once central sensitization occurs (and thence what is termed "sympathetically independent pain: SIP") they are much less likely to be effective.
Other modes of administration
These include transdermal patches e.g. clonidine (an antihypertensive agent, may therefore cause drop in blood pressure) fentanyl (an opiate agonist). Fentanyl patches tend to produce fewer side effects than oral morphine. The FDA has recently approved a new innovation: Actiq is a crystallized form of fentanyl that comes in lozenges for buccal use (put inside the cheek, where it is absorbed rapidly into the bloodstream). This mode of administration allows almost immediate relief from intense flare-ups of pain. It is used in treatment of cancer patients at present.
Ketamine nasal spray is available in the USA. This needs to be investigated further.
Topical application of capsaicin is used to treat pain in peripheral neuropathies such as seen in diabetes mellitus. However, contact with the support group COFWA suggests that many patients find the initial (expected) increase in pain (which occurs prior to the anaesthetic effect) is intolerable, and few remain using it.
These include Transcutaneous Electrical Nerve Stimulation:
3 relatively new techniques are becoming available:
Motor-level electrical stimulation has been used for management of chronic pain with muscular involvement. Wheeler et al (lxxix) describe its use for spinal rehabilitation. There are multiple beneficial effects; some degree of pain relief, interruption of the pain-spasm cycle (and thus reduced myospasm) increased blood flow to muscles, muscle strengthening and neuromuscular re-education. The Wheeler study showed that patients with chronic neck or low back pain with a muscular component, benefited from the treatment, although patients with an inflammatory disorder were excluded from the study. The possibility of this form of treatment being beneficial to arachnoiditis patients needs further investigation.
NMDA receptor antagonists such as dextromethorphan. (NMDA receptors are implicated in the "wind-up" mechanism of spinal sensitization). They look promising for neuropathic pain, but a recent study has shown that dextromethorphan (DM), a widely used non-prescription antitussive (cough medicine) may be teratogenic, causing foetal abnormalities in chicken embryos (lxxix). At this time, I would advise against the use of this drug in pregnant women, until further evidence is put forward. It is of some use in reducing morphine tolerance. MorphiDex has been developed by Algos. This drug combines DM with morphine, thereby increasing the effectiveness of the narcotic without increasing side effects. It is under application to the FDA. Memantine is another NMDA antagonist undergoing trials. Ziconotide (SNX-111) is an experimental drug that shows promise for future use, but further extensive trials will be needed before it reaches clinical use.
ABT-594 is another drug in trials, based on a toxin found in the skin of frogs. This has been found to be 50 times as effective as morphine in animals.
These include treatment of specific symptoms:
Gastroparesis (see under symptomatology): prokinetic drugs such as Cisapride may relieve bowel motility disorders, including reflux oesophagitis.
MULTIPLE CHEMICAL SENSITIVITY
A few arachnoiditis patients may develop multiple chemical sensitivity. A paper in 1996 (lxxx) suggested a causal link between neurotoxic illnesses, MCSD (multiple chemical sensitivity disorder) and exposure to environmental toxins, including organic solvents and dental materials. There is also a link between autoimmune diseases such as lupus and multiple allergies. As described above, some patients with arachnoiditis subsequent to injection of foreign substance into the subarachnoid space, may have features suggestive of Chemically Induced Immune Disorder.
A slightly higher number of patients have new allergies to antibiotics, especially penicillin related.
A number of patients describe adverse reactions to dental anaesthetics, particularly those containing adrenalin. These problems may lead to difficulties in prescribing for patients with arachnoiditis.
LOOKING TO THE FUTURE
Dr. Charles Burton has called arachnoiditis a "scientific orphan". As yet, systematic, coordinated research is lacking.
Areas for future research include:
Other projects include:
Raising public and medical awareness of the syndromic nature of arachnoiditis and of the adverse effects of various types of invasive procedures. Working towards a collaborative approach amongst specialists such as neurologists, neurosurgeons, orthopaedic surgeons, immunologists, physiotherapists, and sufferers, to further understanding of this debilitating condition.
Dr. Sarah Smith MB BS, Patron of the Arachnoiditis Trust. March 1999.
APPENDIX I: AUTOIMMUNE ASPECTS
The following data may be noted to clarify the ideas about the autoimmune aspect of arachnoiditis. They are unfortunately random, as there is a paucity of medical literature relating to this topic. However, my aim is to give the reader an idea of how the hypothesis mentioned in the article came about. MacDonald (lxxxi) noted that 18% of the general population carry a factor in the blood (Histamine Release Factor HRF) which causes a dramatically potentiated, sustained autoimmune reaction to foreign substance in the people who carry this factor. As this factor may be implicated in autoimmune responses, this may be relevant in explaining why there is only a minority of patients with arachnoiditis who develop the condition to a clinically significant degree.
There seems, from anecdotal evidence, to be a significant proportion of arachnoiditis patients who have autoimmune problems.
Vasculitic neuropathies are seen in Rheumatoid Arthritis, Sjogren's, Behcet's syndrome and Systemic Lupus Erythomatosus. The commonest disorder that seems to be diagnosed concurrently with arachnoiditis is Sjogren's syndrome. Various authors describe neurological aspects of this disorder, although there has been no direct reference to a link with arachnoiditis, however, there are similar clinical features between the two conditions (lxxii). Kumazawa et al attribute the chronic sensory neuropathy occasionally seen in Sjogren's to dorsal root ganglionitis with T-cell invasion. (lxxiii). They also describe autonomic dysfunction in Sjogren's syndrome. Nitsche et al (lxxiv) suggest that neurological features are seen frequently in overlap syndrome (a clinical picture of multiple coexistent autoimmune disorders, also known as Mixed Connective Tissue Disease MCTD), and that occasionally a demyelinating type picture of central nervous system involvement may be seen. It is possible that arachnoiditis is part of the clinical spectrum of MCTD. Tesavibul (lxxv) suggests that there are subsets of Multiple Autoimmune Syndrome (MAS) and of particular interest is his proposed Type 2, which includes Sjogren's syndrome, Rheumatoid arthritis, Primary Biliary Cirrhosis, Scleroderma and Autoimmune thyroid disease. (There are isolated cases of each of these disorders seen in patients with arachnoiditis). There is also a recognised, albeit rare, association between the chronic inflammatory condition, sarcoidosis, and arachnoiditis. (lxxxvi) Sarcoidosis is a multisystem, chronic granulomatous (a specific type of chronic inflammation) disorder, which involves an abnormal immune response. The exact source of this reaction is as yet unknown. A study by Sharma (lxxxvii) showed 24% of neurosarcoidosis cases had meningeal involvement.
Marinac(lxxviii) noted that there appears to be an association between the occurrence of hypersensitivity-type reactions in drug and chemical induced meningitis (an acute reaction) and underlying collagen vascular disease (known to be autoimmune).
It has been seen in conditions such as Rheumatoid Arthritis that there may be anti-plasminogen antibodies (plasminogen is part of the fibrinolytic pathway). It may therefore be possible that arachnoiditis involves an autoimmune process that affects fibrinolysis. A recent paper (lxxxix) suggests that in arachnoiditis there is a similar process of inflammation to that seen in serous membranes such as the peritoneum, with "a negligible inflammatory cellular exudate and a prominent fibrinous exudate". It is worth noting that the condition retroperitoneal fibrosis may be seen in association with rheumatoid arthritis.
APPENDIX II: SYRINGOMYELIA
The principle features are:
Later stages may affect bladder, bowel and sexual function. Joint pains worse with straining. Charcot Joints (neurogenic arthropathy= joint damage due to lack of protective sensation) Symptoms may be unilateral or bilateral. An uncommon finding is onset of electric shock sensation running up and down the spine when the head is flexed or extended, occasionally followed by syncope (passing out). This is known as Lhermitte's phenomenon. Some patients may show an increasing scoliosis (lateral curvature of the spine) which is thought to be due to unequal nerve supply to the paraspinal muscles.
Misdiagnoses have included:
Carpal tunnel syndrome (neurological symptoms resulting from compression of the median nerve at the wrist) Ulnar nerve compression (ulnar nerve in the arm) Cervical spondylosis (degenerative disease of the cervical spine).
Diagnosis is by MRI scan of the spine and EMG tests electrical tests to detect muscle weakness) Surgical treatment is usually necessary for symptomatic cases, and early intervention essential, if the syrinx is large and/or increasing in size, to avoid irreversible cord damage. Surgery may provide stabilisation or modest improvement in symptoms for most patients. Recurrence may necessitate further operations. Shunting is used to drain the spinal fluid from the cavity into either the abdomen (syringoperitoneal) chest (syringopleural) or the subarachnoid space. This procedure carries risk of complications such as damage to the spinal cord, haemorrhage, infection, shunt blockage, low CSF pressure and spinal tethering.
A recent paper ( ) suggests that all types of shunts may cause "significant morbidity" and lead to further surgical intervention. A study specifically of syringomyelia secondary to arachnoiditis ( ) found that outcome of surgery depended on the severity of the preoperative arachnoid pathology and that shunting was associated with recurrence rates of over 90%. For patients with focal scarring, microsurgical dissection of the scar and decompression of the subarachnoid space with a fascia lata graft stabilised over 80% of patients (but in cases with extensive scarring this was less than 20%).
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Ahlgren P Invest Radiol 1980 Nov-Dec;15(6 Suppl): S264-6 Early and late side effects of water-soluble contrast media for myelography and cisternography: a short review. Bohutova J, Vojir R, Kolar J, Grepl J Diagn Imaging 1979; 48(6): 320-5 Some unusual complications of myelography and lumbosacral radiculography.
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Adams MD, Hopkins RM, Ferrendelli JA Invest Radiol 1988 Sep; 23 Suppl 1:S217-9 A rat EEG model for evaluating contrast media neurotoxicity.
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Llewellyn CG, Campbell DR, Quartey GR Can Assoc Radiol J 1988 Sep; 39(3): 230-1 Intracranial subdural hematoma complicating metrizamide myelography.
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Wood KM Arguelles J Norenberg MD Reg Anaesth 1980 5:13-15 Degenerative lesions in rat sciatic nerves after local injections of methylprednisolone in aqueous solution.
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Posted 13 April 2016 - 04:13 PM
The report found there was little awareness of the disease, even in the medical community, and recommended the Royal Australian College of General Practitioners provide GPs with educational and training opportunities aimed at raising awareness of the diagnosis, symptoms and treatment of the condition.
Posted 14 April 2016 - 12:00 PM
Posted 14 April 2016 - 07:15 PM
Posted 15 April 2016 - 11:50 AM
Posted 15 April 2016 - 11:52 AM
For even more historical document information please visit the Myodil Action Group website. The Myodil Action Group was solely responsible for the inception of the House of Commons Myodil All Party Group and is the only group working with it and is demanding a public inquiry. If you want justice there are three things you should do. Please join the Myodil Action Group (MAG), chaired by Ursula Coxhead. If you live in the UK you should contact your MP explaining you are a sufferer of Myodil induced Adhesive Arachnoiditis and you want him or her to join the House Of Commons All Party Myodil Action Group you should also sign their e-petition to help them fight for a public inquiry, recognition, and compensation.
There is a conspiracy to hide this huge medical injury scandal. They ignored the warnings Myodil was unsafe but through willful ignorance or willful negligence they continued to use it, which means it is actually unlawful “criminal” injury, manslaughter or murder, the evidence is overwhelming. In the UK there are no statute of limitations on criminal offences.
The spinal cord is a pure environment which should not be insulted with needles and chemicals. If you went in to hospital with back ache and underwent a Myodil Myelogram it doesn’t matter if they found anything wrong with your spine or not, you came out with toxic chemical meningitis (a separate devastating injury far worse than any prior injury you may or may not have had) leading to diffuse Adhesive Arachnoiditis. These conditions are incurable and un-treatable, causing intractable pain and organ dysfunction/failure, both of these problems lead to death however they cover it up by stating death is caused by natural causes from organ failure.
Posted 15 April 2016 - 11:53 AM
21 Sep 2012 – Public roundtable Arachnoiditis
GSK has the utmost sympathy for the people who have been, and are, afflicted by arachnoiditis. Arachnoiditis is a complex condition that may be caused by a number of conditions such as spinal infections, surgery and trauma.
Myodil was an injectable dye used by doctors as a contrast medium for x-ray purposes in myelography and supplied by Glaxo from 1950.
Although a causal link between Myodil and arachnoiditis was not established, when the company became aware of a possible association, it included a precautionary warning in the Myodil product information sheet that there was a possible risk of arachnoiditis from the use of this medicine.
Myodil was not withdrawn from the market in Australia but discontinued in 1987 when newer diagnostic radiographic techniques became available.
All pharmaceutical products have side-effects, which doctors have to take into account by weighing them against the benefit to be gained by using the products.
In Australia, a court action around Myodil was launched against Glaxo and in 1999 Glaxo reached a settlement with claimants. The settlement was without admission of guilt. GSK is not at liberty to divulge the details of the settlement as these are confidential.
GSK believes that it acted responsibly at all times in relation to the supply of Myodil. Glaxo supplied this diagnostic product with the information available at that time to meet the needs of a very knowledgeable and specialist medical profession for many years, until it was superseded by newer products and technology.
GlaxoSmithKline is a global research-based pharmaceutical and healthcare company with a proud history in Australia dating back to 1886. Our mission is to improve the quality of human life by enabling people to do more, feel better and live longer.
Posted 15 April 2016 - 11:55 AM
Worldwide millions of people underwent Myodil Myelogram’s, five million in America, a million in the UK etc. only Russia and Sweden wouldn’t use it because they thought it was dangerous. This medical injury is massive, the biggest ever, bigger than thalidomide. As soon as you mention the phrase Myodil induced Adhesive Arachnoiditis, doctors become embroiled with psychological problems. If you have been lucky enough to have a scan through the NHS, they have purposely been done incorrectly so that it doesn’t show Adhesive Arachnoiditis (this happened to me). They do not want to admit they have been injuring/killing millions of people. So the medical profession have been lying through their teeth conspiring for decades to cover it up by ignoring it or telling you that you don’t have it.Extremely lucrative jobs and reputations are at stake, not to mention the massive possible compensation cost. So they are all working together protecting each other and to contain it to a minimum (aiding and abetting, which is unlawful). Nobody wants to expose Glaxo for selling a dangerous product that has been killing millions of people, once again lucrative jobs and reputations are at stake. Because this medical injury is so big in numbers and so damaging to the human body, the medical profession have had good cause to cover it up, because of this the media haven’t been able to understand just how serious it is.
This medical injury is iatrogenic which means the medical profession and Glaxo caused it, and because they caused it they don’t want to admit to it so you are blacklisted and can’t get a diagnosis or treatment, making you a sufferer of iatrogenic neglect which is cruel and shows how ruthless the medical profession is in guarding themselves over medical injury claims.
It’s not just Myodil Myelogram’s they have been injuring people with, it’s badly performed epidural’s as well.
Posted 15 April 2016 - 11:57 AM
Latest GSK Press Release
04 Mar 2013 – GSK’s response to the public roundtable report on Arachnoiditis
GlaxoSmithKline (GSK) has reviewed the final report of the House of Representatives Standing Committee on Health and Ageing into adhesive arachnoiditis (“Living with the pain of adhesive arachnoiditis”).
The report makes a number of direct references to GSK, so it is important that GSK communicates its position on the report and related issues. Some of the points below reiterate information that GSK has previously provided in its public statements and some reflect responses to the contents of the report.
GSK has the utmost empathy for people who have been, and are, afflicted by arachnoiditis.
• GSK considers it has acted responsibly at all times in regard to the supply of Myodil including appropriate testing and monitoring and timely updates to product information to reflect the available science. We have also engaged in legal settlements where appropriate and been an active participant in the roundtable process.
• All pharmaceutical products may be associated with side-effects. Manufacturers provide prescribing information so that practitioners can make a judgment about the risk/benefit of the product and whether or not to administer it to the patient.
• When GSK became aware of a possible association with arachnoiditis (in 1971), GSK promptly included a precautionary warning in the Myodil prescribing information sheet that there was a possible risk of arachnoiditis following x-ray myelography using Myodil.
GSK respects the work of the committee and for the many people affected by arachnoiditis and recognises the important role it has played in raising awareness of the experiences of patients living with this condition.
However, we believe that it would not be appropriate for GSK to be responsible for establishing a charitable foundation as recommended by the committee.
The report was based on roundtable discussions convened by the Standing Committee in which GSK participated.
The Report by the standing committee makes reference to a range of stakeholders including pharmaceutical companies (e.g., Lafayette Pharmacal, GSK), medical associations (e.g. Royal Australian College of GPs, The Australian and NZ College of Anaesthetists), local health networks (e.g. Medicare Locals), research bodies (e.g., The Australian Research Council, the National Health and Medical Research Council)
The full report can be found here: http://www.aph.gov.a...ditis/index.htm.
Posted 16 April 2016 - 11:49 AM
I received this by e-mail with many thanks
Posted 30 April 2016 - 12:34 PM
This has blown me away and am having trouble putting this into words== I am so wild
First I am out here to help sufferers and do my best
Do I trust ACC and the powers to be the answer is NO
Do I trust people == well I would like to think so
On the 26th April at approximately between 4-30pm-5pm
My wife and I had a knock on our door and found 2 men in blue one Sergeant
They came in one going with my wife to the dining table the Sergeant into the lounge ==He asked me to turn off the TV
He started that the police have had a complaint about me [ An Anonymous caller] That I was going to blow up or planning or threaten to bomb ACC He also added that the police have accessed my blog and that they have been in contact with ACC
My understanding is that they have accessed my PC as well but have not taken it away
The police asked me to look in my garage I said go to it I have nothing to hide
After being here for ¾ of an hour and as they were leaving they mention a name and did I know him My answer was yes
I told police ACC are a pack of mongrels who I have been fighting for years But will not threaten them
My job before as a Fireman is to protect and save people life
On the 28th I rung police and am now wanting answers still as at today nothing
Whoever is making false statements to Police is a very sick= evil vindictive nasty person with no bases to make statements like this
What damage has been done
If any person knows or knows of someone that is so nasty please contact me urgent
This person should be charged what he or she have done is criminal
Posted 01 May 2016 - 10:05 AM
had similar years ago seems when I backed off posting the crap stopped. I do believe ACC does have black operators that make this type of trouble for tail liabilities.
A muppet from wainui? Who was complaining about your blog last week ????
Forgive me John Huntley but I missed your blog. Do you think if it was very serious the cops would've sent more than two sworn staff? FGS you're a retired firefighter, so ACC isn't your sole income now. We know who truly did make threats to bomb ACC Takapuna, New Zealand Plus we all saw those YouTubevideos where that awful Dermot & scruffy David mentioned you. IMHO This reeks of the same nasty trolls connected to the Takapuna Beach plotter and who've since made death threats against myself and my sick disabled mother in care, under their erroneous assumption I am the non university educated blogger who has unsatisfactory English grammar (their, there etc). Why were the cops in your garage/shed so long? Smells of a fishing expedition. You once showed me around your garage before you went overseas for a couple of months & it took only a few minutes, so what took the officers so long in there?https://cmiglobal.co...8560526294fe...
John and I go back a long way, School budies and work mates, He has been shafted by ACC for a long time NO HE wouild not do it, Good luck to YouJohn Huntley
OMG who is this crooked little troll? Is this where he lives? May we see what has been posted about you? Sorry to ask but I've been defamed so badly, my own turned against me.https://www.google.c...3m4!1sBowPYL...
Posted 02 May 2016 - 05:24 PM
Posted 21 June 2016 - 01:48 PM
Scan.pdf 213.6KB 2 downloads
asked my doctor to please explain this document to me
Answer == with myodil in brain it is sending wrong messages with pain through my whole body from head to toes this is picked up in this document
Just a warning == if you have a CT scan and you have myodil in brain you can have side effects With me it was == head in a spin for weeks wanting to vomit
very tired wanting to sleep all the time major pain through my whole body
more X-rays to come soon