By DR. Sarah Smith


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).


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."


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)


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 the second 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):

  1. sExtradural compression (spondylosis/stenosis)
  2. local post-operative changes
  3. arachnoiditis at a single level
  4. arachnoiditis at multiple levels
  5. myelographic block secondary to arachnoiditis
  6. arachnoiditis progressive or ascending greater than 2 levels above operative site.

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.


  • Spinal surgery (especially multiple)
  • Myelographic dyes (especially oil-based such as Myodil (Pantopaque))
  • Epidural steroid injections (e.g.Depo-Medrol)
  • Epidural anaesthesia
  • Other intraspinal drugs such as amphotericin B and methotrexate
  • Multiple lumbar punctures
  • Trauma
  • Infection e.g. meningitis
  • Subarachnoid haemorrhage
  • Spinal stenosis
  • Chronic disc prolapse


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.


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).




  1. Subarachnoid cysts
  2. Syringomyelia
  3. Communicating hydrocephalus

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.

Oral regimes:

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.

Non-pharmacological treatments

These include Transcutaneous Electrical Nerve Stimulation:

  • TENS (of limited use)
  • Acupuncture (contact with patients who have tried this suggests that it is not as useful as could be hoped)
  • Physiotherapy: must be gentle as vigorous exercise may precipitate a flare-up. As in PPS, a non-fatiguing programme is likely to be the most beneficial.
  • Hydrotherapy: often very useful, but the water must not be too warm (heat intolerance is common in arachnoiditis patients)
  • Hypnosis
  • Biofeedback
  • Cognitive techniques
  • Relaxation/meditation: these are all helpful adjuncts to drug treatment, but few patients can manage on these pain management techniques solely.

3 relatively new techniques are becoming available:

  1. APS (Action Potential Simulation) electrical stimulation (non-invasive) similar to TENS but of a different electrical waveform.
  2. LLLT (Low-level Laser Therapy) again, non-invasive, resembling ultrasonic treatment in its application, it has been used with success in patients with various types of neuropathic pain, (e.g. post-herpetic) but mostly in more localized conditions.
  3. PENS (Percutaneous Electrical Nerve Stimulation) is a technique that bridges acupuncture and electrical stimulation (TENS); low level electrical current (cf. TENS) is delivered via a series of ultra-fine, acupuncture-like needles. A recent study (lxxvii) has demonstrated that PENS was more effective than TENS in providing short-term pain relief and improved physical function in patients with chronic low back pain.

    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.

    Experimental treatments

    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.

    Miscellaneous treatments

    These include treatment of specific symptoms:

    Gastroparesis (see under symptomatology): prokinetic drugs such as Cisapride may relieve bowel motility disorders, including reflux oesophagitis.


    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.


    Dr. Charles Burton has called arachnoiditis a "scientific orphan". As yet, systematic, coordinated research is lacking.

    Areas for future research include:

    1. Autoimmune aspects, Aetiology (causes)Pathology (disease process)Possible treatments
    2. Developments in treatment of neuropathic pain

    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.


    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.


    The principle features are:

    • Headache- worsens with cough, sneeze, and strain.
    • Neckache
    • Pain in upper limbs, often exacerbated by valsalva manoeuvres, exertion or coughing.
    • Areas of dissociated sensory loss, which may be in a bizarre distribution over the trunk and upper limbs.
    • Loss of temperature sensation in upper limbs may lead to painless burns.
    • Loss of upper limb reflexes; positive Babinski reflex
    • Atrophy (wasting) of small muscles in the hands
    • Spastic paresis, gradually progressive, leading to difficulty in walking. (increased muscle tone and weakness)
    • Uncoordinated movements
    • Muscle spasms and fasciculations (twitches)
    • Skin rashes
    • Alteration in sweating
    • Raynaud's phenomenon (cold, painful hands due to poor circulation)
    • Horner's syndrome (see above), nystagmus.
    • Dysphagia (difficulty swallowing)
    • Dysphonia (abnormal voice)
    • Abnormal salivation.

    (NB. These symptoms are sometimes seen in uncomplicated arachnoiditis. Jenik et al (xxv) stated that spinal cord syndromes due to non-traumatic adhesive arachnoiditis cause "predominantly syringomyelic sensory deficits.")

    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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    Arachnoiditis explained by Dr. Sarah Smith

    Arachnoiditis is a chronic inflammation of the arachnoid layer of the meninges, which are the coverings of the brain and spinal cord. The most severe form is Adhesive arachnoiditis, which may be progressive.

    The scarring produced by the disease causes many symptoms, the most debilitating of which is pain, typically constant and of a burning nature, sometimes with intermittent sharp, stabbing pains (sometimes described as electric shock sensation). The pain is principally in the lower back and limbs, although it may be found higher up the spine and radiate down the arms. Other sensory symptoms include:

    • Tingling or numbness
    • Heightened skin sensation
    • Normally painless stimuli may be painful
    • Strange sensations e.g. water running down leg.
    • Burning in ankles or feet; sensation like walking on broken glass

    Movement (motor) functions may also be affected. Symptoms include:

    • Weakness (rarely paralysis)
    • Muscle spasms
    • Muscle cramps

    Bladder problems may also occur. These are due to involvement of the nerves that regulate bladder function, and may take one of two general forms: overactive bladder muscle causing urgency and incontinence, or under-active bladder, causing difficulty emptying the bladder, incomplete emptying and thus susceptibility to repeated infections. Similarly, the bowels may be affected.

    Circulation in the extremities may be affected if the autonomic (involuntary) nervous system is involved. This system regulates functions such as blood vessel tone and there may be cold hands or feet, or possibly swelling (oedema).

    From contacting numerous sufferers with arachnoiditis, it is becoming clear that there are often other symptoms, which may not at first glance appear related to the disease. These include:

    • Unexplained skin rashes
    • Joint and muscle pains (some patients have a dual diagnosis of fibromyalgia and arachnoiditis)
    • Heat intolerance
    • Cold chills/intermittent low-grade fevers
    • Difficulty swallowing


    Arachnoiditis has been known to the medical profession for many years as a rare complication of spinal surgery, trauma and meningitis (and other spinal infections such as TB).

    However in more recent years, myelography has come under fire as a cause of this disease. You may well have heard of Myodil, which was banned. In America, there is now a Bill before Congress to ban the myelogram dyes, Pantopaque(oil-based),Amipaque, Omipaque and Isovue (water-based) as there is evidence to suggest that these dyes cause arachnoiditis. Harry Feffer, Professor of Orthopaedic surgery at George Washington University states that patients who have had two or more myelograms stand a 50% chance of developing arachnoiditis.

    More controversial still is the effect of epidural steroid injection. Depo-Medrol has been documented as being neurotoxic due to the benzyl alcohol that the steroid is suspended in. Manufacturers of several steroid preparations state that their use around the spine is contra-indicated. In Australia, legal action is being undertaken by about 100 people after treatment with Depo-Medrol. Dr. Charles Burton, At the Institute of low Back and Neck Care, Minnesota, states that “the most common foreign body causing adhesive arachnoiditis is Depo-Medrol” now that Iophendylate (i.e.Pantopaque) has been withdrawn from use. Whilst it is accepted by the medical community that “any foreign body substance introduced into the subarachnoid space has the potential of causing an inflammatory reaction (adhesions, arachnoiditis or adhesive arachnoiditis) “ (Charles Burton MD. 1997). The incidence of complications is still relatively low, which suggests that some patients have a predisposition to develop the more aggressive, uncontrolled reaction. More research needs to be done about this. There have been papers postulating a defective enzyme and there appears to be a possible autoimmune component. These are areas for further investigation.


    One of the most striking features of stories from patients with arachnoiditis is that they have nearly all had great difficulty obtaining a diagnosis. Many are told they have “Failed Back Surgery Syndrome” (FBSS). Charles Burton writes that “an international study…..has shown that lumbo-sacral adhesive arachnoiditis has been directly responsible for about 11% of all FBSS cases”.

    Bearing in mind that arachnoiditis may be linked to a medical procedure, doctors may be reluctant to diagnose the disease. Also, there is at this time no known cure, but the disease is not generally life-threatening, so that practitioners may not want to give patients such a negative diagnosis. The first step in diagnosis, is, as always, a thorough history-taking and physical examination by the GP or hospital physician (usually a neurologist).

    A high resolution MRI scan will help to exclude other causes, and may be useful in diagnosing arachnoiditis, especially if it is read by an experienced neuroradiologist. For bladder problems, a referral to an urologist for urodynamic testing may be necessary.


    At this time, there is no definitive treatment for the disease process itself, although The Arachnoiditis Trust are setting up a working party of professionals to research the literature and establish international contacts with a view to getting research projects started. There are, however, various treatment modalities for the pain experienced, which tends to be the most debilitating factor. It is a “neurogenic” pain i.e. Generated by nerves, and as such is difficult to treat. Regimes include oral medication with anti-inflammatory agents; opioid drugs; adjuvant therapy with anticonvulsants and antidepressants, which are both very useful in this type of pain. This is not because there is a belief that the patient is either depressed or epileptic, and the drugs tend to be used at different doses to the ones used for depression or epilepsy. There are also other drugs to decrease muscle spasm. TENS machines may be of use, and may lead on to implantation of a spinal cord stimulator (which is like an internal TENS) for those patients who do not obtain good relief from drugs alone. In USA there are intraspinal narcotic pumps, but these may have serious side effects especially after prolonged use. Most encouragingly, there is a large body of research currently underway into a new class of drugs, which look very promising. Many patients suffer from the emotional effects of being in constant pain and the disabilities that this may impose upon them. These may be compounded by difficulties with the doctor/patient therapeutic relationship. However, referral to a specialist pain clinic may be useful in helping patients to gain an element of control over their illness. This can be very beneficial in improving the quality of life. Generally the pain management programmes tend to focus on cognitive/behavioural approaches i.e. using mental exercises to minimise the pain experienced, rather than using drugs, which may carry unacceptable side-effects. Sadly, many patients feel that referral to centres like this implies that they are not being taken seriously and that there is a suggestion that the pain is “in their head”. This is not to say that it is an issue of willpower, or that the patient is weak-willed or has a low pain threshold. Good doctors should take pains to reassure their patients that this is not the case. For some people, it can be a useful adjunct to other therapy.

    Dr. Charles Burton has called arachnoiditis a “scientific orphan” as regards past research. 


    Spinal stenosis is a term that means narrowing of the spinal canal or the nerve root foramina. It is thus divided into central or lateral stenosis. Central stenosis produces compression of the thecal sac. - Soft tissue (ligamentum flavum and disc) may contribute as much as 40% to this compression.

    It is more common in males because their spinal canal is smaller at the L3-L5 level. Lateral stenosis involves impingement of nerve roots lateral to the thecal sac, as they pass through the neural foramina. It is made worse with hypertrophy (overgrowth) of the ligamentum flavum and /or joint capsule. Foraminal stenosis affects the exiting (upper) nerve root.

    Compression of neural structures produces root ischemia and stenosis also compresses vascular supply of nerves so that symptoms are predominately those of neural ischemia. (Inadequate blood supply to nerves)

    There are many different causes of stenosis, the commonest of which is degenerative changes in the spine. This is also referred to as spondylosis, and tends to occur in the older age groups.

    However, there are other causes, including congenital or developmental stenosis. This presents at a much earlier age.

    A further cause is spondylolisthesis, which is slippage of one vertebra on another, usually caused by degenerative problems or trauma. Stenosis may be post-traumatic or post-surgical.

    Stenosis can occur at any level in the spine, but most commonly in the lumbar region. It is the commonest cause of Failed Back Surgery Syndrome(FBSS).

    Cervical stenosis is commonly associated with degenerative spinal changes, but can occur as a congenital problem, which may be asymptomatic until a minor injury such as whiplash causes persistent problems. This is well documented amongst American Football players, who may suffer temporary nerve damage (cord neuropraxia) after injury on the field, or may go on to have recurrent problems, known as the "chronic burner syndrome". It is generally accepted that a narrowed cervical spinal canal confers a risk of serious neurological damage from even minor injury (1,2), especially hyperextension. Symptoms of cervical stenosis are generally pain, tingling, numbness and weakness in the arms (myelopathic symptoms). In addition, there may be leg weakness, with a heavy feeling in the legs and difficulty walking usual distances or up stairs. Bladder problems may occur, and possibly sexual function may be affected.

    Stenosis may also occur at both cervical and lumbar levels. This is known as Tandem Spinal Stenosis (TSS) and is characterised by a triad of intermittent neurogenic claudication, progressive gait disturbances, and findings of mixed myelopathy and polyradiculopathy (multiple nerve root involvement) in both upper and lower extremities. It can mimic other neurological conditions such as amyotrophic lateral sclerosis (ALS). (3) (4)

    Thoracic stenosis is relatively rare.

    Lumbar stenosis:

    In lateral stenosis, the intervertebral foramina decrease in size from L1 to L5, therefore the L5 nerve root tends to be the most frequently involved.

    Regarding central stenosis, Porter suggests that "Pathologically, a developmentally small canal is usually affected by multiple levels of segmental degenerative change, with venous pooling in the cauda equina between two levels of low pressure stenosis."(4) He also states that "the size of the lumbar vertebral canal has clinical importance. The canal develops very early in life, and impaired growth at this time affects other growing systems. The patient with spinal stenosis has more than a spinal disadvantage."(5) He has found through studies on the effects of Antenatal environment on the development of the spinal canal, that the L3 canal was found to be the most sensitive to the influence of the factors such as gestational age and low birth weight. (6) Alvarez (7) describes lumbar stenosis as predominantly a condition of the older age groups. Lumbar stenosis is a condition that progresses slowly, and has few clinical signs, thus often delaying diagnosis. Diagnosis relies mostly on symptomatology raising the possibility of the condition, thereby suggesting relevant investigations. "Symptoms are often chronic, frequently missed, or misdiagnosed in the medical community, and may cause severe disability or reduction in the quality of life."(8)

    The chief symptom is what is termed "neurogenic claudication"(from the Latin "claudico", meaning "I limp") which refers to lower limb pain, often bilateral, which comes on with walking or standing for a length of time. As the condition progresses, walking distance and standing time are progressively decreased. Symptoms are relieved by sitting down or bending forward (compare disc herniation, in which bending exacerbates the pain). Some patients will bend down or squat as if about to tie their shoe-lace, to relieve pain on walking and there is the "shopping cart" sign which is when a patient will lean over the back of the shopping trolley to relieve the pain of standing in a queue. Flexion of the spine reduces symptoms, whereas extension exacerbates them. Neurogenic claudication should be distinguished from vascular intermittent claudication. The circulatory nature of the latter will present other features such as skin pallor or mottling, and impaired peripheral pulses. Significantly, resting in the standing position (unlike neurogenic claudication) relieves the pain of vascular claudication on exercise. The pain tends to be burning, gripping or cramping in nature, and radiates from the buttocks down the leg. The patient may describe it as "vice-like". There may also be dull aching and fatigue in the thighs and legs. Other symptoms may include tingling and numbness, as well as a degree of weakness. In severe cases, urinary incontinence can occur. Low back pain may also be a feature, but not usually a predominant one.

    A study by Jonsson et al (9) concluded that: "Pain was more intense and positive straight leg raising test results were more common in younger patients, whereas reflex disturbances were more common in the elderly." It must be remembered that other spinal conditions may co-exist with stenosis, in particular, disc disease. This may complicate the clinical picture. Clinical examination may not reveal abnormalities in straight leg raising or reflexes, as would be seen in disc disease. Sensory loss tends to be dermatomal (in nerve root distribution). Evaluation may include the Phalen test <19.htm>, which attempts to reproduce the symptoms of leg pain etc. The patient is stood upright and the spine extended by the examiner for a minute or so, which will induce the symptoms. Then the patient is allowed to bend forward and put his hands on a table, with one leg on a stool. This should relieve the symptoms.

    A further useful test is Exercise stress testing on a treadmill. (10)

    Investigation of stenosis is best achieved by CT or MRI scan with axial loading, (11), which is the equivalent of the Upright flexion-extension myelography, which is also used. (12) Bearing in mind that myelography is an invasive procedure and carries risks such as arachnoiditis (see below) the author recommends the latest MRI techniques. For the cervical spine, T2-weighted turbo spin-echo MRI is the investigation of choice. (13) Treatment of stenosis seems to raise controversies amongst the medical profession. Many authors suggest that conservative (non-surgical) treatment is preferable, whereas authors such as Alvarez (7) maintain that this has little proven benefit and that early surgery is the best method of treatment. Jonsson et al (14) suggest that the results from surgical decompression deteriorate with time, and that patients who had had symptoms for less than 4 years (and had insignificant low back pain) had the best outcomes. A review published in 1997 concludes that: "This review of the literature shows that the least invasive surgical procedure can obtain the best results if the correct diagnosis is made and if the operation is carried out within the first years of the disease." (15) Another recent study, by Javid and Hadar (16) suggests that "At 1 to 11 years the success rate was 70.8% for patients with stenosis, 66.6% for those with stenosis and herniated disc, and 63.6% for those with lateral recess stenosis. In conclusion, long-term improvement after laminectomy was maintained in two-thirds of these patients." Decompressive surgery must balance sufficient decompression with inducing spinal instability. The principle causes of failure of surgery are inadequate decompression, recurrence of degenerative hypertrophy (overgrowth), and instability. Arachnoiditis may also occur as a complication. (See below).

    Other modes of treatment have included epidural steroid injections, but Fukusaki et al (17) in a recent paper, state that they are not effective in stenosis patients. Other authors such as Cohen and Kostuik do not endorse their use, although some doctors (such as Rydevik) believe that they can be of use in the elderly population, for whom the risk of surgery is greater. (18) One study in Japan (19) tried using intravenous lipoprostaglandin (Lipo-PGE1) to treat stenosis. It produced symptomatic improvement for a limited period in the treatment of neurogenic claudication associated with stenosis. The drug appeared to exert its effects through an increase in the circulation of blood in the nerve roots and the cauda equina.

    Arachnoiditis and Stenosis

    Stenosis is recognised as being one of the causative factors for arachnoiditis. Jackson and Isherwood (20) from their MRI study, concluded that arachnoiditis features can be seen in stenosis, without other risk factors, but state that the cause of this is unexplained. Arachnoiditis over multiple levels is rare, except where there is multi-level stenosis.

    Epstein et al (21) reported 5 cases of arachnoiditis due to stenosis alone. Another important point to consider is that invasive techniques such as myelograms or epidurals will be entering an already compromised space and this may increase the risk of complications, of which arachnoiditis is one. Some of the studies done on post-myelographic arachnoiditis suggest that stenosis is a factor in the degree of severity. (22)

    Furthermore, adhesive arachnoiditis is considered to be one of the causes for the poor operative results for lumbar spinal stenosis. (23)

    Sarah Smith MB BS December 1998



    1.Katoh S, Ikata T, Hirai N, Okada Y, Nakauchi K Paraplegia 1995 Jun; 33(6): 330-333 Influence of minor trauma to the neck on the neurological outcome in patients with ossification of the posterior longitudinal ligament (OPLL) of the cervical spine.

    2. Pettersson K, Karrholm J, Toolanen G, Hildingsson C Spine 1995 Aug 1; 20(15): 1664-7 Decreased width of the spinal canal in patients with chronic symptoms after whiplash injury.

    3.Dagi TF, Tarkington MA, Leech JJ J Neurosurg 1987 Jun; 66(60): 842-849 Tandem lumbar and cervical spinal stenosis. Natural history, prognostic indices, and results after surgical decompression.

    4. Porter RW Spine 1996 Sep 1; 21(17): 2046-52 Spinal stenosis and neurogenic claudication.

    5. Porter RW The Henderson Trust Lecture. The development of the vertebral canal and associated neuro-physiological abnormalities.

    6.Papp T, Porter RW, Craig CE, Aspden RM, Campbell DM Spine 1997 Aug 15; 22(16): 1805-10 Significant antenatal factors in the development of lumbar spinal stenosis.

    7. Alvarez JA, Hardy RH Jr Am Fam Physician 1998 Apr 15; 57(8): 1825-34, 1839-40 Lumbar spine stenosis: a common cause of back and leg pain.

    8.Goldman SM, Funk JD, Christensen VM J Am Podiatr Med Assoc 1997 Mar; 87(3): 117-24 Spinal stenosis. A common cause of podiatric symptoms.

    9. Jonsson B, Annertz M, Sjoberg C, Stromqvist B Spine 1997 Dec 15; 22(24): 2932-7 A prospective and consecutive study of surgically treated lumbar spinal stenosis. Part I: Clinical features related to radiographic findings.

    10. Deen HG, Zimmerman RS, Lyons MK, McPhee MC, Verheijde JL, Lemens SM Spine 1998 Jan 15; 23(2): 244-8 Use of the exercise treadmill to measure baseline functional status and surgical outcome in patients with severe lumbar spinal stenosis.

    11. Willen J, Danielson B, Gaulitz A, Niklason T, Schonstrom N, Hansson T Spine 1997 Dec 15; 22(24): 2968-76 Dynamic effects on the lumbar spinal canal: axially loaded CT-myelography and MRI in patients with sciatica and/or neurogenic claudication.

    12. Zander DR, Lander PH Can Assoc Radiol J 1998 Aug; 49(4): 256-61 Positionally dependent spinal stenosis: correlation of upright flexion-extension myelography and computed tomographic myelography.

    13. Muhle C, Metzner J, Brinkmann G, Kuhn B, Bischoff L, Hutzelmann A, Wesner F, Heller M Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1997 Nov; 167(5): 467-73 [Comparison of T2-weighted turbo spin-echo and ultrafast HASTE sequence in the diagnosis of cervical myelopathies and spinal stenoses and static and kinematic MRT of the spine].

    14.Jonsson B, Annertz M, Sjoberg C, Stromqvist B Spine 1997 Dec 15; 22(24): 2938-2944 A prospective and conservative study of surgically treated lumbar spine stenosis. Part II: Five-year follow-up by an independent observer.

    15. Niggemeyer O, Strauss JM, Schulitz KP Eur Spine J 1997;6(6): 423-9 Comparison of surgical procedures for degenerative lumbar spinal stenosis: a meta-analysis of the literature from 1975 to 1995.

    16. Javid MJ, Hadar EJ J Neurosurg 1998 Jul; 89(1): 1-7 Long-term follow-up review of patients who underwent laminectomy for lumbar stenosis: a prospective study.

    17. Fukusaki M, Kobayashi I, Hara T, Sumikawa K Clin J Pain 1998 Jun; 14(2): 148-51 Symptoms of spinal stenosis do not improve after epidural steroid injection.

    18. Rydevik BL, Cohen DB, Kostuik JP Spine 1997 Oct 1; 22(19): 2313-7 Spine epidural steroids for patients with lumbar spinal stenosis.

    19. Murakami M, Takahashi K, Sekikawa T, Yasuhara K, Yamagata M, Moriya H J Spinal Disord 1997 Dec; 10(6): 499-504 Effects of intravenous lipoprostaglandin E1 on neurogenic intermittent claudication.

    20.Jackson A, Isherwood I Br J Radiol 1994 Sep; 67(801): 840-847 Does degenerative disease of the lumbar spine cause arachnoiditis? A magnetic resonance study and review of the literature.

    21.Epstein JA, Epstein BS, Lavine LS, Rosenthal AD, Decker RE, Carras R J Neurosurg 1978 Feb; 48(2): 252-258 Obliterative arachnoiditis complicating lumbar spinal stenosis

    22.Laitt R; Isherwood I; Jackson A BrJ Radiol 1996 Aug: 69(824): 693-4 Patterns of chronic adhesive arachnoiditis following Myodil myelography: the significance of spinal canal stenosis and previous surgery.

    23.Kawauchi Y; Sakou T; Yone K Spinal Cord 1996 Jul; 34(7); 403-410 Myeloscopic observation of adhesive arachnoiditis in patients with lumbar spinal canal stenosis.

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