My E E G was B A D and more

I'm scheduled for anterior fusion surgery Feb 22nd, 2013.  I'm looking forward to having my neck fixed.  I can't help feel that when the mechanical issues are fixed, the herniations and the severely compressed cervical spine that I will have less inflammation in the area.  That might mean less attacks of trigeminal neuralgia, less attacks of occipital neuralgia and less pain and symptoms like the carpal in my right hand, the incontinence and the balance issues.  I think it is a good surgery.  I'm grateful to the surgeon.

The back of my neck was feeling funny and low and behold..it's a discoid rash!  A perfect 0!  Here's a .pic.

Also I was given orthotic devices for my carpal tunnel, tarpal and ulnar and perenal.  Above are some pics of those.

The new shockers:  After seeing my neurologist and being told about my abnormal EEG and brain damage and seizure disorder it was difficult to tell my husband.  It's one thing to suspect it, it's another thing to admit it and see it in writing and hear it from your doctor.  I videotaped myself and caught several jerky moments I'm pretty sure were small seizures.  It explains the chipped teeth and bite on my tongue.  I will continue to do  word games and neurophysical exercises to stay sharp.  I'm already on anti-seizure medication.  I take tegretol for my trigeminal neuralgia.
The system wide nerve entrapment syndrome.  I mean WHAT WHAT WHAT?  I'm wearing the orthotics as needed.  I have good days and bad days..I need to try harder to identify the triggers so I have more good days.  Ideas anyone?

Thanks for reading!  HUGS, Julie

Adhesive Arachnoiditis ???

I think I seriously KNOW what may be wrong with me.  I found this info by accident.  However it fits me to a T.
No sense in me highlighting it for you, it's pretty self explanatory.  I did a search for muscle fibrosis and nerve entrapments and lupus and found this condition of adhesive arachnoid syndrome.  This is a disease that is autoimmune or caused by an ai action that causes system wide nerve entrapments because it causes scar tissue between the muscle and nerves IN THE CONNECTIVE TISSUE.
I made the text bigger and bolder and underlined where I want to emphasize the amazing perfect fit and descriptions of my diagnosis's, misdiagnosis's and symptoms.  Some of most incredible cooincidences that MIRROR my condition include having symptoms of cranial neuropathies, burning mouth syndrome, solar urticaria, neurogenic bladder, burning feet pn and the misdiagnosis when having adhesive arachnoiditis of cervical spondlyosis (check), ulnar and carpal tunnel (check), cervical spondylosis (check) and EMG (check again)


THE ADHESIVE ARACHNOIDITIS SYNDROME
Sarah Andreae-Jones MB BS (Smith)
Patron of the Arachnoiditis Trust UK
INTRODUCTION

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.

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.

THE INFLAMMATORY NATURE OF ADHESIVE ARACHNOIDITIS
Arachnoiditis is chronic inflammation of the arachnoid layer of the meninges which consists of trabeculae, a mesh of interwoven collagen fibrils resembling tissue paper. These secrete spinal fluid, which circulates through the cerebrospinal axis and is absorbed through the arachnoid villi in the brain.
The initial phase of the inflammatory process involves influx of white blood cells in response to an insult to the subarachnoid space, such as blood (trauma, surgery), foreign substance (dye, etc) or infectious agent (e.g. meningitis). This is initiated via the action of cytokines, (proteins that act as immune modulators). There is infiltration by macrophages and mesenchymal cells; the latter transform into fibroblasts, which make collagen (scar tissue).
Usually the fibrinolytic process, which breaks down excess scar tissue, limits this, but in arachnoiditis the scar tissue continues to form.
Authors such as Jayson ([4]) 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. ([5])
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 ([6]). 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 ([7]) 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.

PATHOLOGY
In the first stage the spinal nerves are inflamed (radiculitis) and the adjacent blood vessels distended (hyperaemia). The subarachnoid space disappears. Deposition of collagen fibrils (scar tissue) begins. In the second stage, (arachnoiditis) 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 subsequent compression causes them to atrophy. The scarring prevents the arachnoid from producing spinal fluid in that area. These stages were described by Burton in 1978.
In some cases, the scar tissue calcifies (arachnoiditis ossificans).
Benini and Blanco ([8]) 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, especially if there is a foreign body present. They are particularly seen after Pantopaque myelography.
An animal study ([9]) 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.
THE IATROGENIC ASPECT OF ADHESIVE ARACHNOIDITIS
PROGNOSIS
Arachnoiditis has been described as an insidious disease that is incurable. Guyer’s paper on the prognosis of arachnoiditis ([38]) 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 ([39]) 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).

THE SYNDROMIC NATURE OF SYMPTOMS IN ADHESIVE ARACHNOIDITIS

Adhesive arachnoiditis presents with diverse symptoms, which may relate to problems outside the CNS, and could therefore be described as a syndromic picture. However, bearing in mind that the treatments used for the neurological symptoms may cause a variety of side-effects, it is difficult to say exactly which symptoms can be directly and solely ascribed to arachnoiditis and which are more complex in origin.

The medical literature mostly describes symptoms in the lower back and or legs, with pain, weakness and sensory loss. Some authors also discuss bladder and sexual dysfunction. Jenik et al ([40]) 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. ([41])

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).

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.

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.

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 ([42]), 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 ([43]) 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 ([44]) 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 ([45]) 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. ([46])

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. ([47])

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.

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 ([48]) 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.

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. ([49])

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. ([50])

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.

DIFFERENTIAL DIAGNOSIS

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.

TREATMENT OPTIONS

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. ([60])

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 ([61]) 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 ([62]) 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. ([63]) 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.

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.”([64])

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%([65]). There are a number of papers documenting cases in which intrathecal granulomatous tissue has formed at the pump site. ([66]) 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 ([67]) 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” ([68]) 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. ([69])

A study on the neurotoxicity of intrathecal agents ([70]) 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 ([71]) 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 ([72]) 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. ([73])

Complications include wound infection, electrode displacement and fibrosis at the tip of the stimulating electrode. ([74]) 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 ([75]) 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 ([76]) 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 ([77]) 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 ([78]). 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.

LOOKING TO THE FUTURE

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

Areas for future research include:

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.

APPENDIX I: AUTOIMMUNE ASPECTS

The following data may be noted to clarify the ideas about the autoimmune aspect of arachnoiditis. They are unfortunately random, as there is a paucity of medical literature relating to this topic. However, my aim is to give the reader an idea of how the hypothesis mentioned in the article came about.

MacDonald ([80]) 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 ([81]). Kumazawa et al attribute the chronic sensory neuropathy occasionally seen in Sjogren’s to dorsal root ganglionitis with T-cell invasion. ([82]). They also describe autonomic dysfunction in Sjogren’s syndrome.

Nitsche et al ([83]) 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 ([84]) 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. ([85]) 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 ([86]) showed 24% of neurosarcoidosis cases had meningeal involvement.

Marinac ([87]) 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 ([88]) suggests that in arachnoiditis there is a similar process of inflammation to that seen in serous membranes such as the peritoneum, with “a negligible inflammatory cellular exudate and a prominent fibrinous exudate”. It is worth noting that the condition retroperitoneal fibrosis may be seen in association with rheumatoid arthritis.

 APPENDIX II: SYRINGOMYELIA

The principle features are:

• 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 ([89]) suggests that all types of shunts may cause “significant morbidity” and lead to further surgical intervention.

A study specifically of syringomyelia secondary to arachnoiditis ([90]) 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%).

ADDENDUM

It is no longer considered necessary to use a contrast agent in MRI scanning provided that the scan is T2 weighted, high resolution preferably with a stir cycle. Although this scan is considered the diagnostic test, it must however, be remembered that not all scans are sensitive enough to detect arachnoiditis, especially in the early stages. In any case, as regards MRI as a tool to assess the severity of the condition, it is comparable to using a chest X-ray to determine the heart rate and rhythm. Therefore, other tests such as Electromyograms (EMG) and nerve conduction studies (NCV) may be very useful in assessing the extent of nerve impairment.

Sarah Smith, MAY 2000.

REFERENCES

[1] Burton CV Spine 1978 Mar; 3(1): 24-30 Lumbosacral arachnoiditis

[2] Official Report 12 January 1998: Vol.304,c.152

[3] Burton CV, Internet article “Adhesive arachnoiditis: The Global Economic Liability” 1997

[4] Jayson MI, Keegan A, Million R, Tomlinson I Lancet 1984 Nov 24; 2(8413): 1186-7 A fibrinolytic defect in chronic back pain syndromes.

[5] Burton CV appearing in Neurological Surgery, Third Edition, Volume 4, pp: 2856-2865

[6] Koide J, Takada K, Sugiura M, Sekine H, Ito T, Saito K, Mori S, Takeuchi T, Uchida S, Abe T J Virol 1997 Mar; 71(3): 2478-2481 Spontaneous establishment of an Epstein-Barr virus-infected fibroblast line from the synovial tissue of a rheumatoid arthritis patient.

Wen S, Shimizu N, Yoshiyama H, Mizugaki Y, Shinozaki F, Takada K Am J Pathol 1996 Nov; 149(5): 1511-1517 Association of Epstein-Barr virus (EBV) with Sjogren's syndrome: differential EBV expression between epithelial cells and lymphocytes in salivary glands.

James JA, Kaufman KM, Farris AD, Taylor-Albert E, Lehman TJ, Harley JB J Clin Invest 1997 Dec 15; 00(12): 3019-26 An increased prevalence of Epstein-Barr virus infection in young patients suggests a possible etiology for systemic lupus erythematosus.

Dror Y, Blachar Y, Cohen P, Livni N, Rosenmann E, Ashkenazi A Am J Kidney Dis 1998 Nov; 32(5): 825-8 Systemic lupus erythematosus associated with acute Epstein-Barr virus infection.

[7] MacDonald SM, Rafnar T, Langdon J, Lichtenstein LM Science 1995 Aug 4; 269(5224): 688-90 Molecular identification of an IgE-dependent histamine-releasing factor.

[8] Benini A,Blanco J Schweitz Arch Neurol Psychiatr 1990;141(4):293-343 [Chronic fibroplastic leptomeningitis of the spinal cord and cauda equina]

[9] Tatara N Brain Nerve (Tokyo) 1992; 44(12): 1115-1125 Experimental Syringomyelia in rabbits and rats after localized spinal arachnoiditis.

[10] Johnson AJ, Burrows EH Br J Radiol 1978 Mar;51(603):196-202 Thecal deformity after lumbar myelography with iophendylate( Myodil) and meglumine iothalamate (Conray 280)

[11] Junck L, Marshall WH Ann Neurol 1983 May; 13(5): 469-84 Neurotoxicity of radiological contrast agents.

Skalpe IO Spine 1978 Mar; 3(1): 61-4 Adhesive arachnoiditis following lumbar myelography.

Suolanen J Ann Clin Res 1977 Aug; 9(4): 257-60 Adhesive arachnoiditis after lumbar myelography.

Johansen JG, Barthelemy CR, Haughton VM, Lipman BT, Ho KC AJNR Am J Neuroradiol 1984 Jan-Feb;5(1):97-9 Arachnoiditis from myelography and laminectomy in experimental animals

Tabor EN, Batzdorf U Neurosurgery 1996 Nov;39(5):1040-2 Thoracic spinal Pantopaque cyst and associated syrinx resulting in progressive spastic paraparesis: case report

[12] Skalpe IO Radiology 1976 Dec; 121(3 Pt. 1): 647-51 Adhesive arachnoiditis following lumbar radiculography with water-soluble contrast agents. A clinical report with special reference to metrizamide.

Jensen TS, Hein O J Neurol Neurosurg Psychiatry 1978 Feb; 41(2): 108-12 Intraspinal arachnoiditis and hydrocephalus after lumbar myelography using methylglucamine iocarmate.

Tanaka K, Nishiura I, Koyama T No Shinkei Geka 1987 Jan; 15(1): 89-93 Arachnoiditis ossificans after repeated myelographies and spinal operations--a case report and review of the literature].

Ward W, Matheson M, Gonski A Med J Aust 1976 Aug 28; 2(9): 333-5 Three cases of granulomatous arachnoiditis after myelography.

Haughton VM, Ho KC, Larson SJ, Unger GF, Correa-Paz F Radiology 1977 Jun; 123(3): 681-5 Experimental production of arachnoiditis with water-soluble myelographic media.

Haughton VM, Ho KC Radiology 1982 Jun; 143(3): 699-702 Arachnoid response to contrast media: a comparison of iophendylate and metrizamide in experimental animals.

Ahlgren P Invest Radiol 1980 Nov-Dec;15(6 Suppl): S264-6 Early and late side effects of water-soluble contrast media for myelography and cisternography: a short review.

Bohutova J, Vojir R, Kolar J, Grepl J Diagn Imaging 1979; 48(6): 320-5 Some unusual complications of myelography and lumbosacral radiculography.

Hansen EB, Fahrenkrug A, Praestholm J Br J Radiol 1978 May; 51(605): 321-7 Late meningeal effects of myelographic contrast media with special reference to metrizamide.

[13] Nakagawa H, Arita S, Kobayashi S, Ikoma Y, Oshino N Nippon Yakurigaku Zasshi 1989 Mar; 93(3): 187-96 [Neurotropic effects of non-ionic contrast media].

Obeid T, Yaqub B, Panayiotopoulos C, al-Jasser S, Shabaan A, Hawass NE Ann Neurol 1988 Oct; 24(4): 582-4 Absence status epilepticus with computed tomographic brain changes following metrizamide myelography.

Adams MD, Hopkins RM, Ferrendelli JA Invest Radiol 1988 Sep; 23 Suppl 1:S217-9 A rat EEG model for evaluating contrast media neurotoxicity.

Maly P, Bach-Gansmo T, Elmqvist D AJNR Am J Neuroradiol 1988 Sep; 9(5): 879-83 Risk of seizures after myelography: comparison of iohexol and metrizamide.

Llewellyn CG, Campbell DR, Quartey GR Can Assoc Radiol J 1988 Sep; 39(3): 230-1 Intracranial subdural hematoma complicating metrizamide myelography.

Kessler A, Radwan H, Kott E Harefuah 1988 May 1; 114(9): 435-7 [Transient encephalopathy following cervical myelography with metrizamide].

Kassicieh D, Drake ME Jr, Shuttleworth EC, Rammohan KW J Am Osteopath Assoc 1988 Mar; 88(3): 384-6 Conduction aphasia following metrizamide myelography.

Ahmed I, Pepple R, Jones RP Clin Electroencephalogr 1988 Jan; 19(1): 37-42 Absence status epilepticus resulting from metrizamide and omnipaque myelography.

[14] Wood KM Arguelles J Norenberg MD Reg Anaesth 1980 5:13-15 Degenerative lesions in rat sciatic nerves after local injections of methylprednisolone in aqueous solution.

[15] Nelson DA Arch Neurol 1988 Jul;45(7): 804-806 Dangers from methylprednisolone acetate therapy by intraspinal injection

[16] Mackinnon SE, Hudson AR Plast. Reconstr. Surg. 1982; 69: 482-489 Peripheral nerve injection injury with steroid agents.

[17] National Health and Medical Research Council (NHMRC) Australia, 1994 Epidural use of steroids in the management of back pain and sciatica of spinal origin.

[18] Byrod G, Olmarker K Spine 1995 20: 138-143 Rapid transport route between the epidural space and the intraneural capillaries of the nerve roots.

[19] Rosen CD, Kahanovitz N, Bernstein R, Viola K Clin Orthop 1988 Mar; (228):270-2 A retrospective analysis of the efficacy of epidural steroid injections.

[20] Andersen KH, Mosdal C Acta neurochir (Wien) 1987; 87(1-2): 52-3 Epidural application of cortico-steroids in low-back pain and sciatica.

[21] Cuckler JM, Bernini PA, Wiesel SW, Booth RE Jr, Rothman RH, Pickens GT J Bone Joint Surg[Am] 1985 Jan; 67(1):63-6 The use of epidural steroids in the treatment of lumbar radicular pain. A prospective, randomized, double-blind study.

[22] Carette S, Leclaire R, Marcoux S, Morin F, Blaise GA, St-Pierre A, Truchon R, Parent F, Levesque J, Bergeron V, Montminy P, Blanchette C N Engl J Med 1997 Jun 5; 336(23): 1634-40 Epidural corticosteroid injections for sciatica due to herniated nucleus pulposus.

[23] Ringsdal VS, Nielsen NA, Slot O, Kryger P Ugeskr Laeger 1997 Sep 15;159(38): 5653-7 [Epidural glucocorticoid injection in lumbago sciatica]

[24] Agency for Health Care Policy and Research (AHCPR); (Federal Government Agency) 1994 Clinical Practice Guideline No.14; Acute Low back problems in Adults: assessment and treatment.

[25] Vandermeulen E, Gogarten W, Van Aken H Anaesthetist 1997 Sep;46 Suppl 3: S179-S186 [Risks and complications following peridural anesthesia]

[26] Haisa t, Todo T, Mitsui I, Kondo T Neuro Med Chir(Tokyo) 1995 Feb;35(2):107-9 Lumbar adhesive arachnoiditis following attempted epidural anesthesia—case report

[27] Yuen EC, Layzer RB, Weitz SR, Olney RK Neurology 1995 Oct; 45(10): 1795-801 Neurological complications of lumbar epidural anesthesia and analgesia.

[28] Rocco AG, Philip JH, Boas RA, Scott D Reg Anesth 1997 Mar-Apr; 22(2):167-77 Epidural space as a Starling resistor and elevation of inflow resistance in a diseased epidural space.

[29] Hurst E, Weston J. Pathol Bacteriol 1955 38(70): 167-178 Adhesive Arachnoiditis and Vascular Blockage Caused by Detergents and other Chemical Irritants: An Experimental Study.

[30] Austin RT, Zuk JA J R Coll Surg Edinb 1989 Feb; 34(1): 30-2 Epidural adhesions after chymopapain chemonucleolysis.

[31] Moon MS, Kim I, Ok IY, Lee KW Int Orthop 1990;14(1):79-83 The response of nerve tissue to chymopapain

[32] Wehling P, Pak MA, Georgescu HI Acta Orthop Belg 1990; 56(3-4); 539-44 Intrathecal injection of a specific enzyme in rats as a model for chemically induced spinal cord injury.

[33] Kelly JM, Asbury AK, King JS J Neuropathol Exp neurol 1975 Sep; 34(5): 388-400 Neuropathological effects of intrathecal water.

[34] Moore DC, Hain RH JAMA 1954 156: 1050-1053 Importance of the perineural spaces in nerve blocking

[35] Malinovsky JM, Pinaud M Ann Fr Anesth Reanim 1996; 15(5): 647-58 [Neurotoxicity of intrathecally administered agents.]

[36] Sghirlanzoni A, Marazzi R, Pareyson D, Olivieri A, Bracchi M Anaesthesia 1989 Apr;44(4):317-21 Epidural anaesthesia and spinal arachnoiditis

Sklar EM, Quencer RM, Green BA, Montalvo BM, Post MJ Radiology 1991 Nov; 181(2): 549-554 Complications of epidural anesthesia: MR appearance of abnormalities.

[37] Burm AG Clin Pharmacokinet 1989 May; 16(5): 283-311 Clinical pharmacokinetics of epidural and spinal anaesthesia.

[38] Guyer DW, Wiltse LL, Eskay ML and Guyer BH. Spine 1989 Dec; 14(12): 1332-1341 The long range prognosis of arachnoiditis.

[39] Wilkinson HA Alternative therapies for the Failed Back Syndrome in The Adult Spine, JW Frymoyer ed.1991

[40] Jenik F, Tekle-Haimanot R, Hamory BH Paraplegia 1981; 19(3): 140-54 Non-traumatic adhesive arachnoiditis as a cause for spinal cord syndromes. Investigation of 507 patients.

[41] COFWA Survey, Martha Richardson 1999

[42] Brandt T Audiol Neurootol 1996 Jul-Aug; 1(4): 187-96 Cervical vertigo--reality or fiction?

[43] Bowsher D J Neurol Neurosurg Psychiatry 1996 Jul; 61(1): 62-9 Central pain: clinical and physiological characteristics.

[44] Ziegler MG, Ruiz-Ramon P, Shapiro MH Psychosom Med Jul-Aug; 55(4):339-46 Abnormal stress responses in patients with diseases affecting the sympathetic nervous system.

[45] Mathias CJ Hypertension 1991 Nov; 18(5 Suppl): III22-30 Role of sympathetic efferent nerves in blood pressure regulation and in hypertension.

[46] Khurana RK Neurology 1987 Jul; 37(7): 1221-4 Orthostatic hypotension-induced autonomic dysreflexia.

[47] Mathias CJ Hypertension 1991 Nov; 18(5 Suppl): III22-30 Role of sympathetic efferent nerves in blood pressure regulation and in hypertension.

Colachis SC 3d J Am Paraplegia Soc 1992 Jul; 15(3):171-86 Autonomic hyperreflexia with spinal cord injury.

[48] Auld AW Spine 1978 Mar; 3(1): 88-91 Chronic spinal arachnoiditis. A post-operative syndrome that may signal its onset.

[49] Bayer A, Thiel HJ, Zrenner E, Paulus W, Ried S, Schmidt D Nervenarzt 1995 Feb; 66(2): 89-96 [Disorders of color perception and increase glare sensitivity in phenytoin and carbamazepine therapy. Ocular side effects of anticonvulsants.

[50] Luoto S, Taimela S, Hurri H, Alaranta H Spine 1999 Feb 1; 24(3): 255-61 Mechanisms explaining the association between low back trouble and deficits in information processing. A controlled study with follow-up.

Kuhajda MC, Thorn BE, Klinger MRAnn Behav Med 1998 Winter; 20(1): 31-5 The effect of pain on memory for affective words.

[51] Torres D, Bauso Toselli L, Vecchi E, Leiguarda R, Doctorovich D, Merello M, Guevara J, Nogues M Medecina (B Aires) 1993;53(50):391-396 [Spinal arachnoiditis as a complication of peridural anesthesia]

Sklar EM, Quencer RM, Green BA, Montalvo BM, Post MJ Radiology 1991 Nov;18(2):549-554 Complications of epidural anesthesia: MR appearances of abnormalities

Nogues MA, Merello M, Leiguarda R, Guevara J, Figari A Eur Neurol 1992;32(2):99-101 Subarachnoid and intramedullary cysts secondary to epidural anesthesia for gynecological surgery

Tseng SH, Lin SM Clin Neurol Neurosurg 1997 Dec; 99(4): 256-8 Surgical treatment of thoracic arachnoiditis with multiple subarachnoid cysts caused by epidural anesthesia.

[52] Kendall BE, Valentine AR, Keis B, Neuroradiology 1982 Spinal arachnoid cysts: clinical and radiological correlation with prognosis.

[53] Kamada K, Iwasaki Y, Hida K, Abe H, Isu T No Shinkei Geka 1993 Feb;21(2):135-140 [Syringomyelia secondary to adhesive arachnoiditis: clinical profiles and efficacy of shunt operations]

[54] Caplan LR, Norohna AB, Amico LL J Neurol Neurosurg Psychiatry 1990 Feb; 53(2): 106-113 Syringomyelia and arachnoiditis.

[55] Tatara N Brain Nerve (Tokyo) 1992 44(12): 1115-1125 Experimental syringomyelia in rabbits and rats after localised spinal arachnoiditis.

[56] Kelley RE, Daroff RB, Sheremata WA, McCormick JR Arch Neurol 1980 Sep; 37(9): 588-9 Unusual effects of metrizamide lumbar myelography. Constellation of aseptic meningitis, arachnoiditis, communicating hydrocephalus, and Guillaine-Barre syndrome.

[57] Hendler NH, Bergson C, Morrison C Psychosomatics 1993 Dec; 34 (6): 49-501 Overlooked Physical Diagnoses in Chronic Pain Patients Involved in Litigation, Part 2.

[58] Perry, Barnes, Gronley Clin.Orthopaedics and Related Research 1988 Aug; 233:145-162 The Postpolio Syndrome-An Overuse Phenomenon

Perry, James, Fontaine, Mulroy, Downey Journal of Bone and Joint Surgery 1995 Aug;77-A(8):1148-1153 Findings in Post-Poliomyelitis Syndrome

[59] Burton CV, Internet publication( Institute for Low back and neck care website) ,April 1998

[60] Sjogren PM, Jensen NH, Jensen TS Pain 1994 Nov; 59(2): 313-6 Disappearance of morphine-induced hyperalgesia after discontinuing or substituting morphine with other opioid agonists.

[61] Ebert B et al J Pain Symptom Manage 1998 15(5):269-274 Dextropropoxyphene acts as a noncompetitive N-methyl-D-aspartate antagonist.

[62] McQuay HJ, Acta Anesthiol Scand 1997; 41 (1): 175-183 Opioid use in chronic pain

[63] Reimann W, Schlutz H, Selve N Anesth Analg 1999 Jan; 88(1): 141-5 The antinociceptive effects of morphine, desipramine, and serotonin and their combinations after intrathecal injection in the rat.

[64] James A. Stangl and John D. Loeser: Current Review of Pain 1997 1: 353-360. Intraspinal Opioid Infusion Therapy in the Treatment of Chronic Nonmalignant Pain [Review article]

[65] Paice JA, Penn RD, Shott S J Pain Symptom Manage 1996 Feb; 11(2): 71-80 Intraspinal morphine for chronic pain; a retrospective multicenter study.

[66] Bejjani GK, Karim NO, Tzortzidis F Surg Neurol 1997 Sep; 48(3): 288-91 Intrathecal granuloma after implantation of a morphine pump: case report and review of the literature.

Cabbell Kl, Taren JA, Sagher O Neurosurgery 1998 May; 42(5): 1176-80 Spinal cord compression by catheter granulomas in high-dose intrathecal morphine therapy: case report.

[67] Sjoberg M, Karlsson PA, Nordborg C, Wallgren A, Nitescu P, Appelgren L, Linder LE, Curelaru I Anesthesiology 1992 Feb; 76920; 173-86 Neuropathological findings after long-term intrathecal infusion of morphine and bupivicaine for treatment in cancer patients.

[68] Malinovsky JM, Lepage JY, Cozian A, Mussini JM, Pinaudt M, Souron R Anesthesiology 1993 Jan; 78(1):109-115 Is ketamine or its preservative responsible for neurotoxicity in the rabbit?

[69] Nordt SP Ann Pharmacother 1996 Oct;30(10):1179-80 Chlorobutanol toxicity;

DeChristoforo R, Corden BJ, Hood JC, Narang PK, Magrath IT Ann Intern Med 1983 Mar; 98(3): 335-6 High-dose morphine infusion complicated by chlorobutanol-induced somnolence.

[70] Malinovsky JM, Pinaud M Ann Fr Anesth Reanim 1996; 15(5): 647-58 [Neurotoxicity of intrathecally administered agents.]

[71] Kumar K, Nath R, Wyant GM J Neurosurg 1991 Sep; 75(3): 402-7 Treatment of chronic pain by epidural spinal cord stimulation: a 10-year experience.

[72] Meilman PW, Leibrock LG, Leong FT Clin J Pain 1989 Jun; 5(2): 189-93 Outcome of implanted spinal cord stimulation in the treatment of chronic pain: arachnoiditis versus single nerve root injury and mononeuropathy. Brief clinical note.

[73] Ronzoni G, De Vecchis M, Rizzotto A, Raschi R, Cuneo L Ann Urol (Paris) 1988; 22(1): 31-4 [Long-term results of spinal cord electrostimulation in the treatment of micturition disorders associated with neurogenic bladder].

[74] Kumar K, Nath R, Wyant GM J Neurosurg 1991 Sep; 75(3): 402-7 Treatment of chronic pain by epidural spinal cord stimulation: a 10-year experience.

[75] O’Connor M, Brighouse D, Glynn CJ Clin J Pain 1990 Sep; 6(3): 240-2 Unusual complications of the treatment of chronic spinal arachnoiditis.

[76] El-sayed A et al JAMA 1999; 281:818-823 Percutaneous Electrical Nerve Stimulation for Low Back Pain. A Randomised Crossover Study.

[77] Wheeler AH, Tucker CL AJPM 1997; 7(3): 92-97 Electrical muscle stimulation: Portable electrotherapy for neck and low back pain: patient satisfaction and self-care.

[78] Andalaro VJ, Monaghan DT, Rosenquist TH Pediatr Res 1998 Jan; 43(1): 1-7 Dextromethorphan and other N-methyl-D-aspartate receptor anatagonists are teratogenic in the avian model.

[79] Lohmann K, Prohl A, Schwartz E Gesundheitswesen 1996 Jun; 58(6): 322-31 [Multiple chemical sensitivity disorder in patients with neurotoxic illnesses].

[80] MacDonald SM, Rafnar T, Langdon J, Lichtenstein LM Science 1995 Aug 4; 269(5224): 688-90 Molecular identification of an IgE-dependent histamine-releasing factor.

[81]Ecoiffier EB, Tubery M, Adoue D, Durroux R, Juchet H, Ollier S, Arlet P

Presse Med 1997 Jun 21;26(21): 995-999 [Systemic manifestations of primary Gougerot-Sjogren syndrome. Nature and incidence apropos of 34 cases].

Tajima Y, Tsukishima E, Sudo K, Aimoto Y, Tashiro K No To Shinkei 1997 Sep; 49(9): 825-8 [A case of Sjogren syndrome associated with multiple mononeuritis and dysautonomia including bilateral tonic pupils].

Vetrugno R, Liguori R, Cevoli S, Salvi F, Montagna P Ital J Neurol Sci 1997 Oct; 18(5): 293-5 Adie’s tonic pupil as a manifestation of Sjogren’s syndrome.

Font J, Valls J, Cervera R, Pou A, Ingelmo M, Graus F Ann Rheum Dis 1990 Oct; 49(10): 775-8 Pure sensory neuropathy in patients with primary Sjogren’s syndrome: clinical, immunological, and electromyographic findings.

[82] Kumazawa K, Sobue G, Yamamoto K, Shimada N, Mitsuma T Rinsho Shinkeigaku 1993 Oct;33(10): 1059-65 [Autonomic dysfunction in sensory ataxic neuropathy with Sjogren’s syndrome]

[83] Nitsche A, Leiguarda RC, Maldonado Cocco JA, Lazaro MA, Garcia Morteo O Clin Rheumatol 1991 Mar; 10(1): 5-9 Neurological features in overlap syndrome.

[84] Tesavibul : Immunology Service, Massachusetts Eye & Ear Infirmary Harvard Medical School, Boston, MA Multiple Autoimmune Diseases :Internet source

[85] Kendall BE, Tatler GL Br J Radiol 1978 Feb; 51(602): 81-92 Radiological findings in neurosarcoidosis

[86] Sharma OP Chest 1997 Jul;112(1): 220-8 Neurosarcoidosis: a personal perspective based on the study of 37 patients

[87] Marinac JS Ann Pharmacother 1992 Jun; 26(6): 813-822 Drug- and chemical-induced aseptic meningitis: a review of the literature.

[88] Ribiero C, Reis FC Acta Med Port 1998 Jan:11(1): 59-65 [Adhesive lumbar arachnoiditis]

[89] Batzdorf U, Klekamp J, Johnson JP J Neurosurg 1998 Sep;89(3): 382-8 A critical appraisal of syrinx cavity shunting procedures

[90] Klekamp J, Batzdorf U, Samii M, Bothe HW J Neurosurg 1997 Feb; 86(2): 233-40 Treatment of syringomyelia associated with arachnoid scarring caused by arachnoiditis or trauma.

Here's another GREAT sight about the rare type of adhesive arachnoiditis, and this is not about the proposed epidural or chemical induced type of adhesive arachnoiditis.  There are less than 1000 affirmed cases of true adhesive arachnoiditis, too little for any study and extremely rare.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1292616/

I will keep my blog updated on this condition, my neurologist and rheumatologist response to it and any conclusive MRI's or other tests I have to look for and confirm.  Peace Out!!!