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.
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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!!!
