Accurate Education – Arachnoiditis

Arachnoiditis

Arachnoiditis is a disease characterized by inflammation in the two outer membranes that cover and protect the brain, the spinal cord and the nerve roots. These two membranes are the dura (exterior) and the arachnoid (interior). The arachnoid contains the cerebrospinal fluid which circulates from the brain to the sacral area at the base of the spine.

 

Inflammation in the arachnoid can result in scarring and fibrosis which can cause abnormal adhesions and clumping of the nerves at the base of the spinal cord and those exiting the spinal cord. These adhesions and clumping can significantly alter  the function of the nerve and the spinal cord that can lead to severe chronic nerve pain, numbness, tingling, weakness in the legs and a variety of neurological impairments.

See below for causes and treatment


See Also:

Low Back Pain (LBP) – Overview

LBP – Disc Pain

LBP – Facet Pain

LBP – Myofascial Pain

LBP – Sacroiliac (SI) Joint Pain

LBP – Sciatica

LBP – Spinal Stenosis

 

Treatment Procedures:

Epidural Injections

Facet Joint Injections and Nerve Procedures

Heat & Cold Therapy

Inversion Therapy

Massage Therapy

Physical Therapy

Trigger Point Therapy


LBP – Surgery:

Considering Surgery?

Failed Back Surgery

 

“The greatest evil is physical pain”

– Saint Augustine

Arachnoiditis

 Epidemiology

Arachnoiditis is a rare disorder that affects more females than males, probably because two thirds of the pregnant women in the USA receive spinal or epidural anesthesia for the delivery.  However, current evidence does not support the claim that routine, uncomplicated epidural analgesia in obstetrics using preservative-free, low concentration bupivacaine with opioids or plain bupivacaine, if performed in the standard way with disposable equipment, causes arachnoiditis.

 

Unfortunately, the precise prevalence and incidence of arachnoiditis is unknown. According to one estimate, approximately 11,000 new cases occur each year in the USA. The increasing number of neck and back surgeries, pain relief procedures and diagnostic interventions and anesthetic spinal interventions has increased the number of cases considerably. Since some cases of arachnoiditis may go misdiagnosed or undiagnosed, it is difficult to determine its real frequency in the general population.

 

A Quick Review of the Pertinent Anatomy of the Spinal Cord

The spinal cord starts at the base of the brain and extends down the vertebral canal to about the first lumbar vertebra of the lower back. The end is cone-shaped and is known as the “conus medullaris.” At the level of the conus medullaris the spinal cord splits up into about 2 dozen nerves known as nerve roots or collectively as the “cauda equina” (in Latin this means “horses tail” due to the visual similarity).  The cauda equina extends downward to the sacrum.

 

These nerve roots are encased in a protective sac known as the thecal sac. Its lining is called the dura mater (dura), and the inner-most layer is the arachnoid. Within the thecal sac is the cerebrospinal fluid (CSF) which serves to nourish the nerve roots and wash away toxic materials such as elements that may result from inflammation. The small nerve roots are always floating in CSF and protected by the dura. Any contaminant or irritant that enters the thecal sac may initiate an inflammatory process.

 

Signs & Symptoms

Most symptoms are initially due to inflammation in the area of damage to the dura and/or the arachnoid membranes. However, arachnoiditis is usually a progressive disorder. First it is characterized by inflammation of the arachnoid membrane and then invasion of the subarachnoid space where the pain remains localized and can be quite severe. Eventually, as the inflammation spreads to the nerve roots after a few months, they begin to adhere to each other which exerts pressure on the nerve roots eventually resulting to scarring and fibrosis which in turn restricts blood flow to the affected area and also impedes the flow of cerebral spinal fluid (CSF). The progression of the localized pain to other areas depends on which nerves are involved. This condition can occur in the neck but is most common in the lower lumbar spine.

 

As the acute inflammatory process progresses to the chronic condition associated with adhesions, it is referred to as “adhesive arachnoiditis” or AA. Only when inflamed nerve roots stick or adhere (forming an adhesion) to the arachnoid lining does AA occur. Some patients diagnosed with arachnoiditis have the symptoms of this condition but only have nerve root inflammation and have not progressed to the point that the nerve roots have adhered to the arachnoid lining. As the inflammation worsens and spreads to develop adhesions, it can cause severe pain and dysfunction of the nerves that connect to the stomach, intestine, sexual organs, pelvis, legs, and feet.

 

Adhesive Arachnoiditis (AA)

Symptom severity of AA depends initially on the extent and location of the initial injury whereas continued chronic severity depends on the extent of spread of inflammation, severity of adhesions and degree of impairment of the CSF circulation.  Most AA occurs in the lumbar region with the pain usually felt in the lower back, the perineal area between rectum and genitals, the legs and feet.  These symptoms may appear weeks after spinal surgery or an interventional procedure such as an epidural injection or block.  In most cases the pain is intense, accompanied by tingling or burning in the legs or feet and skin sensations like “bugs crawling” or “water dripping.”

 

Frequently patients complain of constant severe pain radiating to the lower extremities, muscle cramps and difficulty walking and  impaired balance. Also, patients may suffer from “centralization” of symptoms, including severe headaches, vision disturbances, hearing problems, dizziness and nausea and fatigue. Bowel, bladder and sexual dysfunction as well as “electric shocks” type of pain are common in patients with severe adhesive arachnoiditis.

 

List of common symptoms associated with adhesive arachnoiditis:

  1. Constant low back pain, often sharp or burning
  2. Back pain worsening with prolonged sitting or standing
  3. Back or neck pain worsening with forward or backward flexion or tilting
  4. Burning or prickling pain or tingling in the bottom of the feet
  5. Difficulty starting or stopping urination
  6. Blurred vision or ringing in the ears
  7. Headaches
  
 
Clinical Course:
Symptoms of arachnoiditis often start many years after the suspected causative event. Chronic arachnoiditis can remain mild to moderate in severity or progress to severe and catastrophic, disrupting quality of life. There may be remissions and relapses but it is possible for resolution of symptoms with treatment. Although the course of chronic arachnoiditis is typically irregular, it has been reported to be progressive in up to 33% of patients and non-progressive in 50-59%.
 

Adhesive arachnoiditis, the most severe type of chronic arachnoiditis, results in scar tissue formation, which compresses nerve roots and disrupts their blood supply and also disrupts the normal flow of CSF. It can progress to arachnoiditis ossificans, an end-stage complication of adhesive arachnoiditis characterised by the pathological ossification of the spinal arachnoid in which calcium is deposited into the matrix of the affected membranes.

 
 

Risk Factors

 

Associated Medical Conditions:

As a consequence of impaired flow of CSF, the development of arachnoid cysts and syrinx (fluid collections in the spinal cord) have been reported.

 

Predisposing Medical Conditions:

  1. Ehlers-Danlos Syndrome
  2. Marfan’s Syndrome
  3. Tarlov Cysts
  4. Kyphoscoliosis
  5. Rheumatoid Spondylitis
  6. Spinal Stenosis
  7. Osteoporosis
  8. Herniated Discs
  9. Spinal cord compression
  10. Spinal cord trauma
  11. Infection
  12. Toxic reactions to medications and toxins

 

Predisposing Procedures:

  1. Spinal surgery – especially multiple spinal surgeries
  2. Spinal injections (i.e. epidural injections, epidural blocks, myelograms), especially multiple
  3. Epidural spinal injections or myelogram dyes mistakenly injected into the intrathecal space
  4. One or multiple spinal taps.
  5. Difficult epidural blood patches (injection >20ml).
  6. Infections associated with meningitis (viral, fungal or bacterial).

 

 

In a 2017 publication reviewing 489 patients with adhesive arachnoiditis, the precise probable cause of AA was identified in 472 cases (96.5%); in the remaining 17 cases (3.5%), probable cause was deduced from the timing of sudden changes in the patient’s symptom intensity and frequency. The breakdown incidence of these 489 patients is shown below:

 

Myelogram with Pantopaque, (pre-1986) 12

Myelogram* followed by spinal surgery (post-1986) 16

One Laminectomy (first) 38

Laminectomy plus another procedure 18

Laminectomy, (2nd or multiple) 76

Spinal fusion with bone graft 36

Spinal fusion with hardware 71

Spinal anesthesia 45

Epidural anesthesia (Lumbar) 51

Epidural steroid injections (with incidental dural puncture) 53

Pseudomeningocele following dural tears at laminectomy 27

Other pain relief related procedure 29

Thoracic epidural anesthesia  (syringomyelia) 5

Neuroplasty 5

Vertebroplasty 4

Spinal “taps” 3

Total: 489 patients

*In 1986, the production of oil-soluble contrast media for myelograms was discontinued in the USA.

 

 

Diagnosis of Adhesive Arachnoiditis

A diagnosis of AA is based upon assessment of a detailed patient history identifying key symptoms and risk factors such as having had an invasive procedure, surgery or serious illness within the spine.  In addition, a physical exam and imaging tests such as an MRI for confirmation is essential.  Since the symptoms of adhesive arachnoiditis resemble those associated with other spinal conditions, it is important to consider a multitude of alternative diagnoses.

 

Physical Examination

In patients with adhesive arachnoiditis, physical examination can reveal changes in reflexes, sensation and/or weakness. Exploration of proprioception (joint position awareness) can confirm symptoms of impaired balance.

 

Abnormal findings on physical exam may include:

  1. Pain on extension of arms
  2. Weakness of upper and/or lower extremities
  3. Inability to straight leg raise
  4. Indentation of lower spine (?)
  5. Asymmetry of paraspinal area muscle groups
  6. Reduced reflexes in lower extremities

 

Clinical Testing

 

Imaging

Magnetic resonance imaging (MRI) of the lumbosacral spine with contrast is the best imaging study because it is the most precise and less injurious compared with a computed tomography (CT) scan. The MRI uses a magnetic field and radio waves to produce cross-sectional images of particular organs and bodily tissues and does not expose the patient to radiation.

 

However, the presence of certain non-titanium metal objects (screws, wires, etc.) makes the MRI contraindicated since it may heat these metals. If an MRI is contraindicated, the diagnosis of arachnoiditis can be made using a contrast CT scan, but this requires injecting contrast media into the intrathecal compartment of the spinal cord which is invasive and potentially could make the condition worse.

 

When routine MRI is inconclusive, an MRI performed after the administration of intrathecal gadopentate dimeglumine (Gd-DTPA) as a contrast agent has been described as a safe, effective technique to diagnose or exclude the diagnosis of arachnoiditis. It should be noted that although a large multicenter study failed to demonstrate behavioral changes, neurologic alteration, or seizure activity with intrathecal gadolinium, the administration of intrathecal gadolinium is not approved for use by the FDA and is used off-label. Gadolinium-based contrast agents have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). These conditions have occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. NSF/NFD is a debilitating and sometimes fatal disease and should therefore be avoided in patients with impaired kidney function.

 

While MRI is the gold standard in the diagnosis of arachnoiditis,  unenhanced CT scan better identifies the presence and extent of calcification associated with arachnoid ossifications.

 

Laboratory studies

Laboratory studies are not helpful in the diagnosis of adhesive arachnoiditis nor is clinical neurophysiological testing (e.g. electromyelography).

  

While definitive diagnosis of AA requires imaging, other tests contribute to understanding the risks of AA and may provide clues to the selection of treatment options. These tests include those that assess the presence of inflammation and altered hormonal balances that frequently accompany severe chronic pain. Addressing these conditions may prove helpful in reducing pain and improving function and quality of life.

 

Elevated Inflammatory Markers (blood tests):

    1. C-Reactive Protein-High Sensitivity (CRP-HS)

    2. Erythrocyte Sedimentation Rate (ESR)

    3. Interleukins (IL-6)

 

Hormone Assessments:

1. Pregnenolone

2.DHEA

3.Cortisol

4.Progesterone

5.Estradiol

6.Testosterone

 

Treatment of Adhesive Arachnoiditis (AA)

 

Because adhesive arachnoiditis is a rare disorder, there is no consensus on standard treatment of AA. There have been no well-designed studies to investigate specifice medical interventions. However, it clear that treatment is available that can provide significant improvement in symptoms and a return to a better quality of life.

 

Goals in Management of AA:

  1. Pain control
  2. Reduction of neuroinflammation
  3. Exercises to improve flow of spinal fluid
  4. Regeneration of damaged nerves

 

 

Pain Control

Because of the adhesive nature of the condition, sudden movements such as being bumped or jolted can be very painful. To help protect against this, spine bracing can be effective and AA patients may benefit from the periodic use of a lumbar or cervidal brace to protect them. Care should be taken when walking in unfamiliar areas while shopping or attending social events.

 

The pain associated with AA is often severe and aggressive effort is required to provide relief. Medications directed at neuropathic (nerve) pain are indicated and should be initiated early with gradual increased dosing to achieve optimal benefit and avoid side effects. These medications include gabapentin (Neurontin), pregabalin (Lyrica) and complementary and alternative supplements including L acetyl-carnitine and lipoic acid.
See Neuropathic (Nerve) Pain

 

Because of the severity of AA, it is often necessary to turn to opioids to provide adequate pain control and improve function. While it always the case to limit the quantity and potency of opioids chosen for pain management as possible, it may be necessary to use higher potency opioids. However, the opioids which have greater effect on neuropathic pain may be preferred. These opioids include tramadol (Ultram), tapentadol (Nucynta), levorphanol and methadone.

 

However, any medication for pain may be only marginally effective unless spinal cord inflammation is first controlled.

 

Reduction of Neuroinflammation

Every AA patient must have a daily regimen to keep neuroinflammation from accumulating. This can be the missing link to relief and recovery. This regimen includes gentle exercises to improve flow of spinal fluid and limit or reverse the adhesive process. The use of medications to reduce inflammation should also be included.

 

Recent advances in research into the inflammatory processes involving the nervous system (neuroinflammation) have provided insights into some of the unique mechanisms involved. Immune cells within the nervous system called the microglial cells are believed to play a role in the initiation and maintainence of neuroinflammation. Unfortunately, unlike other mechanisms of inflammation, microglial cells do not respond well, if at all, to standard anti-inflammatory drugs including ibuprofen and other NSAIDs or corticosteroid anti-inflammatories including hydrocortisone. Methylprednisolone 4 mg or prednisone 5 to 10 mg at 3:00 pm on 5 days a week may be recommended but corticosteroids must be used with caution under the guidance of a physician due significant side effects associated with prolonged use.

 

There is a strong effort being made by the medical community to identify medications that can reduce microglial activation of neuroinflammation but a definitively potent and effective medication is still elusive. However, there is a growing body of research that suggests some alternative medications may be safe and effective and should be considered, especially for those with severe symptoms. These medications include minocycline and palmitoylethanolamide (PEA), both with evidence that they reduce microglia-induced neuroinflammation.

See: Minocycline

See: Palmitoylethanolamide (PEA)

 

The role of an anti-inflammatory diet and anti-inflammatory supplements should not be overlooked. The Mediterranean, or anti-inflammatory, diet is an important component of chronic pain management, especially with conditions associated with chronic inflammation. Nutritional supplements, especially curcumin and other NRF2 activators are highly recommended for their antioxidant benefits related to inflammation.

See: Meriva (Curcumin)

See: Nutrition & Pain

 

 

Exercises to improve flow of spinal fluid

Mild physical therapy including stretching is recommended for affected individuals to restore motion, preserve function and to help them remain active. Other approaches include massage, hydrotherapy, and hot or cold compresses. Surgery as a treatment of adhesive arachnoiditis is generally not recommended because of the possibility of worsening the inflammation and the condition.

 

It is particularly important that patient improve and maintain the range of motion of their spine and extremities as much as possible. This involves daily stretching so that eventually the patient can attain full range of motion, at least of their arms and legs. Patients should walk outside their home daily.

 

The following spinal cord exercises have been recommended by Dr. Forest Tennant, a leading authority in the management of adhesive arachnoiditis:

 

FULL-BODY STRETCH LAYING DOWN
Lay down on the floor and do a full-body stretch. Count up to 10.

 

FULL-BODY STRETCH STANDING
Spread hands and reach “to the sky” until you feel pressure and tugging in your back. Count up to 10.

 

SIT AND STRETCH ARMS
Stretch your arms and spread your fingers. Count up to 10. Can do while sitting in a car or plane.

 

LEG RAISE WHILE LAYING DOWN
Raise your leg until you feel tugging in your back. Count up to 10.

 

LEG RAISE WHILE STANDING
Stabilize yourself next to a table or wall. Raise your leg and flex your foot.

 

KNEE PULL WHILE LAYING DOWN
Pull your knee back until you feel tugging in your back. Count up to 10.

 

INVERSION TABLE
If able, a short episode on an inversion table may assist in pulling adhesions and cauda equina nerves apart to prevent scarring.

 

Regeneration of damaged nerves

Nutritional and hormone support may facilitate the body’s ability to repair damaged nerves. When hormonal deficiencies are identified, replacement therapy can be helpful in restoring nerve health.

 

  1. Supplement deficient hormones as determined by serum or saliva testing:

    a) Pregnenolone

    b) DHEA

    c) Thyroid

    d) Testosterone

    e) Cortisol

    f) Estradiol

    g) Progesterone

     

  2. Vitamin B12: 2 to 3 times a week (sublingual or oral)

     

  3. OPTIONAL: Human Chorionic Gonadotropin (HCG): 500 units, given sublingual or injection, 3 days a week. This treatment is off-label and lacks consensus of medical opinion as to it’s effectiveness.

     

  4. OPTIONAL: Add oxytocin (40 units per ml) given 1⁄2 ml sublingual twice daily if patient is making progress. This treatment is off-label and lacks consensus of medical opinion as to it’s effectiveness.

 

References

  1. National Organization of Rare Diseases – Arachnoiditis
  2. Arachnoiditis Imaging

 

Adhesive Arachnoiditis Overview 

  1. Suspecting and Diagnosing Arachnoiditis – 2017
  2. Arachnoiditis – Clinical Progression, Evaluation, and Management- 2013
  3. Obstetric epidurals and chronic adhesive arachnoiditis – 2004
  4. Postlumbar puncture arachnoiditis mimicking epidural abscess – 2013
  5. Thoracic arachnoiditis, arachnoid cyst and syrinx formation secondary to myelography with Myodil, 30 years previously – 2006
  6. Adhesive arachnoiditis in mixed connective tissue disease – a rare neurological manifestation – 2016

 

Adhesive Arachnoiditis – Treatment

  1. Arachnoiditis handbook for Relief and Recovery – Forest Tenant 2016
  2. Arachnoiditis – Clinical Progression, Evaluation, and Management- 2013

 

 

Arachnoiditis Treatment Minocyline

  1. Minocycline blocks lipopolysaccharide induced hyperalgesia by suppression of microglia but not astrocytes – 2015
  2. A novel role of minocycline: attenuating morphine antinociceptive tolerance by inhibition of p38 MAPK in the activated spinal microglia. – PubMed – NCBI
  3. Minocycline, a microglial inhibitor, blocks spinal CCL2-induced heat hyperalgesia and augmentation of glutamatergic transmission in substantia gelatinosa neurons – 2014
  4. Pathological pain and the neuroimmune interface – 2014
  5. Minocycline attenuates the development of diabetic neuropathic pain: possible anti-inflammatory and anti-oxidant mechanisms. 2011 – PubMed – NCBI
  6. Minocycline Provides Neuroprotection Against N-Methyl-d-aspartate Neurotoxicity by Inhibiting Microglia – 2001
  7. Minocycline targets multiple secondary injury mechanisms in traumatic spinal cord injury

 

Emphasis on Education

 

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