SPINAL STENOSIS
Sarah Andreae-Jones MB BS (Smith)
Patron of The Arachnoiditis Trust UK

 

Spinal stenosis is a term that means narrowing of the spinal canal or the nerve root foramina. It is thus divided into central or lateral stenosis. Central stenosis produces compression of the thecal sac. Soft tissue (ligamentum flavum and disc) may contribute as much as 40% to this compression. It is more common in males because their spinal canal is smaller at the L3—L5 level.

Lateral stenosis involves impingement of the nerve roots lateral to the thecal sac, as they pass through the neural foramina. It is made worse with hypertrophy (overgrowth) of the ligamentum flavum and / or joint capsule. Foraminal stenosis affects the exiting (upper) nerve root.

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

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

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

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

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

Cervical stenosis is commonly associated with degenerative spinal changes, but can occur as a congenital problem, which may be asymptomatic until a minor injury such as whiplash causes persistent problems.

This is well documented amongst American Football players, who may suffer temporary nerve damage (cord neuropraxia) after injury on the field, or may go on to have recurrent problems, known as the “Chronic Burner Syndrome”. It is generally accepted that a narrowed cervical spinal canal confers a risk of serious neurological damage from even a minor injury (1,2), especially hyperextension.

Symptoms of cervical stenosis are generally pain, tingling, numbness and weakness in the arms (myelopathic symptoms). In addition, there may be leg weakness, with a heavy feeling in the legs and difficulty walking usual distances or up stairs. Bladder problems may occur, and possibly sexual function may be affected.

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

Thoracic stenosis is relatively rare.

 

Lumbar stenosis:

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

Regarding central stenosis, Porter suggests that “Pathologically, a developmentally small canal is usually affected by multiple levels of segmental degenerative change, with venous pooling in the cauda equina between two levels of low pressure stenosis.” (4)

He also states that “the size of the lumbar vertebral canal has clinical importance. The patient with spinal stenosis has more than a spinal disadvantage.” (5). He has found through studies on the effects of Antenatal environment on the development of the spinal canal, that the L3 canal was found to be the most sensitive to the influence of the factors such as gestational age and low birth weight. (6). Alvarez (7) describes lumbar stenosis as predominantly a condition of the older age groups.

Lumbar stenosis is a condition that progresses slowly, and has few clinical signs, thus delaying diagnosis. Diagnosis relies mostly on symptomatology raising the possibility of the condition, thereby suggesting relevant investigations. “Symptoms are often chronic, frequently missed, or misdiagnosed in the medical community, and may cause severe disability or reduction in the quality of life.” (8)

The chief symptom is what is termed “neurogenic claudication” (from the Latin “claudico”, meaning “I limp”) which refers to lower limb pain, often bilateral, which comes on with walking or standing for a length of time. As the condition progresses, walking distance and standing time are progressively decreased. Symptoms are relieved by sitting down or bending forward (compare disc herniation, in which bending exacerbates the pain). Some patients will bend down or squat as if about to tie their shoe lace, to relieve pain on walking and there is the “shopping cart” sign, which is when a patient will

Lean over the back of the shopping trolley to relieve the pain on standing in a queue. Flexion of the spine reduces symptoms, whereas extension exacerbates them.

Neurogenic claudication should be distinguished from vascular intermittent claudication. The circulatory nature of the latter will present other features such as skin pallor or mottling, and impaired peripheral pulses. Significantly, resting in the standing position (unlike neurogenic claudication) relieves the pain of vascular claudication on exercise.

The pain tends to be burning, gripping or cramping in nature, and radiates from the buttocks down the leg. The patient may describe it as “vice—like”. There may also be dull aching and fatigue in the thighs and legs. Other symptoms may include tingling and numbness, as well as a degree of weakness. In severe cases, urinary incontinence can occur. Low back pain may also be a feature, but not usually a predominant one.

A study by Jonsson et al (9) concluded that: “Pain was more intense and positive straight leg raising test results were more common in younger patients, whereas reflex disturbances were more common in the elderly.”

It must be remembered that other spinal conditions may co—exist with stenosis, in particular, disc disease. This may complicate the clinical picture.

Clinical examination may not reveal abnormalities in straight leg raising or reflexes, as would be seen in disc disease. Sensory loss tends to be dermatomal (in nerve root distribution). Evaluation may include the Phalen test, which attempts to reproduce the symptoms of leg pain etc.

The patient is stood upright and the spine extended by the examiner for a minute or so, which will induce the symptoms. Then the patient is allowed to bend forward and put his hands on a table, with one leg on a stool. This should relieve the symptoms.

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

Investigation of stenosis is best achieved by CT or MRI scan with axial loading, (11), which is the equivalent of the Upright flexion—extension myelography, which is also used. (12)

Bearing in mind that myelography is an invasive procedure and carries risks such as arachnoiditis (see below) the author recommends the latest MRI techniques.

For cervical spine, T2— weighted turbo spin—echo MRI is the investigation of choice. (13).

Treatment of stenosis seems to raise controversies amongst the medical profession. Many authors suggest that conservative (non—surgical) treatment is preferable, where as authors such as Alvarez (7) maintain that this has little proven benefit and that early surgery is the best method of treatment. Jonsson et al (14) suggest that the results from surgical decompression deteriorate with time, and that patients who had had symptoms for less than 4 years (and had insignificant low back pain) had the best outcomes.

A review published in 1997 concludes that: “This review of the literature shows that the least invasive surgical procedure can obtain the best results if the correct diagnosis is made and if the operation is carried out within the first years of the disease.” (15)

Another recent stud, by Javid and Hadar (16) suggests that “At 1 to 11 years the success rate was 70.8% for patients with stenosis. 66.6% for those with stenosis and herniated disc, and 63.6% for those with lateral recess stenosis.

In conclusion, long term improvement after laminectomy was maintained in two thirds of these patients”

Decompressive surgery must balance sufficient decompression with inducing spinal instability.

The principle causes of failure of surgery are inadequate decompression, recurrence of degenerative hypertrophy (overgrowth), and instability.

Arachnoiditis may also occur as a complication. (See below).

Other modes of treatment have included epidural steroid injections, but Fukusaki et al (17) in a recent paper, state that they are not effective in stenosis patients.

Other authors such as Cohen and Kostuik do not endorse their use, although some doctors (such as Rydevik) believe that they can be of use in the elderly population, for whom the risk of surgery is greater. (18)

One study in Japan (19) tried using intravenous lipoprostaglandin (Lipo—PGEI) to treat stenosis.

It produced symptomatic improvement for a limited period in the treatment of neurogenic claudication associated with stenosis.

The drug appeared to exert its effects through an increase in the circulation of blood in the nerve roots and the cauda equina.

 

Arachnoiditis and Stenosis

Stenosis is recognised as being one of the causative factors for arachnoiditis.

Jackson and Isherwood (20) from their MRI study, concluded that arachnoiditis features can be seen in stenosis without other risk factors, but state that the cause of this is unexplained.

Arachnoiditis over multiple levels is rare, except where there is multi—level stenosis.

Epstein et al (21) reported 5 cases of arachnoiditis due to stenosis alone.

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

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

 

Sarah Smith MB BS December 1998

 

 

References:

1. Katoh S, Ikata T, Hirai N, Okada Y Nakauchi k Paraplegia 1995 Jun; 33(6): 330-333

Influence of minor trauma to the neck on the neurological outcome in Patients with ossification of the posterior longitudinal ligament (OPLL) Of the cervical spine.

2. Pettersson K, Karrholm J, Toolanen G, Hildingsson C. Spine 1995 Aug 1; 20(15): 1664-7

Decreased width of the spinal canal in patients with chronic symptoms after whiplash injury.

3. Dagi TF, Tarkington MA, Leech JJ. J Neurosurg 1987 Jun; 66(60): 842-849

Tamden lumbar and cervical spinal stenosis. Natural history, prognostic indices, and results after surgical decompression.

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

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

6. Papp T, Porter RW, Craig CE, Aspden RM, Campbell DM. Spine 1997 Aug 15; 22(16): 1805-10

Significant antenatal factors in the development of lumbar spinal stenosis

7. Alvarez JA, Hardy RH Jr Am Fam Physician 1998 Apr 15; 57(8): 1825-34, 1839-40

Lumbar spine stenosis: A common cause of back and leg pain

8. Goldman SM, Funk JD, Christensen VM J Am Podiatr Med Assoc 1997 Mar; 87(3): 117-24

Spinal stenosis. A common cause of podiatric symptoms

9. Jonsson B, Annertz M, Sjoberg C, Stromqvist B Spine 1997 Dec 15; 22(24): 2932-7

A Prospective and consecutive study of surgically treated lumbar spinal stenosis. Part 1: Clinical features related to radiographic findings.

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

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

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

13. Muhle C, Metzner J, Brinkmann G, Kuhn B, Bischoff L, Huttzelmann A, Wesner F, Heller M. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1997 Nov; 167(5): 467-73

[Comparison of T2-weighted turbo spin-echo and ultrafast HASTE sequence in the diagnosis of cervical myelopathies and spinal stenoses and static and kinematic MRT of the spine]

14. Jonsson B, Annertz M, Sjoberg C, Stromqvist B Spine 1997 Dec 15; 22(24): 2938-2944

A prospective and conservative study of surgically treated lumbar spine stenosis. Part II: Five-year follow-up by an independent observer.

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

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

17. Fukusaki M, Kobayashi I, Hara T, Sumikawa K Clin J Pain 1998 Jun; 14(2): 148-51

Symptoms of spinal stenosis do not improve after epidural steroid Injection.

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

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

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

21. Epstein JA, Epstein BS, Lavine LS, Rosenthal AD, Carras R J Neurosurg 1978 Feb; 48(2): 252-258

Obliterative arachnoiditis complicating lumbar spinal stenosis.

22. Laitt R, Isherwood I, Jackson A Br J Radiol 1996 Aug: 69(824): 393-4 Patterns of chronic adhesive arachnoiditis following Myodil Myelography: The significance of spinal canal stenosis and previous surgery.

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