Lumbar spinal stenosis (LSS) is a common pain condition that causes lumbar back pain, radiating leg pain, and possible functional impairment. MILD is an emerging minimally invasive treatment for LSS. It is an image-guided percutaneous procedure designed to debulk hypertrophied ligamentum flavum. However, the exact short- and long-term efficacy, safety profile, indication criteria, and certain procedure details reported in medical literature vary.

This narrative review was to elucidate efficacy, safety profile, certain procedure details, advantages, and limitations of MILD.

This is a narrative review.

All included articles are clinic trials including analytic studies and descriptive studies.

PubMed, Cochrane Library, and Scopus were searched. Only clinical trials of MILD procedure were included. Information of indications, contraindications, VAS scores, ODI scores, effective rate, efficacy durations, and certain procedure details was focused on.

According to the literature, for the MILD procedure, the VAS score could be reduced from a pre-treatment level of 6.3-9.6 to a post-treatment level of 2.3-5.8. The ODI score could be reduced from a pre-treatment level of 38.8-55.3 to a post-treatment level of 27.4-39.8. The effective rate of the MILD procedure was reported to be 57.1%-88%. A 2-year postoperative stability of efficacy was also supported. One RCT study testified superior efficacy of MILD over epidural steroid injection.

There is few high-quality literature in the review. Moreover, the long-term efficacy of MILD cannot be revealed according to the current literature.

Based on the reviewed literature, MILD is an effective and safe procedure. MILD can reduce pain intensity and improve functional status significantly. Therefore, it is a preferable option for LSS patients who failed conservative treatments, but not for those who require immediate invasive decompression surgery.

Degenerative changes in posterior elements of the spine such as thickening or hypertrophy of the ligamentum flavum (LF) may result in spinal stenosis. In the present study, we aimed to investigate the potential factors including age, intervertebral disc degeneration (IDD), facet joint degeneration (FJD), end plate degeneration (EPD), which may affect LF thickening and to reveal the relationship among those factors at each level of lumbar spine by evaluating the magnetic resonance images (MRI).

A total of 200 individuals with low back and/or leg pain complaints who had undergone lumbar MRI were included in this study. The thickness of LF, FJD, IDD and EPD were assessed at all lumbar levels.

Totally 1000 end plates, 1000 intervertebral discs and 2000 facet joints were evaluated and the thicknesses of 2000 LFs were measured from MRI images of 200 patients (100 males and 100 females). The mean age was 46.87 ± 12.47 years. LF thickness was strongly associated with FJD especially on the ipsilateral side. Age and IDD were correlated at whole vertebral levels. The age related changes (LF thickness, FJD, IDD and EPD) were more prominent at L4-L5 vertebral level. However, gender had no effect on LF thickness.

The results of this study suggest that LF thickening may occur independently or could be associated with FJD especially on the ipsilateral side and this relationship is due to the vertebral level. The degree of disc degeneration increases with age and age related changes may be predominantly observed at L4-L5 vertebral level.

The purpose of this study was to evaluate magnetic resonance (MR)-detected redundant nerve roots (RNRs) of the cauda equina in patients with lumbar spinal canal stenosis.

A total of 500 lumbar MR studies in patients with lumbar spinal canal stenosis were reviewed for the presence and characteristics of RNRs of the cauda equina. The length of the RNRs relative to the height of the upper vertebral body of the level of the stenosis was used as a prognostic indicator.

RNRs were detected in 15% of the patients, the majority above the level of the stenosis (85%) and loop shaped (72%). Advanced age (i.e., ≥56 years old, odds ratio=1), a lumbar spinal canal stenosis at L2-4 (odds ratio=2.5), and the presence of an intracanal protuberance with sharp margin in the site of the stenosis (odds ratio=7.2) were independent risk factors for the development of RNRs. A direct, significant correlation was found between the relative length of the RNRs and patients' age (Pearson r=0.36, p=0.001). The mean relative length of the RNRs was significantly higher in patients with RNRs located above the level of the stenosis than those with RNRs located below the site of the block. The degree of stenosis was associated with neither the presence nor the relative length of the RNRs.

With an occurrence rate of 15%, RNRs of the cauda equina are not uncommon in cases with lumbar spinal canal stenosis. Advanced age, a canal stenosis at L2-4, and the presence of a sharp intracanal protuberance in the site of the stenosis are the related risk factors. Patients' age and the location of RNRs may be of prognostic value.

Spinal nerve roots have a peculiar structure, different from the arrangements in the peripheral nerve. The nerve roots are devoid of lymphatic vessels but are immersed in the cerebrospinal fluid (CSF) within the subarachnoid space. The blood supply of nerve roots depends on the blood flow from both peripheral direction (ascending) and the spinal cord direction (descending). There is no hypovascular region in the nerve root, although there exists a so-called water-shed of the bloodstream in the radicular artery itself. Increased mechanical compression promotes the disturbance of CSF flow, circulatory disturbance starting from the venous congestion and intraradicular edema formation resulting from the breakdown of the blood-nerve barrier. Although this edema may diffuse into CSF when the subarachnoid space is preserved, the endoneurial fluid pressure may increase when the area is closed by increased compression. On the other hand, the nerve root tissue has already degenerated under the compression and the numerous macrophages releasing various chemical mediators, aggravating radicular symptoms that appear in the area of Wallerian degeneration. Prostaglandin E1 (PGE1) is a potent vasodilator as well as an inhibitor of platelet aggregation and has therefore attracted interest as a therapeutic drug for lumbar canal stenosis. However, investigations in the clinical setting have shown that PGE1 is effective in some patients but not in others, although the reason for this is unclear.

Thickening of the LF is ascribed to buckling due to DSN. Uncertainty exists as to whether this can occur without DSN. Our primary hypothesis was that facet degenerative changes alone, independent of DSN, can thicken the LF. Our secondary hypothesis was that inflammatory changes surrounding degenerative facet joints may incite thickening.

Fifty-two patients were divided into 1 of 3 groups: group 1 (normal lumbar spine, n = 21), group 2 (LF thickening and FH with normal height of the L4-5 disk, n = 18), and group 3 (LF thickening and FH with decreased height of the L4-5 disk, n = 13). LF thickness measured on axial T1WI at the midpoint of the LF length was compared with that in group 1. Facet joints were evaluated for spurring, joint fluid, and cortical irregularity, indicating facet degeneration. Enhancement of the facet joints and LF thickening were also evaluated (n = 2). The Student t test was used to compare groups.

Normal LF thickness (group 1) was 3.1 mm, whereas LF thickness averaged 4.9 mm in group 2 and 5.3 mm in group 3 (both P < .001). Patients with asymmetric LF thickness showed greater LF thickness on the side with greater FH. There was more LF enhancement on the side with greater facet degenerative disease.

LF thickening can be secondary to facet degenerative changes, independent of DSN. Inflammatory changes may be an inciting factor for LF thickening.

As the ligamentum flavum (LF) covers most of the posterolateral part of the lumbar spinal canal, its thickening can be attributed to the development of lumbar canal encroachment. Nevertheless, there have been few reports describing the natural history of the LF.

To investigate the natural history and to subsequently clarify the pathogenesis of LF thickening, we conducted a transverse radiological study of the LF at the lumbar spine using magnetic resonance images.

One hundred and sixty-two patients complaining of low back pain and/or leg pain were evaluated (n = 162; mean age 52.1 years). The thickness of LF was measured at L2-3, L3-4, L4-5 and L5-S levels (n = 648). The relationships among thickness, age, and spinal level were examined.

One hundred and sixty-two patients complaining of low back pain and/or leg pain were evaluated (n = 162; mean age 52.1 years). The thickness of LF was measured at L2-3, L3-4, L4-5 and L5-S levels (n = 648). The relationships among thickness, age, and spinal level were examined.

The following results were obtained. (1) LF thickness increased with age; however, the increments at L4-5 and L3-4 were larger than one at L2-3 and L5-S1. (2) At L4-5, LF was over 3.0 mm thick in patients in the 20-29 age bracket, and in many of them it was more than 3.5 mm thick. (3) All patients with a thickened LF at L2-3 (>3.0 mm) had very thick LFs at all spinal levels. (4) In elderly patients, there was no correlation between the thickness of LF and the decrease of the disc height. In this study, we concluded that thickening of LF at L4-5 had already started in patients in the 30-39 age bracket and that thickening of the LF was not the buckling of the LF into the spinal canal with disc degeneration. The thickness of LF at L2-3 may serve as an indicator of lumbar spinal canal stenosis at multiple levels.

The development of radiculopathy in patients with lumbar canal stenosis is thought to be closely related to intraradicular edema resulting from compression. However, there is little agreement as to question which is more essential for intermittent claudication: ischemia or congestion. The aim of the present experimental investigation was to examine the effect of ischemia and congestion on the nerve root using dogs. The aorta was clamped as an ischemia model of the nerve root and the inferior vena cava was clamped as a congestion model at the sixth costal level for 30 min using forceps transpleurally. Measurements of blood flow, partial oxygen pressure, and conduction velocity in the nerve root were repeated over a period of 1 h after release of clamping. Finally, we examined the status of intraradicular blood-nerve barrier under fluorescence and transmission electron microscope. Immediately after clamping of the inferior vena cava, the central venous pressure increased by about four times and marked extravasation of protein tracers was induced in the lumbar nerve root. Blood flow, partial oxygen pressure, and conduction velocity of the nerve root were more severely affected by aorta clamp, but this ischemia model did not show any intraradicular edema. The blood-nerve barrier in the nerve root was more easily broken by venous congestion than by arterial ishemia. In conclusion, venous congestion may be an essential factor precipitating circulatory disturbance in compressed nerve roots and inducing neurogenic intermittent claudication.

The aim of this study was to evaluate the significance of redundant nerve roots (RNR) in lumbar stenosis by comparative analysis of a group of patients with RNR with a group without RNR.

A total of 68 patients who underwent decompressive laminotomies for single-level lumbar stenosis were divided into two groups. Group I included patients with RNR, and group II included patients with no RNR (NRNR). RNR were defined as a tortuosity of elongated and coiled nerve roots in the subarachnoid space associated with spinal stenosis demonstrable by sagittal images of MRI. Comparative analysis was performed.

RNR was found in 33.8% of patients with stenosis. Patients in the RNR groups were older than those in the NRNR group. There were no statistically significant differences between the two groups with regard to the duration of symptoms, preoperative and final Japanese Orthopaedic Association's (JOA) scores, diameter of the spinal canal, recovery rate, and success rate of the surgery. However, the final JOA scores, recovery rate, and success rate showed a tendency to be better in the NRNR group. In the RNR group, the longer the relative length of RNR, the better the outcome.

RNR is a relatively common finding in association with spinal stenosis. It tends to develop in patients of more advanced age than patients with no RNR. Surgical outcomes in the RNR group were not statistically different from those in the NRNR group, although NRNR group showed slightly better outcomes.

Previous reports of redundant nerve roots (RNRs) of the cauda equina have been limited to evaluations based on myelography. Neither the imaging nor the clinical features of RNRs in relation to magnetic resonance (MR) imaging have been elaborated. The MR imaging characteristics of RNRs were evaluated using the Japanese Orthopaedic Association score before and after the surgery.

There were 44 patients with L4-5 spondylolisthesis in which a complete blockage was demonstrated on myelography. All patients underwent posterior L4-5 interbody fusion. Based the myelographic and MR imaging findings, the patients were stratified into the following three groups: RNRs recognized on both myelographic and MR imaging (Group A); RNRs recognized on myelography but not very evident on MR imaging (Group B); and RNRs not recognized on either myelographic or MR imaging (Group C). Among these three groups, pre- and postoperative clinical symptoms were compared.

There were 16 patients in Group A, 14 in Group B, and 14 in Group C. In terms of preoperative clinical symptoms, there was a significant difference between Groups A and C in the incidence of leg pain and tingling sensation. Significant differences were also noted between Groups A and C and between Groups B and C in ambulatory ability. Evaluation of postoperative clinical symptoms showed a significant difference between Groups A and C in ambulatory ability.

Patients with MR imaging evidence of RNRs presented with more severe clinical symptoms. It is believed that the RNR features derived from MR images represent important findings.

Computed tomography aided evaluation of spinal decompression by ultrasound-guided spinal fracture repositioning, ligamentotaxis, and remodeling after thoracolumbar burst fractures.

To determine the necessity of spinal canal widening by ultrasound-guided fracture repositioning for fractures with and without neurologic deficit.

Ultrasound-guided spinal fracture repositioning is an alternative new approach. Reports have varied concerning ligamentotaxis and remodeling.

Computed tomography aided planimetry of the spinal canal (64 consecutive burst fractures) and neurologic evaluation by Frankel grades.

Ultrasound-guided spinal fracture repositioning (n = 37) reduced the stenosis of the spinal canal area from 45% before surgery to 20% after surgery of the estimated original area. Fifteen patients had a primary neurologic deficit, which improved markedly in 11 cases after treatment. Patients with neurologic symptoms had a greater preoperative spinal stenosis than those without. No correlation was seen between the degree of pretreatment spinal stenosis, fracture type, and severity of the neurologic deficit. Ligamentotaxis (n = 27) reduced the stenosis from 30% before surgery to 18% after surgery and remodeling (n = 11) from 25% after surgery to 13% after metal removal.

Ultrasound-guided fracture repositioning is an efficient method for spinal canal decompression of burst fractures with neurologic symptoms. The marked degree of widening of the spinal canal due to the effects of ligamentotaxis and remodeling may render the reposition of retropulsed fragments unnecessary in cases of fractures without a neurologic deficit.

A pathologic study of the ligamentum flavum in degenerative lumbar disease.

To elucidate the clinical significance of each pathologic finding of the ligamentum flavum.

In many reports, researchers observed the ligamentum flavum removed partially during surgery and did not evaluate the whole image of the ligamentum flavum. In addition, there are only a few reports that examined the possible association between various histologic findings and clinical findings. And, thus, there are many unclear points in the clinical significance indicated by each pathologic finding.

The study participants were 50 patients with degenerative lumbar diseases who underwent surgical decompression with removal of the ligamentum flavum of the affected spinal level. Tissue specimens of the removed ligamentum flavum in cross section were prepared, and changes in the elastic fibers and collagen fibers were evaluated in three grades to evaluate the whole image. In addition, we observed the presence or absence of any focal lesions and statistically analyzed the possible association between these histologic findings and clinical symptoms or image findings.

In regard to the association between histologic findings and clinical symptoms or image findings, calcification was observed in significantly older patients, who tended to have low scores in preoperative JOA score, and was frequently observed in patients with cauda equina symptoms. Patients with ossification had a significantly greater % slip, and chondroid cells were frequently observed in patients with spondylolisthesis.

Various pathologic findings provided important foundations for discussing the pathogenesis of lesions in ligamentum flavum. Calcification was frequently observed in elderly patients and those with cauda equina symptoms, and these patients tended to have severer preoperative symptoms. Chondroid cells were frequently observed in patients with spondylolisthesis, and patients with ossification had a greater % slip, suggesting involvement of mechanical load in ossification of ligaments. The pathologic findings were significantly related to the clinical features, and these findings will be profitable for understanding the pathogenesis of degenerative lumbar disease.

There is evidence to suggest that cauda equina intermittent claudication is caused by local circulatory disturbances in the cauda equina as well as compression of the cauda equina. We evaluated the role of magnetic resonance phlebography (MRP) in identifying circulatory disturbances of the vertebral venous system in patients with lumbar spinal canal stenosis. Extensive filling defects of the anterior internal vertebral venous plexus were evident in patients with lumbar spinal canal stenosis ( n = 53), whereas only milder abnormalities were noted in patients with other lumbar diseases ( n = 16) and none in normal subjects ( n = 13). The extent of the defect on MRP correlated with the time at which intermittent claudication appeared. In patients with lumbar spinal canal stenosis, extensive defects of the internal vertebral venous plexus on MRP were noted in the neutral spine position, but the defect diminished with anterior flexion of the spine. This phenomenon correlated closely with the time at which intermittent claudication appeared. Our results highlight the importance of MRP for assessing the underlying mechanism of cauda equina intermittent claudication in patients with lumbar spinal canal stenosis and suggest that congestive venous ischemia is involved in the development of intermittent claudication in these patients.

The history and physical examination are an essential component in the assessment of patients with lumbar spinal stenosis. The differential diagnosis is broad, and many conditions may be ruled out with a thorough office evaluation. Peripheral neuropathy, arteriovascular disease, and hip arthrosis are common entities with similar symptoms. Imaging studies provide poor specificity. Clinical decision making should be based on a collection of data, including the history and physical findings, functional status, imaging and electrodiagnostic studies, and other adjunctive studies.

This article reviews the history, classification, and pathoanatomy of lumbar spinal stenosis. An understanding of the pathoanatomy of lumbar spinal stenosis is essential for the clinician to treat the patient with clinically symptomatic lumbar spinal stenosis more effectively.

The entire concept of spinal stenosis is based on the assumption that there is a minimal space necessary for the function of the neural content of the spinal canal, and this space, under certain circumstances, gets too small. This may seem self evident, but it was not until the middle of the previous century that there was sufficient focus on this concept to establish the diagnosis of lumbar spine stenosis.

Degenerative central lumbar stenosis has traditionally been considered to be a result of bony narrowing of the spinal canal. In two consecutive patients with degenerative central lumbar stenosis and complete myelographic blocks, the cauda equina was compressed by a thickened ligamentum flavum (cross-sectional area [CSA], > 150 mm2). This ligamentous stenosis occurred within bony canals of normal dimensions (anteroposterior diameter, interpediculate distance, interfacet distance, and CSA). High-resolution computed tomographic myelography was used to calculate quantitative values for the CSA, the length, and the volume of the lumbar ligamentum flavum. Excision of the thickened ligamentum flavum restored the dural sac to normal (CSA, 130-230 mm2), and both patients received relief from their symptoms. Unilateral laminotomy was used successfully to achieve bilateral ligamentectomy. Therefore, in a well-defined subgroup of patients with degenerative central lumbar stenosis, the dural sac can be decompressed by selective resection of the ligamentum flavum, and bilateral ligamentectomy can be performed via unilateral laminotomy.

This paper deals with the effect of motion upon the stenotic lumbar spinal canal and its contents. A review is presented of personal investigations and relevant data from the literature. The normal spinal canal and its lateral recesses are naturally narrowed by retroflexion and/or axial loading, as shown by anatomical, myelographic and computerized tomographic studies. Due to enough free play and protection by safety cushions, cauda equina and exiting nerve roots are not endangered. In stenosis this protection is lost, causing clinical symptoms of nervous compression of a posture-dependent character. Stenosis of the central portion of the spinal canal and of the lateral recess are dealt with separately. The more stenotic narrowing progresses, the greater the narrowing effect of retroflexion will become. This 'rule of progressive narrowing' explains why in severe stenosis even small motions will have a marked functional effect. The author contests the view of some investigators that vertebral 'instability' is essential to explain posture-dependent nerve root compression. Relative narrowing of the spinal canal is shown to predispose to manifestation of lumbosacral nerve root compression by other causes, for example disc herniation. Relative roominess of the canal is thought to explain why abnormal myelograms, suggestive of stenosis or disc herniation, occur in a relatively large percentage of asymptomatic individuals.

Human cadaver spine specimens, consisting of the third and fourth lumbar vertebral laminae and the intervening ligamentum flavum, were studied. The specimens were loaded in axial traction with 1, 2, 4, and 8 kg respectively. To avoid contact deformation the thinning of the yellow ligament was recorded through an opto-electronic laser system. An average elongation of 6 mm was found at 8 kg of traction with a corresponding average thinning of 2 mm. The results indicated that the thickness changes of the ligamentum flavum might affect the dimensions of the lumbar spinal canal during, for example, normal changes in body posture.

The variation in the dimensions of the lumbar spinal canal under both flexion-extension and axial compression-distraction was studied using computerized tomography (CT) scans in human cadaver lumbar spine specimens. In 3-mm-thick CT slices through the disk at L3-L4, the cross-sectional area of the spinal canal was reduced by around 40 mm2, corresponding to a 16% reduction of the initial area when the lumbar spines were moved both from flexion to extension and from distraction to compression. A corresponding reduction in the midsagittal diameter of the canal of 2 mm was found. During these motions, the ligamentum flavum did not appear to be a significant factor for the dynamic changes affecting the dimensions of the canal. This held true even after the disk had been excised in order to produce a total collapse of the disk space.

Two patients with rheumatoid arthritis affecting the lumbar spine showed the clinical, roentgenological, and operative characteristics of lumbar spinal stenosis, which is a neurological complication of rheumatoid arthritis that can be treated by surgery. The clinical history is a prerequisite for suspicion of the syndrome, and lumbar myelography including roentgenograms of the extended lumbar spine may verify the diagnosis.

The authors describe a simple clinical adjunct to the routine neurological examination of patients with intermittent cauda equina compression syndrome. The "bicycle test" helps exclude intermittent claudication due to vascular insufficiency and frequently confirms the relationship of posture to radicular pain.

The cases of four patients with intermittent claudication due to compression of the cauda equina are reported. The cause of this syndrome is considered to be a compression of the cauda equina by a thickening of the ligamentum flavum. The clinical, neuro-radiological and surgical characteristics are discussed.

Authors experience based on 15 cases of iatrogenic stenosis of spinal canal in thoracic and lumbar region. The stenosis was the sequelae of spondylodesis made for spinal tuberculosis, spondylolisthesis traumatic and idiopathic, spinal fractures and assimilation faults. The onset of signs of stenosis appeared from 1 to 7 years after the first operation. The treatment was operative in 8 cases, conservative in 7. The first gave the best results. Observation time was up to 14 years after the second operation.

Intermittent claudication is known as a specific symptom in patients with chronic occlusive arterial lesions. Clinically it is important that neurogenic intermittent pseudo-claudication should be differentiated from true intermittent claudication. Nevertheless confusion still exists in differential diagnosis between these two entities. This paper deals with general review of intermittent pseudo-claudication and a particular emphasis is placed on the different concepts of the pathophysiology and the differential diagnosis from the standpoint of vascular surgery. Recently one case of the neurogenic intermittent pseudo-claudication was encountered and presented in this paper.

Hypertrophy of the ligamentum flavum has been reported to occur in the prolapsed intervertebral disc syndrome. The ligaments from 28 patients were compared with a necropsy control group (18). Only minor histological anomalies were noted in two patients and the ligament was not thickened in cases of disc prolapse. In addition, there was no evidence to suggest previous trauma to the ligaments associated with disc protrusion or that the elastic fibres in the ligament degenerate with age, although some degeneration of the collagen fibres had apparently occurred in the two oldest control cases.