Degenerative lumbar spinal stenosis refers to the narrowing of the spinal canal due to degenerative changes in spinal joints, intervertebral discs, and ligamentum flavum [1]. As the space surrounding the neurovascular tissue becomes narrower, major clinical symptoms may appear, such as neurogenic claudication, radiating pain in the lower extremities, low back pain, and urination– defecation impairment. Clinical symptoms may include decreasing sensation and fatigue in the lower extremities, as well as increasing pain in both buttocks or lower limbs, which may worsen when walking or standing for a long time (neurogenic intermittent claudication) [2]. Patients may experience alleviation of symptoms when they sit or bend forward [3], and if the pain caused by a walking or standing posture becomes severe, it may become difficult to perform daily and independent activities or the risk of fall may increase [3-5].

Degenerative lumbar spinal stenosis is a progressive disease that involves all the movement segments of the spine [6]. The relative instability initiated by degeneration of the intervertebral disc leads to hypermobility of the vertebral segments, resulting in increased pressure on the posterior facet joints, followed by a narrowing of the intervertebral disc space, an increased extension angle, and hypertrophy of the facet joints, especially the hypertrophy of the superior articular process. As it gradually progresses, the joints become ankylosed. The hypertrophic articular process causes localized joint stiffness (ankylosis). In addition, calcification or thickening of the yellow ligament is an important mechanism in stenosis. Joint tropism can also be a factor leading to degenerative lumbar spinal stenosis [7]. Consequently, this causes the stenosis of the spinal canal and compression of nerve structures, which may lead to intermittent neurogenic claudication due to congestion of the epidural venous blood and increased vascular pressure. Although minor trauma or repetitive stimulation associated with work does not significantly contribute to the occurrence of such stenosis, it can worsen the symptoms of existing stenosis. No symptoms can be felt when resting; however, symptoms appear due to the following reason when walking or standing. As the lumbar is extended, the spinal canal becomes narrower and the neural tissue is compressed, and simultaneously, the metabolic rate of nerve roots by the lower extremity movement increases, but the increase in blood flow cannot catch up with it. The cauda equina nerve roots gain metabolic energy from the blood circulation of the arteries located on the surface of nerve roots and the diffusion of cerebrospinal fluid. In lumbar spinal stenosis, when the nerve roots are under increased pressure in the spinal canal, neural ischemia and defective nerve conduction can occur. Symptoms can also occur due to venous congestion and may contribute to the etiology of lumbar spinal stenosis involving two or more segments. If the nerve roots are damaged, central sensitization of pain perception can occur, which can result in chronic pain.

Lumbar spinal stenosis is classified according to the anatomical location in which the spine is affected or to the etiology (Table 1). In degenerative lumbar spinal stenosis, the redundancy and loosening of yellow ligaments due to the narrowing of the disk space result in the narrowing of space in the spinal canal, which may be accompanied by instability. This relative hypermobility causes overgrowth and thickening of the posterior facet joints and surrounding ligaments. The yellow ligaments can thicken, especially in the area where they are attached to the spinal articular capsule around the lateral recess, which may compress the nerve roots (Fig. 1). These processes occur individually or simultaneously, resulting in symptoms of lumbar spinal stenosis.

Central stenosis refers to the narrowing of the space between both the posterior facet joints, primarily the space occupied by the dura sac and internal neural structures. The stenosis of this region is caused by the intervertebral disc extrusion, bulging of the annulus fibrosis, osteophyte formation, and folded or thickened yellow ligaments. Symptomatic central stenosis results in neurogenic claudication with pain in the lower extremities. The lateral side of the dural sac is known as the lateral canal, through which nerve roots pass, and when the nerve roots are compressed, there might be radiating pain.

The lateral recess is known as the “entrance zone,” which begins at the medial border of the superior articular process and extends to the medial border of the pedicle [6]. In this region, the nerve roots that have emerged from the dura sac pass through the distal and lateral parts. The boundaries of the lateral recess comprise a vertebral pedicle on the lateral side, a superior articular process of the posterior joint on the dorsal side, an intervertebral disc and posterior ligaments on the anterior side, and a spinal canal on the medial side. The primary causes of stenosis in the entrance zone are a posteriorly herniated intervertebral disc and hypertrophic osteoarthritis of the posterior joints, wherein the nerve roots are compressed by the thickened superior articular process.

The mid-zone refers to the foraminal region located in front of the pars [8]. The anatomical structure corresponds to the ventral part of the pars. Regarding the boundary structures, they medially border on the lateral recess, anteriorly on the vertebral body and intervertebral disc, posteriorly on the pars and intertransverse ligaments, and laterally on the surface of the pedicle. Stenosis occurs in this region following the thickening of the fibrocartilage tissue at defective pars or by compression due to osteophytes. The thickening of the yellow ligament sometimes causes stenosis up to the neural foramen, and the formation of osteophytes under the pars defect is also related to stenosis occurring in this region (Fig. 2). In spondylolisthesis and degenerative scoliosis, one vertebral pedicle is relatively lowered due to the rotational malalignment of the vertebral body or asymmetrical narrowing of the intervertebral disc. This can also cause neural compression at this level.

The exit zone is shaped as an inverted teardrop created by the intervertebral foramen, and the neural foramen is the space between the lower part of the upper pedicle and the upper part of the pedicle of the lower vertebrae, which borders posteriorly on the pars, inferior articular process of the upper vertebrae, and the superior articular process of the lower spine and anteriorly on the posterior surface of the vertebral body and the intervertebral disc [6]. The dorsal root ganglions and ventral motor roots occupy approximately 30% of this space. This is the region that changes into the epineurium, which wraps the nerve roots in the dura. Nerve roots are located in this region and can be compressed by the protrusion of the far lateral disk, subluxation related to spondylolisthesis, or arthritis [9]. The most common cause is degenerative spinal arthritis.

Degenerative lumbar spinal stenosis primarily proceeds due to the degenerative process of the vertebral joint and yellow ligament [10], and imaging studies can reveal progressed spondyloarthrosis. These abnormal findings can be found primarily on both sides, and the most common regions are between L4 and L5, followed by between L5 and sacrum and between L3 and L4 [11]. In addition, disk herniation and spondylolisthesis can exacerbate acutely such stenosis-related clinical symptom. Spondylolisthesis and degenerative spondyloarthropathy rarely cause stenosis in young patients, but when these degenerative changes occur with aging, spondylolisthesis, and spondyloarthropathy in patients aged >50 years, they can result in lateral recess or foraminal stenosis.

Lumbar spinal stenosis is often asymptomatic. Studies have reported no close association between clinical symptoms and anteroposterior diameter of the spinal canal. The natural course of lumbar spinal stenosis in the majority of cases includes gradual development of symptoms; however, in some cases, it becomes acute following some trauma or severe physical activity. In several patients, even when imaging tests lead to the diagnosis of stenosis, symptoms and physical examination may only reveal negligent abnormalities. Several studies have reported that patients who received surgical treatment, such as decompression, exhibit better progress than those who received nonsurgical treatment; however, 50% of the patients who received nonsurgical treatment and were followed up for 8–10 years showed improvements in back pain and leg pain. In a prospective randomized study involving 100 patients with symptoms of stenosis who were provided surgical or nonsurgical treatment, it was observed that symptoms improved after approximately 3 months irrespective of the type of treatment, and some patients showed symptom improvement after 12 months. In the nonsurgical treatment group, symptoms worsened over time, but after 4 years, approximately 50% of the patients displayed excellent or fair progress. In contrast, 80% of the patients who received surgical treatment exhibited good results at the 4-year follow-up [12]. In another study, the majority of patients diagnosed with lumbar spinal stenosis exhibited stable disease progression, and 15%–50% of those who received nonsurgical treatment showed good results. Worsening of symptoms even with appropriate conservative treatment may be an indication for surgical treatment. According to Weinstein et al. [12], the surgical treatment group showed improvement in all primary outcomes compared with the nonsurgical treatment group.

The overall prevalence of lumbar spinal stenosis varies among studies. The prevalence in the group based on clinical diagnostic criteria has been reported to be approximately 11% in the general population [13-15]. According to the diagnosis based on imaging studies, the prevalence was found to be 11% in the asymptomatic general population and 38% in the general population. Prevalence increases with age, and the diagnosis based on imaging tests such as magnetic resonance imaging (MRI) and computed tomography (CT) scan is known to be made a decade earlier than the diagnosis based on clinical symptoms. In some studies in which the International Classification of Diseases codes were used, the prevalence was reported as 7%–23%. Some expert opinions reported a prevalence of 4%–53%. Considering the progression of this degenerative disease, the prevalence of degenerative lumbar spinal stenosis can be significantly influenced by age. For instance, one study reported a prevalence of approximately 78% in the target patients with an average age of 67 years (age range, 40–93 years), whereas the prevalence was only approximately 12% in patients with an average age of 40 years [8]. Some prevalence studies used only central stenosis as the diagnostic criterion. In other studies, both foraminal and lateral access stenosis were included. Moreover, a bias may be introduced due to the average age of the target patient group. Therefore, it is important to consider these aspects when interpreting the results of the abovementioned previous studies [3,9,10,16,17]. Previously, lumbar spinal stenosis has been reported to be more common in men; however, recent reports have mentioned that it is 3–5 times more common in women [11,18].

Till date, there exists some ambiguity in the clinical diagnostic criteria for degenerative lumbar spinal stenosis. According to a study conducted in 2016, the consensus of experts on clinical symptoms included (1) pain in the lower extremities or buttocks while walking, (2) symptom relief resulting from bending the lower back forward, (3) symptom relief from bending the back forward while using a shopping cart or riding a bicycle, (4) motor or sensory disturbance while walking, (5) normal and symmetrical pulse of the dorsalis pedis artery, (6) weakening of lower extremity, and (7) lower back pain [13,14]. In other studies, detailed history, gait, and some physical examination findings were also included in the classification criteria [13,15,19].

Patients with lumbar spinal stenosis generally test negative in the straight leg raising test, and findings of motor neurological disorders are rare. Sudden appearance or exacerbation of sciatic neuralgia suggests the possibility of occurrence of intervertebral disc herniation in addition to existing spinal stenosis. Radiating pain occurs often in the lateral access and foraminal stenosis, and L5 neurological symptoms are the most common [20]. In neurological examination, motor deficit can be primarily observed due to the compression of L5 nerve roots in severe stenosis or degenerative spondylolisthesis. In the event of paresthesia, peripheral neuropathy caused by diabetes, alcoholism, or drug use should be suspected. For detecting the interruption in blood circulation, the dorsalis pedis and popliteal arteries should be palpated, and the edema and varicose veins in lower extremities should be excluded [21]. Moreover, it must be differentiated from the symptoms of lesions in the lower limbs, such as hip joints and knees [22].

Nonsurgical treatment is appropriate for patients with mild to moderate symptoms. Commonly used treatment strategies include bed rest for a short period of approximately 1 week, medication (anti-inflammatory drugs, oral adrenal corticosteroids, muscle relaxants, prostaglandin E1 analogs, antidepressants, and anticonvulsants such as gabapentin), lumbar exercise (isometric flexion exercise and hyperextension exercise), physical therapy, orthosis usage, thermal therapy, ultrasound, massage, electrical stimulation, and traction therapy [21,32].

Patients with lumbar spinal stenosis may exhibit symptoms such as back pain, radiating pain, and neurogenic claudication. Although long-term outcome of treatments manifests similar results for both nonsurgical and surgical treatments, positive effects such as short-term improvement in symptoms and decreased fall risk may be expected with surgery. Surgical treatment is basically decompression, and a combination of treatments can be added, depending on the degree of decompression and the accompanying instability. Recently, minimally invasive surgery has been reported to be excellent in the treatment of lumbar spinal stenosis. Therefore, better treatment effects can be expected with an approach aimed at understanding the overall pathophysiology and treatment methods of lumbar spinal stenosis.