Slip disc Relief
Low back pain (LBP) affects approximately 60–85% of adults during some point in their lives. Fortunately, for the large majority of individuals, symptoms are mild and transient, with 90% subsiding within 6 weeks. Chronic low back pain, defined as pain symptoms persisting beyond 3 months, affects an estimated 15–45% of the population. For the minority with intractable symptoms, the impact on quality of life and economic implications are considerable. Despite the high prevalence of low back pain within the general population, the diagnostic approach and therapeutic options are diverse and often inconsistent, resulting in rising costs and variability in management throughout the country. In part, this is due to the difficulty establishing a clear etiology for most patients, with known nociceptive pain generators identified throughout the axial spine. Back pain has been termed as “an illness in search of a disease.” Indeed, once “red flag” diagnoses such as cancer and fracture have been ruled out, the differential sources of low back pain remain broad, including the extensive realm of degenerative changes within the axial spine for which radiological evaluation is nonspecific and causal relationships are tentative. We will elaborate on these degenerative processes and their clinical implications. We will further discuss diagnostic approaches and the efficacy of existing treatment options.
Introduction
Low back pain (LBP) affects approximately 60–85% of adults during some point in their lives . Fortunately, for the large majority of individuals, symptoms are mild and transient, with 90% subsiding within 6 weeks . Chronic low back pain, defined as pain symptoms persisting beyond 3 months, affects an estimated 15–45% of the population . For the minority with intractable symptoms, the impact on quality of life and economic implications are considerable.
Despite the high prevalence of low back pain within the general population, the diagnostic approach and therapeutic options are diverse and often inconsistent, resulting in rising costs and variability in management throughout the country . In part, this is due to the difficulty establishing a clear etiology for most patients, with known nociceptive pain generators identified throughout the axial spine . Back pain has been termed as “an illness in search of a disease”. Indeed, once “red flag” diagnoses such as cancer and fracture have been ruled out, the differential sources of low back pain remain broad, including the extensive realm of degenerative changes within the axial spine for which radiological evaluation is nonspecific and causal relationships are tentative .
We will elaborate on these degenerative processes and their clinical implications. We will further discuss the diagnostic approaches and the efficacy of existing treatment options.
The terms lumbar osteoarthritis, disk degeneration, degenerative disk disease, and spondylosis are used in the literature to describe anatomical changes to the vertebral bodies and intervertebral disk spaces that may be associated with clinical pain syndromes.
Spinal osteoarthritis (OA) is a degenerative process defined radiologically by joint space narrowing, osteophytosis, subchondral sclerosis, and cyst formation . Osteophytes included within this definition fall into one of the two primary clinical categorie. The first, spondylosis deformans describes bony outgrowths arising primarily along the anterior and lateral perimeters of the vertebral end-plate apophyses. These hypertrophic changes are believed to develop at sites of stress to the annular ligament and most commonly occur at thoracic T9–10 and lumbar L3 levels . These osteophytes have minimal effect on intervertebral disk height and are frequently asymptomatic, with only rare complications arising from their close anatomic relationship to organs anterior to the spine .
By contrast, intervertebral osteochondrosis describes the formation of more pathological end-plate osteophytes, associated with disk space narrowing, vacuum phenomenon, and vertebral body reactive changes . If protruding within the spinal canal or intervertebral foramina, these bony growths may compress nerves with resulting radiculopathy or spinal stenosis. Moreover, these bony projections may limit joint mobility and invade other organs or tissues . The term “osteoarthritis” suggests pathology limited to bone. Nevertheless, in this context, it has clear implications for the health of neighboring disks and nerve roots.
Comparatively, degenerative disk disease (DDD) refers to back pain symptoms attributable to intervertebral disk degeneration. Such pathologic changes include disk desiccation, fibrosis, and narrowing. The anulus may bulge, fissure, or undergo mucinous degeneration. Also included within the anatomic definition of DDD are defects and sclerosis of the end-plates, and osteophytes at the vertebral apophyses . With these bony changes included in the radiographic description of both OA and DDD, there exists diagnostic overlap between the conditions. As a result, these terms are often used interchangeably in the medical literature to describe similar phenomena.
Spondylosis
Spondylosis is a term referring to degenerative osteoarthritis of the joints between the centre of the spinal vertebrae and/or neural foraminae. If this condition occurs in the zygapophysial joints, it can be considered facet syndrome. If severe, it may cause pressure on nerve roots with subsequent sensory and/or motor disturbances, such as pain, paresthesia, or muscle weakness in the limbs.
When the space between two adjacent vertebrae narrows, compression of a nerve root emerging from the spinal cord may result in radiculopathy (sensory and motor disturbances, such as severe pain in the neck, shoulder, arm, back, and/or leg, accompanied by muscle weakness). Less commonly, direct pressure on the spinal cord (typically in the cervical spine) may result in myelopathy, characterized by global weakness, gait dysfunction, loss of balance, and loss of bowel and/or bladder control. The patient may experience a phenomenon of shocks (paresthesia) in hands and legs because of nerve compression and lack of blood flow. If vertebrae of the neck are involved it is labelled cervical spondylosis. Lower back spondylosis is labeled lumbar spondylosis.
Causes
•Repetitive strain injury (RSI) caused due to lifestyle without ergonomic care, e.g., while working in front of computers, driving, traveling, intense work in farm, etc.
•Age related degeneration
•Rugby
diagnosis
•Spurling's test
•Pain while coughing with neck in hyperextended position
Treatment
Treatment is usually conservative in nature. Patient education on lifestyle modifications and HOMOEOPATHIC MEDICATIONS, Physical Therapy ACCUPRESSURE MASSAGE BED TREATMENT,)have been shown to manage such conditions..
It is often argued, however, that the cause of spondylosis is simply old age, and that posture modification treatment is often practiced by those who have a financial interest (such as Worker's Compensation) in proving that it is caused by work conditions and poor physical habits. Understanding anatomy is the key to conservative management of spondylosis.
Surgery
Many surgical procedures have been developed to alleviate the signs and symptoms associated with spondylosis. The vertebral column can be approached by the surgeon from the front, side, or rear. Osteophytes and sometimes portions of an intervertebral disc are commonly removed in an effort to relieve pressure on adjacent nerve roots and/or the spinal cord.
Complications
A major problem related to this disease is vertebrobasilar insufficiency. This is a result of the vertebral artery becoming occluded as it passes up in the transverse foramen. The spinal joints become stiff in cervical spondylosis. Thus the chondrocytes which maintain the disc become deprived of nutrition and die. The weakened disc bulges and grows out as a result of incoming osteophytes. A ‘drop attack’ in older people is a sign of vertebrobasilar insufficiency, which is the cause of 25% of the strokes and TIA’s in the USA.
Spondylosis of the lumbar spine, the subject of this paper, is a term with many definitions. In the literature, it has been utilized in many different contexts, employed synonymously with arthrosis, spondylitis, hypertrophic arthritis, and osteoarthritis. In other instances, spondylosis is considered mechanistically, as the hypertrophic response of adjacent vertebral bone to disk degeneration (although osteophytes may infrequently form in the absence of diseased disks) [17]. Finally, spondylosis may be applied nonspecifically to any and all degenerative conditions affecting the disks, vertebral bodies, and/or associated joints of the lumbar spine [17, 18]. For purposes of this review, we will use this final, broad definition of spondylosis, recognizing the high incidence of coincident degenerative changes, and the dynamic interplay between adjacent disks, vertebra, and nerves that create the clinical pain syndromes within the axial spine and associated nerves.
Pathogenesis
The high incidence of simultaneous degenerative changes to the intervertebral disk, vertebral body, and associated joints suggests a progressive and dynamic mechanism, with interdependent changes occurring secondary to disk space narrowing .
Intervertebral disks are believed to undergo what “degenerative cascade” of three overlapping phases that may occur over the course of decades. Phase I (Dysfunction Phase) describes the initial effects of repetitive microtrauma with the development of circumferential painful tears of the outer, innervated anulus, and associated end-plate separation that may compromise disk nutritional supply and waste removal. Such tears may coalesce to become radial tears, more prone to protrusion, and impact the disk’s capacity to maintain water, resulting in desiccation and reduced disk height. Fissures may become ingrown by vascular tissue and nerve endings, increasing innervation and the disk’s capacity for pain signal transmission . Phase II (Instability Phase) is characterized by the loss of mechanical integrity, with progressive disk changes of resorption, internal disruption, and additional annular tears, combined with further facet degeneration that may induce subluxation and instability. During Phase III (Stabilization Phase), continued disk space narrowing and fibrosis occurs along with the formation of osteophytes and transdiscal bridging .
The spectrum of pathological changes in facial joints and the disk and the interaction of these changes. The upper light horizontal bar represents dysfunction, the middle darker bar instability, and the lower dark bar stabilization.
THERE are several implications of disk space narrowing. Adjacent pedicles approximate with a narrowing of the superior–inferior dimension of the intervertebral canal. Laxity due to modest redundancy of the longitudinal ligaments enables bulging of the ligamentum flavum and potential for spine instability. Increased spine movement permits subluxation of the superior articular process (SAP), causing a narrowed anteroposterior dimension of the intervertebral and upper nerve root canals. Laxity may also translate into altered weight mechanisms and pressure relationships on vertebral bone and joint spaces believed to influence osteophyte formation and facet hypertrophy to both inferior and superior articular processes with risks for projection into the intervertebral canal and central canal, respectively. Oblique orientations of the articular processes may further cause retrospondylolisthesis, with resulting anterior encroachment of the spinal canal, nerve root canal, and intervertebral canal.
Biochemical research exploring osteophyte formation supports the above process. Osteophyte lipping is believed to form at periosteum through the proliferation of peripheral articular cartilage which subsequently undergoes endochondral calcification and ossification [28]. Changing weight mechanics and pressure forces as well as alterations in oxygen tension and dynamic fluid pressure appear to be influential factors in osteophyte formation . Mesenchymal stem cells of the synovium or periostium are likely precursors, with synovial macrophages and a milieu of growth factors and extracellular matrix molecules acting as probable mediators in this process .
Clinical presentation
Pain within the axial spine at the site of these degenerate changes is not surprising as nociceptive pain generators have been identified within facet joints, intervertebral disks, sacroiliac joints, nerve root dura, and myofascial structures within the axial spine
These degenerative anatomical changes may culminate in a clinical presentation of spinal stenosis, or narrowing within the spinal canal through progressive ingrowth of osteophytes, hypertrophy of the inferior articular process , disk herniation, bulging of the ligamentum flavum , or spondylolisthesis. The clinical result: a constellation of pain symptoms encompassed in the term neurogenic claudication (NC). NC may include (to varying extents) lower back pain, leg pain, as well as numbness and motor weakness to lower extremities that worsen with upright stance and walking, and improve with sitting and supine positioning
Clinical presentations of radiculopathy may emanate from many sources, all of which can be explained by the degenerative process. Disk bulging may affect descending rootlets of the cauda equina, nerve roots exiting at the next lower intervertebral canal, or the spinal nerve within its ventral ramus, if protruding centrally, posterolaterally, or laterally, respectively . Osteophyte lipping along the posterior aspect of vertebral bodies, along upper or lower margins, may similarly impinge upon the same neural structures as the bulging disk just described . Hypertrophic changes to the superior articular process may intrude upon nerve roots within the upper nerve root canal, dural sac, or prior to exiting from next lower intervertebral canal, depending on their projection . These theoretical forms of impingement have been substantiated through cadaver studies. A 70% reduction or 30% residual diameter of neuroforminal space is cited as the critical amount of occlusion to induce neural compromise . Moreover, compression of the posterior disk to less than 4 mm height, or foraminal height to less than 15 mm has also been determined as critical dimensions for foraminal stenosis and nerve impingement .
Etiology/risk factors
What factors mediate this degenerative progression? What leads a large portion of the population to manifest spondylosis, even early on in their lives? Given the substantial variability in the number and degree of spine changes observed in individuals and the wide range of clinical presentations, answers to these questions hold promise to broaden treatment options.
The influence of age
Large studies of osteoarthritis have long recognized the aging process to be the strongest risk factor for bony degeneration, particularly within the spine [36]. An extensive autopsy study in 1926 reported evidence of spondylitis deformans to increase in a linear fashion from 0% to 72% between the ages of 39 and 70 years.
The impact of activity and occupation
Disk generation has long been associated with certain activities. Retrospective studies cite Body Mass Index (BMI), incident back trauma, daily spine loading (twisting, lifting, bending, and sustained nonneutral postures), and whole body vibration (such as vehicular driving) to be factors which increase both the likelihood and severity of spondylosis . While these correlations exist, a study following progressive radiographic changes in lumber DDD did not find significant associations with the extent of physical activity, noting only age, back pain, and associated hip OA to be predictive of DDD and osteophyte changes .
The role of heredity
Genetic factors likely influence the formation of osteophytes and disk degeneration. 50% of the variability found in osteoarthritis can be attributed to heritable factors. Similarly, twin studies evaluating the progression of degenerative changes in lumbar MRI imaging suggest that approximately half (47–66%) of the variance could be explained by genetic and environmental factors, attributing only 2–10% of variance to physical loading and resistance training [44]. Another twin study revealed a high degree of similarity in signal intensity, disk height narrowing, disk bulging, and end-plate changes . A search for these underlying genetic factors has identified polymorphisms in genes regulating inflammatory pathways and a Vitamin D Receptor allele to correspond to radiographic progression of lumbar disk degeneration .
A functional adaptation?
Is osteophyte formation inherently pathological? question if osteophyte formation may represent a remodeling process, functionally adapting to the instability or the changes in the demands of the spine .. Osteophytes may form in the absence of other degenerative processes, and cartilaginous damage may exist without corresponding osteophytes . Although there remains a strong association between the presence of osteophytes and other degenerative spine changes, isolated instances of one without the other occur, in the absence of overt symptoms.
A diagnostic approach
The initial evaluation for patients with low back pain begins with an accurate history and thorough physical exam with appropriate provocative testing. These first steps are complicated by the subjectivity of patient experiences of chronic spinal pain and the inherent difficulty isolating the anatomic region of interest during provocative testing without the influence of neighboring structures.
Radiographic studies, whether plain film, CT, CT myelogram, or MRI, may provide useful confirmatory evidence to support an exam finding and localize a degenerative lesion or area of nerve compression. However, imaging is an imperfect science, identifying the underlying cause of LBP in only 15% of patients in the absence of clear disk herniation or neurological deficit . Furthermore, there remains a frequent disconnection between the symptom severity and the degree of anatomical or radiographic changes . While correlations between the number and severity of osteophytes and back pain exist , the prevalence of degenerative changes among asymptomatic patients underlies the difficulty assigning clinical relevance to observed radiographic changes in patients with LBP.
Nerve compression symptoms by clinical history may also be confirmed by electromyographic studies demonstrating normal distal motor and sensory nerve conduction studies with abnormal needle exam. Diagnostic injections can facilitate localization by isolating and anesthetizing irritated nerve roots (via epidural), or by blocking suspected pain generators within facet joints, sacroiliac joints, or the disk space itself .
Intervention and treatment options.
We will briefly describe these treatment options for the management of chronic low back pain syndromes within each of the four primary categories: physical therapy (and associated modalities and behavioral techniques), pharmacotherapy(HOMOEOPATHIC MEDICATIONS), and surgical intervention.
Exercise-based and behavioral interventions
Exercise therapy
Exercise therapy (ET) remains one of the conservative mainstays of treatment for chronic lumbar spine pain, and may be tailored to include aerobic exercise, muscle strengthening, and stretching exercises . Significant variation in regimen, intensity, and frequency of prescribed programs presents challenges to assessing efficacy among patients . One meta-analysis of the current literature exploring the role of ET in patients with varying duration of symptoms found a graded exercise program implemented within the occupational setting demonstrated some effectiveness in subacute LBP. Among those suffering chronic pain symptoms, small, but statistically significant improvements were observed among patients, with regard to pain reduction and functional improvement . The optimal approach to exercise therapy in chronic low back pain sufferers appears to be those regimens involving an individually-designed exercise program emphasizing stretching and muscle strengthening, administered in a supervised fashion, with high frequency and close adherence. Such results are complemented by other conservative approaches, including NSAIDS, manual therapies, and daily physical activity .
Transcutaneous electrical nerve stimulation (TENS)
A “TENS” unit is a therapeutic modality involving skin surface electrodes which deliver electrical stimulation to peripheral nerves in an effort to relieve pain noninvasively. Such devices are frequently available in outpatient exercise therapy settings, with up to a third of patients experiencing mild skin irritation following treatment . While one small study identified an immediate reduction in pain symptoms 1 h following TENS application, there remains little evidence of long-term relief. Another larger study did not discover significant improvement with TENS compared with placebo with regard to pain, functional status, or range of motion .
Lumbar supports
Lumbar back supports may provide benefit to patients suffering chronic LBP secondary to degenerative processes through several potential, debated mechanisms. Supports are designed to limit spine motion, stabilize, correct deformity, and reduce mechanical forces. They may further have effects by massaging painful areas and applying beneficial heat; however, they may also function as a placebo. There is moderate available evidence evaluating efficacy of lumbar supports within a mixed population of acute, subacute, and chronic LBP sufferers to suggest that lumbar supports are not more effective than other treatment forms; data is conflicting with regard to patient improvement and functional ability to return to work .
Traction
Lumbar traction applies a longitudinal force to the axial spine through use of a harness attached to the iliac crest and lower rib cage to relieve chronic low back pain. The forces, which open intervertebral space and decrease spine lordosis, are adjusted both with regard to level and duration and may closely be measured in motorized and bed rest devices. Temporary spine realignments are theorized to improve symptoms related to degenerative spine disease by relieving mechanical stress, nerve compression, and adhesions of the facet and annulus, as well as through disruption of nociceptive pain signals . Nonetheless, patients with chronic symptoms and radicular pain have not found traction to provide significant improvement in pain nor daily functioning . Little is known with regard to the risks associated with the applied forces. Isolated case reports cite nerve impingement with heavy forces, and the potential for respiratory constraints or blood pressure changes due to the harness placement and positioning .
Spine manipulation
Spine manipulation is a manual therapy approach involving low-velocity, long lever manipulation of a joint beyond the accustomed, but not anatomical range of motion. The precise mechanism for improvement in low back pain sufferers remains unclear. Manipulative therapy may function through: “ release for the entrapped synovial folds, relaxation of hypertonic muscle, disruption of articular or periarticular adhesion, unbuckling of motion segments that have undergone disproportionate displacement, reduction of disk bulge, repositioning of miniscule structures within the articular surface, mechanical stimulation of nociceptive joint fibers, change in neurophysiological function, and reduction of muscle spasm” .
Available research regarding its efficacy in the context of chronic LBP finds spinal manipulation to be “more effective” compared to sham manipulation with regard to both short- and long-term relief of pain, as well as short-term functional improvement . Compared with other conventional, conservative treatment approaches such as exercise therapy, back school, and NSAID prescription, spinal manipulation appears comparable in its effectiveness both in short- and long-term benefits [52, 59]. Research exploring the safety of such therapy among trained therapists found a very low risk of complications, with clinically worsened disk herniation or cauda equina syndrome occurring in fewer than 1/3.7 million .
Massage therapy
