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Cervical Degenerative Disc Disease


Cervical Degenerative Disc Disease

Article Author:
Jordan Fakhoury
Article Editor:
Thomas Dowling
Updated:
7/28/2020 7:33:35 PM
For CME on this topic:
Cervical Degenerative Disc Disease CME
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Cervical Degenerative Disc Disease

Introduction

Degenerative disc disease of the cervical spine typically develops in the aging population equally in terms of patient sex. Patients most commonly present with pain. Pain, or in combination with other neurological symptoms, may require surgical intervention. Treatment options range from nonoperative measures to decompression, instrumented fusion, or a combination of both laminoplasty or instrumentation or a combination of both. This chapter will examine the anatomy, natural history, etiology, pathophysiology, evaluation, and treatment options.

The cervical spine, C1 to C7, provide exceptional function and range of motion. The upper cervical spine, C1 (the atlas, which articulates with the occiput), and C2 (the axis) are highly specialized, allowing for significant ranges of motion (rotation, flexion, extension, and side-bending) related to facet orientation allowing for more rotation. Structures adjacent to the cervical vertebrae include the spinal cord and nerve roots, blood vessels as well as the trachea and esophagus.

The intervertebral disc (IVD) is found from the C2-C3 level down, aids in cervical spine mobility and stabilization. In contrast to the thoracic and lumbar vertebrae, the cervical vertebrae have a unique bony prominence called the uncinate process, which articulates with the adjacent level to form the joint of Luschka or uncovertebral joint. This joint helps to reinforce the IVD and provides additional stability and motion.[1] The IVD is an intricate structure composed mainly of two parts, the peripherally located annulus fibrosus (AF) and the centrally located nucleus pulpous (NP) which are responsible for its’ load distribution function. The anterior and posterior longitudinal ligaments reinforce the IVD.

The AF of the intervertebral discs is mostly of type I collagen in layers (lamellae), proteoglycans, glycoproteins, elastic fibers, and extracellular matrix (ECM) secreting cells. These collagen layers are uniquely positioned to form a strong shell for the inner contents, the NP.

The NP has a gel-like consistency composed mainly of water, which decreases with age (~90% at birth and 70% by the age of 60). The remaining minority of the NP contents then consists of type II collagen and proteoglycans.  A critical proteoglycan in the NP is aggrecan, which, when bound to hyaluronic acid, helps to keep water within the NP, allowing for load resistance.

After the first years of life, the IVD becomes the largest avascular structure in the body. Most of the nutrition delivery is via metabolite diffusion from the vertebral endplates. Over time, the IVD not only begins to lose its water content but its proteoglycan supply as well, leading to a more fibrotic consistency of the NP and subsequent fissuring As those vertebral endplates calcify with aging.

There are different types of NP herniations. If the NP herniates but remains contained by the annulus, it is referred to as a disc protrusion. However, the NP can also penetrate through injured annular fibers, and NP contents can extrude through a defect in the annulus, referred to as a disc extrusion. Furthermore, NP fragments can be separated from the extruded disc material, yielding disc sequestration.[2]

The degenerative process of the cervical spine classifies into three distinct stages: (1) dysfunction, (2) instability, and (3) stabilization. Dysfunction occurs between the ages of 15 to 45 years old. During this stage, radial and circumferential tears can occur in the annulus accompanied by facet joint localized synovitis. Instability (2) can occur in individuals between the ages of 35 to 70 years old. This stage is characterized by disruption of the inner disc with progressive resorption, as well as facet joint degeneration. This condition leads to the final stage of the process, stabilization, occurring most commonly after 60 years of age. Here, hypertrophic bone develops around the facet joints as well as the disc, promoting stiff and possible ankylosing spine.

Interestingly, each spine segment may be at a different degenerative stage. One level could be completing the dysfunction stage while another beginning the stabilization phase. Disc herniations appear to occur as a result of dysfunction and instability phase while spinal stenosis occurs as a result of the late instability stage and early stabilization stage as a result of the bony overgrowth and disk space narrowing  It is, for this reason, one may find a patient whose cervical spine segments have a combination of disc herniations and spinal stenosis at different levels.C5-6 is most commonly affected due to biomechanics of the cervical spine.

When discussing the natural history of the cervical degenerative disc disease and treatment options, symptomatic patients can experience an array of symptoms from pain intermittent or constant, along with possible neurological symptoms without pain. Patients generally receive nonoperative treatment when experiencing nonprogressive pain and/or minimal neurological issues. If surgery is necessary, it is typically elective, and it can be delayed with the hope of symptomatic improvement. However, an exception is patients diagnosed with cervical myelopathy who should have more urgent surgical treatment to avoid progression.

The proper diagnosis and treatment for spondylolytic cervical myelopathy can be extremely challenging, especially in patients with or even without ongoing axial neck pain with possible radiculopathy. One must also be aware that 20% of patients with cervical stenosis may also have lumbar stenosis. While many patients may have straightforward diagnosis with a thorough history and physical examination accompanied by confirmatory imaging modalities, there is a significant subset of patients who have pain without experiencing neurological findings (aside from possible sensory changes) and whose imaging may not easily correlate with physical exam findings. It is instances such as this in which other diagnostic modalities should support a careful history and physical examination for an accurate diagnosis. Thus, a systematic assessment is imperative to diagnose and treat these patients appropriately and adequately.

Etiology

Since IVD dependence upon intervertebral endplate diffusion for nutrition, cervical degeneration is a normal part of aging, which starts early on-the second decade of life. As the discs lose water content, they can become less compliant and fissure leading to decrease disk height and collapse. This change in alignment can further put stress on the posterior aspect of the cervical spine and lead to spondylotic changes as well (i.e., facet hypertrophy). The less hydrated NP, as it degenerates, the load of the cervical spine and the increased forces exerted on the NP are then further transmitted to the AF, which then begins to tear and fissure, weakening the AF. This further causes the IVD to lose height, as the AF starts to bulge and increase in diameter and then fissure.

While aging, some environmental and genetic factors can predispose individuals to the development of cervical degenerative disc disease. Of interest, with increasing use of electronics (such as handheld devices such as smartphones) while sitting, chronic flexion at the neck can lead to increased stress on the discs.  In the neutral position, the head weighs approximately 12 lbs.  With increasing flexion, the relative weight seen on the discs increases to 27 lbs at 15, 40 lb at 30, 49 lbs at 45 and 60 lbs at 60 degrees of flexion. This chronically added weight yields more chronic stress on the IVD, particularly the NP, poor diffusion, and nutrition to the IVD and subsequent degeneration.[3] 

Other possible risk factors and causes have been objects of research, including smoking, occupation, genetics, atherosclerosis, contact sports, and prior surgeries. However, studies have found contradictory evidence demonstrates uncertain contributions of body mass index, sex, sports, smoking, and alcohol consumption.[4] Gore et al. showed no evidence suggesting cigarette smoking is a causative agent in cervical spine degeneration. Sports such as weightlifting was also not found to increase the risk of degeneration.[5]

Epidemiology

Similar to the lumbar spine, cervical disc degeneration is a naturally occurring age-related phenomenon. The prevalence of cervical DDD increases with age regardless of the patient's symptomatology (or lack thereof).[6][7] Literature has demonstrated that in a select population, a quarter of patients less than the age of 40 showed evidence of disk degeneration or narrowing at one level. This evidence was found in about 60% of patients the same population who were greater than 40 years old.[8] Lehto et al. demonstrated similar findings in asymptomatic patients older than the age of 40, in which 62% showed abnormalities on MRI.[9] 

In a Japanese study evaluating 497 asymptomatic patients, Matsumoto et al. showed almost 90% of patients (men and women) over 60 years of age had abnormal findings while 17% and 12% of men and women respectively, in their 20s demonstrated abnormalities. [10] Several studies have acknowledged the most common disc-level involved in degeneration was C5-6, and the second most common being C6-7. Research has also demonstrated that cervical DDD was associated with lumbar degenerative changes in both men and women but did appear later in life. An association has also been found in the pain distribution in the neck-shoulder-brachial region in patients with moderate to severe cervical DDD.[9][10][11] 

Pathophysiology

The pathophysiology of cervical spine degenerative disc disease is comparable to the thoracic and lumbar spine. Typically, physiologic changes occur within the nucleus pulposus first, followed by progressive degeneration of the annulus. This normal degenerative process may lead to extrusion of the nucleus components. The segments begin to become hypermobile leading to additional degenerative arthritic changes and instability. Unlike the lumbar spine, these hypertrophic changes mainly occur at the uncinate process, which forms the ventral wall of the foramen (uncovertebral joint). The facet joints and vertebral bodies also eventually begin to experience these hypertrophic changes due to altered loads. As aforementioned, these changes lead to stiffness and a decrease in motion of the cervical spine.

Once an HNP occurs, pain, which is the most common finding in CDD, is dependent upon the level affected and the location of the herniation. However, HNP's may also be asymptomatic. Most herniations occur posterolaterally given the AF's thinner and weaker structure in this area due to the PLL (posterior longitudinal ligament not covering this area as thickly. Given the posterolateral location of the nerve root, the HNP can produce pain in two ways; one is if the dorsal root ganglion (DRG) becomes compressed, the presenting symptoms will typically follow a dermatomal pattern. However, if the HNP is directly posterior, the second way is that spinal cord compression can occur, with symptoms distal to the injury. 

History and Physical

A careful history is paramount to ensure that presenting symptoms are caused by degenerative changes and not more serious conditions.  Discussion with the patient about possible constitutional symptoms (weight loss, fever, chills, and/or sweats) and infections can be crucial, along with oncologic history and trauma.  If pain is a presenting symptom, a thorough pain history such as functional limitation, intensity, onset, alleviating and exacerbating symptoms, radiation, and related symptoms are needed.  A comprehensive history of neurologic complaints such as weakness, sensory loss, and gait are imperative.

Physical exam should always begin with the patient's vitals (i.e., fever). A thorough neurologic examination is necessary, which at a minimum should include motor testing of the upper and lower extremities, cranial nerve testing, gait and balance assessment, sensation, and reflexes (including Hofmann's and Babinski) and any clonus.  The range of motion of the cervical spine should undergo evaluation for both degrees of movement and elicit any symptoms.

Most commonly, patients present with axial neck pain and difficulty with movement.[12] A small subset of patients may complain of headaches, while others tend to suffer from shoulder pain.[13] Unilateral radicular symptoms are also quite prevalent and most commonly result from posterolateral disc herniations and osteophytes located at the neural foramen.

Other signs and symptoms include changes of deep tendon reflexes, muscle atrophy, hypesthesias, paresthesias, or weakness demonstrated by specific nerve root signs. A significant proportion of flexion/extension motion of the cervical spine occurs between C4-C6. Interestingly, research shows that the C5-C6 interspace has the earliest and most significant amount of degeneration.[14] The most common nerve roots affected by a disk protrusion are C6 and C7. C6 is between C5-C6.[15]

Provocative testing such as a Spurling test and a shoulder abduction (relief) test can evaluate for any radicular symptoms. A Lhermitte's sign can also help diagnose potential cervical myelopathy. Evaluation of the paraspinal muscular for spasm and trigger points is necessary. An assessment of the upper extremity would also be helpful, to help further distinguish presenting symptoms. For example, a patient may be complaining of a vague numbness and tingling in the hand, which may be secondary to carpal tunnel syndrome, double crush syndrome, or cervical radiculopathy.[16]

Cervical disc disease may be asymptomatic and degenerative changes only found on imaging such as CT scan, X-rays, or MRI. A posterolateral symptomatic HNP will present with dermatomal pain, myotomal weakness, or sensory change.  The most common HNP is at C6-7, just anterior to the C7 nerve root.  When the C7 nerve root is inflamed or compressed, the patient will complain of pain from the neck radiating to the lateral forearm and then palm and possible radiation to the middle finger. Muscle weakness may be present in the ipsilateral triceps muscle, making extension at the elbow difficult.  The triceps reflex may also be depressed and asymmetrical. 

C5 root compression can present with neck pain radiating to the shoulder along with peri-scapula pain. The deltoid may be affected, and weakness during shoulder abduction, external rotation, and elbow flexion may occur. The biceps and brachioradialis reflex may also be depressed and asymmetrical.  

When the C6 nerve is affected, neck pain will radiate to the neck, shoulder down to the thumb and index finger, in addition to periscapular pain. This nerve root innervates the biceps along with the wrist extenders, and weakness during elbow flexion and wrist extension may be present. The biceps and brachioradialis reflex may also be depressed and asymmetrical. 

The C8 nerve root provides sensation from the neck to the medial forearm and medial hand.  The muscle groups innervated are the finger extensors, and weakness during the thumb extension may occur.

Similar to the C8 nerve root, the T1 nerve root, when involved, will present with pain in the neck radiating to the medial arm and forearm but will rarely go to the hand. First dorsal interosseous muscle weakness may be present. 

Severe cervical spondylosis, ossification of the posterior longitudinal ligament, or disc herniation or any combination of these may cause cervical spondylotic myelopathy. This condition most commonly occurs in patients in their 50s or later. The signs and symptoms are widely variable and unique, describing their legs as feeling stiff and/or wooden. Some may complain of numbness and tingling originating from the fingertips to the hands as if they were wearing gloves).[17] Writing and other fine motor functions (dexterity) may also become altered. Hyperreflexia, a positive Hoffman sign, ankle clonus, and a Babinski reflex may also be present. Gait disturbances can occur. With severe cases, bladder and bowel changes can occur.[18]

Evaluation

Laboratory testing may help in diagnosis, especially if an infection (i.e., Lyme disease), autoimmune arthritis, or a metabolic disorder (folate or vitamin B12 deficiency) is high on the differential diagnosis. A CBC with differential along with an ESR and CRP are also necessary; however, all lack specificity for spinal infection. Blood cultures may also be indicated when an infection is suspected.

Imaging should begin with a radiographic evaluation, which may indicate a decrease in normal cervical lordosis, hypertrophic changes, and disc space narrowing. They are also helpful in ruling out additional problems like fractures or instability. Computed tomography (CT) may also be helpful for preoperative planning, especially in patients with dorsal osteophytes and OPLL. MRI is the gold standard for patients when considering degeneration of the cervical spine as a potential diagnosis as ligaments, disc, and neural structures visible. Magnetic resonance (MR) imaging allows for the evaluation of both soft tissue and boney structures and accurately measures functionally relevant spinal canal and spinal cord dimensions in various planes.[19] 

Reduced spinal canal width increases the risk of cervical cord compression and myelopathy.[20] Because space around the cord becomes relatively decreased in the lower cervical spine segments, the risk is higher at these levels.[21][22][23] On MRI, the inner disk spaces tend to have a moderately high signal intensity, and the surrounding rim, the annulus fibrosus, is of low signal intensity. An area of medium-intensity dorsal demonstrates central or paracentral disc herniations to the disk space. Myelopathic patients may not initially present with cord changes but may be present with time. These changes are demonstrated by hyperintensity at the level of the cord compression with cord edema or even myelomalacia.

It is also important to note further modalities to assist in ruling out other potential diagnoses. For example, EMG may be beneficial to exclude compressive and/or peripheral neuropathies caused by occupational exposures, diabetes, or folate/vitamin B12 deficiencies.

Treatment / Management

Treatment for cervical disc disease is centered around decreasing pain, improving function, and minimizing recurrence and duration of symptoms. Treatment typically beings with nonoperative care and can lead to operative intervention.

Nonoperative

Conservative modalities include rest, modification of activity, pharmacological agents, physical therapy, manipulation, different types of injections, and acupuncture. Initial short term immobilization may be beneficial. Medications may provide symptomatic relief. These may include nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, and/or muscle relaxants. NSAIDs are commonly used and provide relief via interfering with prostaglandin synthesis leading to the inhibition of the inflammatory cascade.

Steroids may be beneficial in initial management for short-term usage as they are associated with deleterious side-effects. Muscle relaxants are an option when patients are experiencing muscle spasms. Gross et al. demonstrated cervical mobilization and manipulation might provide immediate or short-term relief for neck pain.[24] GABA class drugs like gabapentin and serotonin uptake inhibitors may be considerations as well. Tricyclic antidepressants may also play a role. Clinicians should avoid using opioids.

A cervical collar may be recommended in patients who present with intractable neck pain. Controversy exists over the efficacy of cervical traction for treatment of HNP as there is no evidence to suggest a reduction in the degree of disc herniation.[25] It, however, may allow for some neuroforaminal decompression.

Physical therapy should start early in the treatment algorithm. Passive modalities should be used and include but are not limited to heat, mechanical traction, massage, and a soft cervical collar.[26] Heat has shown to decrease pain and reduce muscle spasms.[27][28] Evidence suggests cryotherapy can help decrease inflammation and reduce muscle guarding.[29][30] Massaging the area of intensity allows for mechanical stimulation leading to an increase of circulation and the promotion of muscle relaxation.[31] Cervical traction may allow for joint distraction and potentially relieving pressure off nerve roots/disks; this may improve epidural blood flow in the area and reduce pain, inflammation, and spasms.

Active modalities should also be part of rehabilitation. These include aerobic conditioning, dynamic muscle training, isometric, and range of motion exercises. Postural training may help. Isometric exercises allow for the strengthening of paravertebral muscles with avoidance of certain motions that can cause pain. Recent reports suggest there was no strong evidence for patients with chronic neck pain to undergo neck strengthening and stretching exercises.[32]

As stated previously, the diagnosis and treatment of cervical myelopathy may be difficult and unpredictable. Some patients may develop a rapid onset and decline of symptoms while some may experience a plateau in symptoms, but in general, it is usually progressive as a timeline may be variable.[33] Unfortunately, spontaneous improvement rarely occurs. Sometimes, close observation may be a consideration in patients with symptoms that appear not to be progressing and are mild.

Operative Treatment

Patients who fail to respond to nonoperative treatment, especially those experiencing intractable pain, progressive or significant neurological compromise, myelopathy may require surgical intervention. One surgical option is decompression. Decompression procedures may include fusion with or without instrumentation. However, typically most decompressions will consist of a fusion to minimize the potential for post-surgical deformity.

Pain management procedures may also be beneficial. Nerve root injections or epidural steroid injections can not only be used as a diagnostic tool but can also be therapeutic. However, they are not without undesirable complications.[34][35] Historically, trigger point injection has also been used, but no evidence has shown its long-term effectiveness.

There are a variety of surgical approaches to the cervical spine. Commonly, the neural structures become compressed anteriorly; therefore, an anterior approach is necessary to directly remove a disk, causing decompression and will most likely include a fusion (ACDF). The approach of choice in patients with normal to kyphotic alignment is the anterior approach as a laminectomy in these patients may further cause kyphosis secondary to the destabilization that occurs.[36] During an ACDF, compressive and degenerative structures are removed with a fusion across the segments adjacent to the decompression. Furthermore, several disks can be removed with multi-level fusions (with or without strut graft). A corpectomy with strut grafting may be necessary for multi-level decompressions. An anterior cervical plate can be inserted to increase stability and earlier mobilization. Distraction across the disk space with an interbody implant can lead to further indirect decompression of the neural foramen.

Some studies demonstrate a fusion rate of up to 94% after an ACDF.[37] However, for fusion to be successful, appropriate patient selection and precise operative techniques are key. Current literature shows support for major symptomatic improvement of most patients.[38][39][40] Although recurrent symptoms, evening worsening, may still occur most likely secondary to adjacent level degeneration to the fusion. Furthermore, neurological compromise is rare (0.01%).[41] Other potential causes of complications include soft tissue dissection when using the anterior approach followed by grafting and plating. During dissection, the recurrent laryngeal nerve may suffer injury, causing a palsy, potentially leading to hoarseness. Additionally, the esophagus and/or trachea may be injured, possibly perforated, and graft may become dislodged and subside. Hoarseness and/or dysphasia can be noted postoperatively, especially with higher levels operated on or with multi-level cases.

When an indirect decompression is warranted, the posterior approach to the spinal cord can be utilized. This approach is mainly for patients with neutral or lordotic cervical spine alignment. Furthermore, the posterior approach is quite helpful with patients who have multi-level compression and congenital stenosis, usually involving C3-C6 or C7. The muscles attaching to the second cervical segment are protected to avoid progressive kyphosis and postoperative neck pain. Posterior decompression provides the spinal cord with additional space, moving away from the disk/bony ridges compressing anteriorly. Options include laminectomy (either with or without fusion) or open-door laminoplasty. Both of which can achieve the same goal, to increase the diameter of the canal.

Highsmith et al. showed similar neurological outcomes between the two, but patients who underwent a laminectomy with fusion had less neck pain compared to laminoplasty.[42] If neck pain is present, fusion should be done to address this as just doing a decompression may allow for neurological recovery but not alter pain from DDD. Laminoplasty is usually reserved for patients with cord compression without or with minimal neck pain. Laminoplasty may minimize the risk of postoperative kyphosis in patients with neutral to lordotic spine. Currently, laminectomies are usually accompanied by instrumented fusion, which increases stability and can maintain or restore lordosis. Lees et al. demonstrated satisfactory results in 70 to 80% of patients who underwent a laminectomy.[43] Hirabayashi et al. described the expansive open-door laminoplasty, which has shown good results in 66% of patients.[44] However, these techniques are not without their complications, which range from hematoma, dural injury, paralysis, postoperative C5 palsy, and postlaminectomy kyphosis and neck pain. Moreover, a foraminotomy is an option for direct decompression of nerve roots in patients with only radiculopathy.

Recently, cervical disk arthroplasty has gained popularity. Some studies show no significant difference between fusion and arthroplasty regarding revision rates two years postoperatively.[45] However, this procedure is not indicated for degenerative disc disease but rather herniated discs.

A combined approach (anterior and posterior) may be needed when a multi-level corpectomy is indicated or when there is diminished bone quality secondary to the patients’ metabolic state.

Differential Diagnosis

  • Brachial plexopathy
  • Carpal/cubital tunnel syndrome
  • Peripheral neuropathy or neuritis
  • Complex regional pain syndrome
  • Demyelinating disorder
  • Radiation plexopathy
  • Malignancy (Pancoast tumor for neuropathic symptoms)
  • Myofascial pain
  • Cervical spondylosis
  • Sprained ligaments
  • Cervical sprain and strain
  • Rheumatologic disorder
  • Fibromyalgia
  • Shoulder pathology/rotator cuff injury                
  • Thoracic outlet syndrome
  • Infectious etiology/osteodiscitis

Prognosis

The prognosis and disease development are difficult to predict and extremely variable from patient to patient. In an article published in 1956, Clark and associates followed 120 patients with cervical spondylosis. They found that in 75% of patients, the disease processed weakened in an episodic manner, in 20% of patients, symptoms gradually progressed, and in 5%, patients became symptomatic rapidly.[46] 

Several years later, Lees et al. further demonstrated the unpredictability of the disease.[43] In his study of 37 patients, Nurick et al. found that there was an initial phase of deterioration, then a nonprogressive phase which, in some cases, lasted for years. Older patients were more prone to further deterioration.[47] In another study, 26% of patients’ conditions worsened, 38% remained stable, and over one-third improved.[48]

Complications

Patients with cervical disc disease can experience a significant impact from pain and disability, often not correlated to the level of pathologic changes in the discs itself.  This disability can yield loss of productive days at work, worsening of roles in personal life along with overall poor health from being more sedentary in their lifestyle. Neurologic complications can occur as outlined above with loss of lower extremity function and incontinence being a very catastrophic, albeit rare, complication with myelopathy.

Deterrence and Patient Education

Cervical disc disease has the potential to carry immense morbidity leading to poor quality of life and disability. Patients concerned with cervical disc degeneration should receive education about their diagnosis. A diagnosis early on is imperative and can avoid potential impairments or restrictions. Primary physicians should also educate themselves to avoid missing common physical exam signs. If the patient's primary care physician is concerned, a referral system should be in place. 

Enhancing Healthcare Team Outcomes

Patients with cervical disc disease require an interprofessional approach. Physical therapists can help with not only acute exacerbations but also prevent chronic issues from being permanent. They also play a vital role in acting as educators for patients for proper posture and home exercises.

Clinicians such as the patient's primary care physician, their physiatrists, neurologist, orthopedists, and/or neurosurgeons should work together with the patient for a concise diagnosis and treatment plan (including a nonoperative and/or operative approach). Cervical epidural injections, facet blocks, nerve root injections, when warranted, should be performed by a pain management physician with significant expertise given the catastrophic consequences of a complication.[49] Given the possible disability and impact, obtaining coping mechanisms is incredibly important, and mental health providers play a crucial role. They can aid in helping developing skills through cognitive behavioral therapy (CBT) and decreasing pain by performing biofeedback.[50][51]


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