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CATEGORY	DETAILS
Risk Factors	Age > 40 years, repetitive spinal loading (manual labor, heavy lifting), obesity, smoking, prior spinal trauma, sedentary lifestyle, genetic predisposition, poor posture
Etiology	Progressive age-related degeneration of intervertebral discs, vertebral bodies, and facet joints
Patient Presentation	Chronic, insidious neck or low back pain and stiffness that worsens with activity and improves with rest; may present with radiculopathy (radiating limb pain, numbness, weakness) or myelopathy (gait instability, hand clumsiness)
Classic Physical Exam	Decreased spinal range of motion, paravertebral muscle tenderness, crepitus on motion, Spurling test positive (cervical radiculopathy), Lhermitte sign (myelopathy), hyperreflexia and Hoffmann sign (upper motor neuron involvement in cervical myelopathy), straight leg raise positive (lumbar radiculopathy)
Key Diagnostic Results	X-ray: osteophytes, disc space narrowing, endplate sclerosis, facet joint hypertrophy. MRI: disc desiccation, disc bulging or herniation, neural foraminal narrowing, spinal cord compression (in myelopathy)
Management	Conservative first: NSAIDs (ibuprofen 400 to 800 mg TID or naproxen 500 mg BID), physical therapy, activity modification. Epidural corticosteroid injections for radiculopathy refractory to conservative therapy. Surgical decompression (laminectomy, anterior cervical discectomy and fusion) for progressive myelopathy or failed conservative management
Keywords	"Osteophytes," "disc space narrowing," "bone spurs," "age-related spine degeneration," "stiffness worse in the morning that improves with movement," "Spurling test positive," "crepitus on neck rotation"

1. Pathophysiology

Spondylosis is fundamentally a disease of cumulative mechanical wear on the spine. The process begins in the intervertebral disc, which is composed of a gelatinous nucleus pulposus surrounded by the annulus fibrosus. With age and repetitive loading, the nucleus pulposus progressively loses its water content through proteoglycan degradation. This desiccation reduces the disc's ability to distribute axial loads evenly across the vertebral endplates. As a result, the disc height decreases, and the annulus fibrosus bears disproportionate stress, leading to tears and fissures.

The loss of disc height triggers a cascade of secondary changes. The facet joints, which are synovial joints that guide spinal motion posteriorly, now bear increased load because the anterior column can no longer support its share. This leads to facet joint arthropathy, characterized by cartilage loss, subchondral sclerosis, and joint capsule hypertrophy. Simultaneously, the vertebral bodies respond to altered biomechanics by forming osteophytes (bone spurs) at their margins. This is the body's attempt to stabilize the segment by increasing the surface area for load distribution. While compensatory, osteophytes become clinically significant when they encroach on the spinal canal (causing central stenosis and myelopathy), the neural foramina (causing foraminal stenosis and radiculopathy), or the vertebral arteries in the cervical spine.

Cervical myelopathy deserves special attention. When posterior osteophytes, disc bulges, and hypertrophied ligamentum flavum collectively narrow the spinal canal, the spinal cord itself becomes compressed. This causes upper motor neuron signs: hyperreflexia, spasticity, gait ataxia, and a positive Hoffmann sign. The pathophysiology here is direct mechanical compression combined with ischemia of the cord's watershed zones. This is the most dangerous manifestation of spondylosis because cord damage can become irreversible.

Radiculopathy occurs when a nerve root is compressed, typically at the neural foramen. The compressed root develops intraneural edema, demyelination, and eventually axonal injury if untreated. This produces dermatomal pain, sensory loss, and myotomal weakness. In the lumbar spine, the most commonly affected levels are L4-L5 and L5-S1. In the cervical spine, C5-C6 and C6-C7 are most frequently involved.

The reason patients report stiffness that is worse in the morning and improves with gentle activity is that immobility allows periarticular edema and synovial thickening to stiffen the joints, while movement promotes synovial fluid circulation and reduces stiffness. This pattern helps distinguish spondylosis from inflammatory conditions like ankylosing spondylitis, where morning stiffness lasts longer (typically more than 30 to 60 minutes) and improves significantly with exercise rather than just mild activity.

2. Classification and Clinical Manifestation

Spondylosis is classified primarily by anatomical location and the type of neurological involvement.

By Location

LOCATION	LEVELS MOST AFFECTED	CHARACTERISTIC FEATURES
Cervical spondylosis	C5-C6, C6-C7	Neck pain and stiffness, occipital headaches, radiculopathy to upper extremities, myelopathy with gait disturbance
Thoracic spondylosis	T6-T10	Least common; midback pain, band-like radicular pain around the thorax; rarely causes myelopathy unless severe
Lumbar spondylosis	L4-L5, L5-S1	Low back pain, radiculopathy to lower extremities, neurogenic claudication if associated spinal stenosis develops

By Neurological Involvement

TYPE	MECHANISM	CLINICAL FEATURES
Axial (uncomplicated)	Disc and facet degeneration without neural compression	Localized pain and stiffness; no neurological deficits; pain worsens with extension and loading
Radiculopathy	Nerve root compression by osteophytes or disc material at the foramen	Dermatomal pain radiating to the limb, numbness, paresthesias, segmental weakness, decreased deep tendon reflexes at the affected level
Myelopathy	Spinal cord compression in the central canal (cervical or thoracic)	Gait ataxia, hand clumsiness (loss of fine motor control), hyperreflexia, spasticity, positive Babinski sign, bowel or bladder dysfunction in advanced cases
Neurogenic claudication	Lumbar central stenosis compressing the cauda equina	Bilateral leg pain, heaviness, and weakness with walking or standing that improves with forward flexion (shopping cart sign); must be distinguished from vascular claudication

Common Dermatomal Patterns in Radiculopathy

NERVE ROOT	MOTOR DEFICIT	SENSORY DEFICIT	REFLEX AFFECTED
C5	Deltoid weakness (shoulder abduction)	Lateral arm	Biceps reflex
C6	Wrist extensors, biceps weakness	Lateral forearm, thumb, index finger	Brachioradialis reflex
C7	Triceps, wrist flexors, finger extensors	Middle finger	Triceps reflex
C8	Hand intrinsics, finger flexors	Medial forearm, ring and little finger	None reliably tested
L4	Tibialis anterior (ankle dorsiflexion), quadriceps	Medial leg	Patellar reflex
L5	Extensor hallucis longus (great toe dorsiflexion), hip abductors	Lateral leg, dorsum of foot	None reliably tested
S1	Gastrocnemius, peroneus longus (ankle plantarflexion, eversion)	Lateral foot, sole	Achilles reflex

3. Diagnostic Workup

TEST	ROLE	KEY FINDINGS
Plain radiograph (X-ray) of the spine	Best initial test for evaluating chronic axial neck or back pain	Osteophyte formation, disc space narrowing, endplate sclerosis, facet joint hypertrophy, loss of lordosis
MRI of the spine	Most accurate test and gold standard for evaluating neural compression	Disc desiccation (dark disc on T2), disc herniation or bulge, spinal cord compression and signal changes (T2 hyperintensity indicates myelomalacia), foraminal stenosis, ligamentum flavum hypertrophy
CT myelography	Alternative to MRI when MRI is contraindicated (e.g., pacemaker, claustrophobia)	Excellent bony detail; shows canal narrowing with contrast outlining the thecal sac and nerve roots
Electromyography and nerve conduction studies (EMG/NCS)	Used when the clinical picture is ambiguous or to differentiate radiculopathy from peripheral neuropathy or plexopathy	Denervation potentials (fibrillations, positive sharp waves) in a myotomal distribution confirm radiculopathy; normal sensory nerve action potentials distinguish root-level lesions from plexus or peripheral nerve lesions
Flexion-extension radiographs	Assess segmental instability	Abnormal translation or angulation between vertebral bodies during flexion and extension

The workup for spondylosis follows a logical sequence. When a patient older than 40 presents with chronic, progressive neck or low back pain and stiffness, the best initial test is a plain X-ray. Radiographs are inexpensive, widely available, and effectively demonstrate the hallmark structural changes of spondylosis: osteophytes at the vertebral body margins, narrowing of disc spaces, sclerosis of the vertebral endplates, and hypertrophy of the facet joints. X-rays also help exclude other causes of back pain such as fractures, tumors, or destructive lesions.

However, X-rays cannot visualize soft tissues. If the patient has neurological symptoms (radiculopathy or myelopathy), the next step is an MRI of the affected spinal region. MRI is the most accurate test because it directly visualizes the intervertebral discs, nerve roots, spinal cord, and surrounding soft tissues without radiation. On T2-weighted images, degenerative discs appear dark (loss of the normal bright signal from hydrated nucleus pulposus). MRI also reveals disc herniations, foraminal stenosis compressing nerve roots, and, critically, T2 hyperintensity within the spinal cord in cases of myelopathy, which indicates myelomalacia (cord damage) and carries prognostic significance.

CT myelography is reserved for patients who cannot undergo MRI. It provides superior bony resolution compared to MRI and, when combined with intrathecal contrast, clearly delineates the thecal sac and nerve root sleeves.

EMG and nerve conduction studies are not part of the routine workup but become valuable when there is diagnostic uncertainty. For instance, if a patient has upper extremity numbness and the clinical question is whether the problem originates at the cervical nerve root (radiculopathy) or at the peripheral nerve (carpal tunnel syndrome, ulnar neuropathy), EMG/NCS can localize the lesion. A key principle: in radiculopathy, the sensory nerve action potential (SNAP) remains normal because the lesion is proximal to the dorsal root ganglion, leaving the peripheral sensory nerve intact. In peripheral neuropathy, the SNAP is abnormal. This distinction is frequently tested.

4. Management and Treatment

STAGE	INTERVENTION	DETAILS
First-line conservative therapy	NSAIDs	Ibuprofen 400 to 800 mg orally three times daily with food, or naproxen 500 mg orally twice daily; use for 2 to 4 weeks; add a proton pump inhibitor for GI protection if prolonged use is anticipated
First-line conservative therapy	Physical therapy	Structured program focusing on strengthening paraspinal and core muscles, improving flexibility, and postural retraining; typically 6 to 12 weeks
First-line conservative therapy	Activity modification	Avoid prolonged static postures, use ergonomic supports, limit heavy lifting
Adjunctive pharmacotherapy	Muscle relaxants	Cyclobenzaprine 5 to 10 mg orally at bedtime for acute muscle spasm; short-term use only (2 to 3 weeks)
Adjunctive pharmacotherapy	Neuropathic pain agents (for radiculopathy)	Gabapentin starting at 300 mg orally at bedtime, titrated up to 1800 to 3600 mg daily in divided doses; or pregabalin 75 mg orally twice daily titrated to 150 to 300 mg twice daily
Interventional	Epidural corticosteroid injection	Fluoroscopy-guided transforaminal or interlaminar injection; indicated for radiculopathy refractory to 4 to 6 weeks of conservative therapy; may be repeated up to 3 times per year
Surgical	Anterior cervical discectomy and fusion (ACDF)	Indicated for cervical radiculopathy or myelopathy failing conservative therapy or with progressive neurological deficits
Surgical	Cervical laminoplasty or laminectomy with fusion	Indicated for multilevel cervical myelopathy with canal stenosis
Surgical	Lumbar decompressive laminectomy	Indicated for lumbar stenosis with neurogenic claudication refractory to conservative care, or progressive neurological deficit
Urgent surgical	Emergent decompression	Required for cauda equina syndrome (saddle anesthesia, urinary retention, bilateral leg weakness) or rapidly progressive myelopathy

Acute stabilization and initial management. For the vast majority of patients with uncomplicated spondylosis (axial pain without neurological compromise), management is entirely conservative. The cornerstone is NSAIDs combined with physical therapy. NSAIDs reduce inflammation in the degenerative facet joints and periarticular tissues. Physical therapy is not merely symptomatic; it addresses the biomechanical contributors by strengthening the muscles that dynamically stabilize the spine.

For patients with radicular symptoms, gabapentin or pregabalin is added to target neuropathic pain. These agents modulate calcium channels at the dorsal horn and reduce aberrant nerve signaling. Oral corticosteroid tapers (e.g., prednisone 60 mg daily tapered over 7 to 14 days) can provide short-term relief during acute radicular flares, but this is not a long-term strategy.

When to escalate. If 4 to 6 weeks of conservative therapy fails to relieve radicular pain, the next best step is an epidural corticosteroid injection. This delivers anti-inflammatory medication directly to the site of nerve root inflammation and can provide relief lasting weeks to months. It serves both a therapeutic and a diagnostic role: pain relief with a targeted injection supports the clinical localization.

Surgical indications are critical for exam purposes. Surgery is considered in three scenarios: (1) progressive myelopathy, which is the strongest indication because cord damage is potentially irreversible if decompression is delayed; (2) radiculopathy that has failed at least 6 to 12 weeks of conservative and interventional management with persistent significant functional limitation; and (3) cauda equina syndrome, which is a surgical emergency requiring decompression within 24 to 48 hours to preserve bowel and bladder function.

Contraindications and cautions. NSAIDs should be used with caution in patients with renal insufficiency (eGFR < 30), active peptic ulcer disease, or cardiovascular risk. In these patients, acetaminophen (up to 3000 mg daily in divided doses) can serve as an alternative analgesic, though it lacks anti-inflammatory properties. Gabapentin requires dose adjustment in renal impairment. In pregnant patients, acetaminophen is considered safe; NSAIDs should be avoided especially in the third trimester due to the risk of premature closure of the ductus arteriosus.

5. Differential Diagnosis and Distractors

DIFFERENTIAL	WHY IT IS SIMILAR	KEY DISCRIMINATOR
Ankylosing spondylitis	Both cause chronic back pain and stiffness; both show changes on spinal imaging	Ankylosing spondylitis presents in young males (< 40), with prolonged morning stiffness lasting > 30 minutes that improves dramatically with exercise, sacroiliac joint involvement on imaging (sacroiliitis), positive HLA-B27, and elevated ESR/CRP. Spondylosis presents in older adults, with brief morning stiffness, and shows degenerative changes (osteophytes, disc narrowing) rather than syndesmophytes and bamboo spine
Spondylolysis	The name is nearly identical, and both involve the lumbar spine	Spondylolysis is a stress fracture of the pars interarticularis, commonly seen in young athletes (gymnasts, football linemen). Diagnosed by oblique X-ray showing the "Scotty dog with a collar" sign. Spondylosis is a degenerative disc and joint disease of aging
Spondylolisthesis	Also frequently confused by name; can coexist with spondylosis	Spondylolisthesis is the anterior displacement of one vertebral body over the one below it, often resulting from bilateral spondylolysis or degenerative facet disease. Diagnosed by the visible "step-off" on lateral X-ray. Spondylosis refers to degeneration without vertebral slippage
Disc herniation (acute)	Both cause radiculopathy with similar dermatomal findings	Acute disc herniation typically presents suddenly in a younger patient (30 to 50) after a lifting or twisting event. MRI shows focal disc extrusion. Spondylosis develops gradually over years with broad-based disc bulges, osteophytes, and multisegmental changes
Multiple sclerosis	Cervical spondylotic myelopathy and MS can both present with upper motor neuron signs, gait ataxia, and hyperreflexia	MS presents in younger patients (20 to 40), often female, with symptoms that are disseminated in time and space (episodes involving different CNS regions). MRI of the brain shows periventricular white matter lesions (Dawson fingers), and CSF shows oligoclonal bands. In spondylotic myelopathy, MRI shows structural cord compression at a single level with no brain lesions
Peripheral arterial disease (vascular claudication)	Lumbar stenosis with neurogenic claudication can mimic vascular claudication (both cause leg pain with walking)	Neurogenic claudication improves with spinal flexion (leaning forward on a shopping cart), worsens with extension, and pulses are intact. Vascular claudication improves with rest regardless of posture, worsens with continued ambulation, and is associated with diminished peripheral pulses and an abnormal ankle-brachial index (ABI < 0.9)
Fibromyalgia	Both cause chronic, widespread musculoskeletal pain	Fibromyalgia presents with diffuse tender points (not confined to the spine), fatigue, sleep disturbance, and cognitive dysfunction. Imaging and labs are normal. Spondylosis has characteristic degenerative findings on X-ray and MRI

6. Traps and High-Yield Pearls

The single most common trap with spondylosis on licensing exams is confusing the terminology. Spondylosis, spondylolysis, and spondylolisthesis sound nearly identical but represent entirely different pathologies. Test writers exploit this ruthlessly. Remember the mnemonics: spondylo-sis involves degen-eration (aging spine), spondylo-lysis involves lysis (a fracture/break of the pars interarticularis), and spondylo-listhesis involves slipping (vertebral displacement). If the vignette describes an elderly patient with chronic stiffness and osteophytes, the answer is spondylosis. If it describes a teenage gymnast with focal low back pain, think spondylolysis. If lateral X-ray shows one vertebral body slid forward on another, that is spondylolisthesis.

Another high-yield trap involves the patient with cervical spondylotic myelopathy who presents with gait instability and hand clumsiness. The distractor answer is often multiple sclerosis or vitamin B12 deficiency (subacute combined degeneration). The key discriminator is the MRI: if it shows structural compression of the cord at the cervical level with T2 signal change confined to the compression site and no brain lesions, the answer is spondylotic myelopathy. Do not be distracted by upper motor neuron signs alone.

The neurogenic versus vascular claudication distinction is a perennial favorite. The vignette will describe an older patient with bilateral leg symptoms on walking. The shopping cart sign (symptoms relieved by leaning forward) and intact pedal pulses confirm neurogenic claudication from lumbar spinal stenosis, which is a late consequence of lumbar spondylosis.

Finally, remember the surgical urgency hierarchy. Progressive myelopathy requires timely surgical decompression because cord damage can be irreversible. Cauda equina syndrome (saddle anesthesia, urinary retention, bilateral lower extremity weakness) is a surgical emergency. A vignette presenting these findings is testing whether you recognize the need for immediate intervention rather than continued conservative management. The next best step is always emergent MRI followed by surgical decompression.

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