Spondilosis

01Pathophysiology

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.

02Classification and Clinical Manifestation

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

By Location

By Neurological Involvement

Common Dermatomal Patterns in Radiculopathy

03Diagnostic Workup

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.

04Management and Treatment

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.

05Differential Diagnosis and Distractors

06Traps 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.