Cervical Spondylotic Myelopathy — Pathophysiology & Surgery

Overview & Pathophysiology

Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction in adults over 55 years and the most common cause of acquired non-traumatic spinal cord compromise worldwide. It results from chronic mechanical compression of the cervical spinal cord by degenerative spondylotic changes — osteophytes, disc herniations, buckled ligamentum flavum, facet hypertrophy, and in severe cases, ossification of the posterior longitudinal ligament (OPLL). The natural history is variable but typically progressive, and CSM represents a major source of disability that can be mitigated or reversed by timely surgical decompression.

Pathophysiology — mechanical and vascular mechanisms: (1) Static compression: the anterior spondylotic bar (disc-osteophyte complex) and posterior hypertrophied ligamentum flavum reduce the anteroposterior diameter of the cervical canal; a canal AP diameter <13 mm = relative stenosis; <10 mm = absolute stenosis; the `Torg-Pavlov ratio` (ratio of the spinal canal AP diameter to the vertebral body AP diameter on lateral X-ray) <0.8 indicates developmental canal narrowing predisposing to CSM; (2) Dynamic compression: in addition to static compression, neck movement — particularly extension — causes further narrowing (ligamentum flavum buckles inward; disc herniates further; intervertebral foramina narrow); hyperlordotic extension posture causes maximal cord compression; flexion may cause cord traction and stretch; (3) Vascular compromise: compression of the anterior spinal artery and the radicular arteries causes cord ischaemia, contributing to the neuronal damage independently of direct mechanical compression
Pathological changes in the cord: Wallerian degeneration of the corticospinal tracts (upper motor neuron signs in the lower limbs); degeneration of the posterior columns (proprioception loss, Romberg positive); anterior horn cell loss at the level of compression (lower motor neuron signs in the upper limbs at the affected level); the typical CSM pattern is therefore: lower limb UMN signs (spasticity, hyperreflexia, Babinski, clonus) + upper limb LMN signs (wasting, weakness, hyporeflexia at the compressive level) + sensory loss (impaired proprioception and vibration)
OPLL (Ossification of the Posterior Longitudinal Ligament): a separate but closely related entity — the PLL undergoes heterotopic ossification, creating a hard bony mass that compresses the spinal cord anteriorly; OPLL is most common in East Asian populations (particularly Japanese — prevalence 2–4%); higher risk of catastrophic cord injury with relatively minor trauma (minor fall → quadriplegia); segmental, continuous, mixed, or circumscribed subtypes; management is particularly challenging as anterior decompression (discectomy/corpectomy) risks dural tear (the dura may be adherent to or incorporated within the OPLL)

Clinical Features & Examination

Feature / Sign	Description	Anatomical Basis
Gait disturbance	Wide-based spastic gait; difficulty walking on uneven surfaces; frequent falls; difficulty climbing stairs; the first and most common presenting feature of CSM — often described by patients as `clumsy walking` or `unsteadiness`	Corticospinal tract compression (UMN); posterior column dysfunction (proprioception)
Hand clumsiness	Difficulty with fine motor tasks — buttoning, writing, chopsticks, typing; hand weakness; intrinsic hand muscle wasting in severe cases; `myelopathic hand` — characterised by loss of rapid alternating hand movement (rapid grip-release test)	Anterior horn cell compression at C6-C8 level (LMN at level of compression); corticospinal tract dysfunction (UMN) at all sublesional levels
Lhermitte`s sign (electric shock phenomenon)	Electric shock-like sensation radiating down the spine and into the limbs on neck flexion; caused by stretch of a compressed cord and sensitised posterior columns	Posterior column/dorsal funiculus irritability; cord traction on flexion at the spondylotic level
Hyperreflexia (lower limbs)	Exaggerated knee and ankle jerks; upgoing plantar response (Babinski sign); clonus; Hoffman`s sign in the hand (flicking the terminal phalanx of the middle finger causes reflex flexion of the index finger and thumb — indicates UMN lesion at or above the level tested)	Corticospinal tract compression — UMN signs below the level of lesion
Hoffman`s sign	Flicking or snapping the terminal phalanx of the middle finger; positive if the index finger and thumb involuntarily flex in response; highly specific for a cervical cord UMN lesion; bilateral Hoffman`s is particularly significant	The most reliable clinical sign for cervical cord UMN pathology; should be routinely tested in any patient with hand or gait symptoms
Inverted supinator reflex	Tapping the brachioradialis tendon (at C5-6) elicits finger flexion rather than the normal wrist/elbow flexion; indicates a cord lesion at C5-6 — the LMN at C5-6 is disrupted (absent normal brachioradialis response) and the UMN to C7-C8 (finger flexors) is released	Pathognomonic for C5-6 cord lesion; combination of LMN loss at the level + UMN release below it; requires both LMN and UMN involvement at the same level
Bladder dysfunction	Urinary urgency, frequency, hesitancy; retention or incontinence in advanced cases	Involvement of descending autonomic pathways; usually a late feature; poor prognostic sign

Functional Grading — Nurick & Modified JOA

Nurick Grade	Description	Clinical Implications
Grade 0	Root signs; no cord involvement; asymptomatic cervical spondylosis	Conservative management; close monitoring
Grade 1	Signs of cord involvement but no difficulty walking	Conservative or surgical depending on progression and severity
Grade 2	Slight difficulty walking; can perform full-time employment	Surgical intervention should be considered — further deterioration likely without surgery
Grade 3	Difficulty walking; requires assistance or aids; unable to work full-time	Surgical decompression recommended — significant disability; good potential for improvement
Grade 4	Can walk only with assistance; severe disability	Urgent surgical decompression; prognosis guarded — improvement possible but outcomes less predictable than earlier intervention
Grade 5	Chairbound or bedbound; unable to walk	Surgical decompression still indicated to prevent further deterioration and for pain relief; limited functional recovery expected

Modified Japanese Orthopaedic Association (mJOA) score: the most widely used quantitative outcome measure for CSM; scores upper limb motor function (0–4), lower limb motor function (0–4), upper limb sensation (0–2), lower limb sensation (0–2), and bladder function (0–3); maximum score 18 (normal); mild CSM = 15–17; moderate = 12–14; severe = <12; the recovery rate (Hirabayashi formula) = (post-op mJOA − pre-op mJOA) / (18 − pre-op mJOA) × 100%; a recovery rate >50% is considered a good surgical outcome

Investigations

MRI cervical spine (gold standard): the primary investigation for CSM; demonstrates the level(s) and extent of cord compression; T2-weighted sequences show high signal within the cord at the compression level — `myelomalacia` (T2 hyperintensity) indicates cord damage and is associated with worse prognosis; T1 hypointense signal within the cord (rare) indicates severe irreversible myelomalacia; a `snake eye` appearance (bilateral T2 hyperintensity in the anterior horn cells on axial T2 MRI) indicates ischaemic anterior horn cell damage and portends poor recovery; sagittal T2 and STIR sequences for cervical alignment, cord signal, and multi-level disease assessment; axial T2 for central canal diameter and cord-canal ratio
Plain X-ray lateral cervical spine: assesses cervical alignment (kyphosis vs lordosis — critical for surgical planning); Torg-Pavlov ratio (<0.8 = narrow canal); osteophytes; disc space height loss; dynamic (flexion-extension) views for instability; OPLL visible as a dense line behind the vertebral bodies
CT cervical spine: optimal for bony detail; OPLL characterisation (size, type, extent); canal diameter on CT; foraminal stenosis; bony facet hypertrophy; pre-operative planning for anterior vs posterior approach
Electrodiagnostics: nerve conduction studies (NCS) and electromyography (EMG) to exclude peripheral nerve disease (carpal tunnel syndrome, peripheral neuropathy) contributing to hand symptoms; somatosensory evoked potentials (SSEPs) and motor evoked potentials (MEPs) for intraoperative monitoring and pre-operative functional assessment

Surgical Management — Approach Selection

Approach	Procedure	Indications	Advantages / Disadvantages
Anterior — ACDF	Anterior cervical discectomy and fusion (ACDF); Smith-Robinson anterior approach; disc removal + osteophyte excision + interbody fusion (cage + plate); 1–3 level disease predominantly	1–3 level CSM with preserved or lordotic alignment; anterior disc/osteophyte causing compression; normal or mild kyphosis; best for cord compression anterior to the cord	Direct anterior decompression; excellent fusion rates with modern cages; restores disc height; indirect foraminotomy; DISADVANTAGE — adjacent segment disease; dysphagia post-op; recurrent laryngeal nerve (C2-C5 left-sided approach preferred) or superior laryngeal nerve injury; limited to 3 levels (more = higher non-union risk)
Anterior — corpectomy	Anterior cervical corpectomy and fusion (ACCF); vertebral body removal + OPLL resection + strut graft + plate; typically 1–2 vertebral body levels	OPLL spanning multiple disc levels; retrovertebral body compression not accessible by ACDF; multi-level anterior disease >3 levels	Allows resection of OPLL and retrovertebral pathology; DISADVANTAGE — highest anterior approach morbidity; strut graft subsidence/extrusion; pseudarthrosis risk higher than ACDF; C5 palsy risk (C5 nerve root stretching after decompression)
Posterior — laminectomy ± fusion	Bilateral laminectomy (with or without lateral mass screws and rod fixation); indirect cord decompression by allowing cord to drift posteriorly away from anterior pathology	Multi-level CSM (>3 levels); cervical lordosis preserved (cord can drift posteriorly if lordosis maintained — laminectomy alone ineffective in kyphosis); cannot use if significant kyphosis present (cord cannot drift posteriorly)	Wide decompression; less surgical risk than multi-level anterior; DISADVANTAGE — post-laminectomy kyphosis (in up to 30% without fusion); C5 palsy risk; reduced range of motion; indirect (cord must drift posteriorly to decompress — does not directly address anterior osteophytes)
Posterior — laminoplasty	Expansion of the spinal canal by `opening` the laminae — either open-door (Hirabayashi — one side completely cut, contralateral side greenstick — laminae hinged open) or French door (central split, laminae hinged bilaterally); preserves the laminae (unlike laminectomy); maintains some posterior tension band	Multi-level CSM with preserved lordosis; OPLL; avoidance of post-laminectomy kyphosis; alternative to laminectomy in younger patients; particularly popular in Japan for OPLL	Avoids laminectomy membrane (pseudomeningocele); maintains some posterior stability; DISADVANTAGE — `closure` of the door (loss of opening) in some patients; C5 palsy; axial neck pain; reduced range of motion; does NOT address kyphosis; may not provide adequate decompression in OPLL involving >60% of the canal
Combined anterior-posterior	360° circumferential decompression — anterior decompression + posterior stabilisation (laminectomy/laminoplasty + lateral mass fusion); or posterior correction of kyphosis + anterior decompression	Severe multi-level disease with significant kyphosis; OPLL with >60% canal involvement; failed prior anterior or posterior surgery; cervical kyphosis requiring correction	Maximum decompression and stabilisation; corrects kyphosis and addresses anterior compression; DISADVANTAGE — highest morbidity; usually staged; reserved for complex cases

Exam Pearls

CSM: most common cause of spinal cord dysfunction in adults >55 years; chronic mechanical compression from degenerative changes (disc, osteophytes, ligamentum flavum, facet hypertrophy); static + dynamic + vascular mechanisms
Clinical pattern: lower limb UMN signs (spastic gait, hyperreflexia, Babinski, clonus) + upper limb LMN signs at level of compression (wasting, hyporeflexia) + posterior column loss (proprioception, vibration, Romberg+)
Hoffman`s sign: flick middle finger terminal phalanx → index + thumb flex = positive UMN cervical cord lesion; bilateral Hoffman`s = highly significant; most reliable clinical sign for CSM
Inverted supinator reflex: absent brachioradialis + finger flexors fire = C5-6 cord lesion pathognomonic; combined LMN at level + UMN below
MRI: T2 cord hyperintensity = myelomalacia (associated with worse prognosis); `snake eye` sign (bilateral anterior horn T2 hyperintensity on axial) = ischaemic LMN damage, poor recovery prognosis; T1 hypointensity = severe irreversible damage
Torg-Pavlov ratio: canal AP / vertebral body AP on lateral X-ray; <0.8 = developmentally narrow canal; predisposes to CSM; absolute canal <13 mm = relative stenosis; <10 mm = absolute stenosis
mJOA score: maximum 18; mild ≥15; moderate 12–14; severe <12; recovery rate (Hirabayashi) = (post-pre)/(18-pre) × 100%; >50% = good outcome
Anterior vs posterior: anterior (ACDF/corpectomy) = 1–3 levels, anterior pathology, lordosis preserved, best direct decompression; posterior (laminectomy/laminoplasty) = multi-level (>3), lordosis preserved (cord must drift back), OPLL, avoid if kyphosis present
OPLL: ossification of PLL; East Asian patients; higher cord injury risk with minor trauma; dural adhesion risk during anterior corpectomy; laminoplasty preferred by many Japanese surgeons; complex anterior resection risks dural tear
C5 palsy: post-decompression deltoid/biceps weakness; occurs after anterior or posterior decompression; thought to be from tethering of C5 root when cord drifts posteriorly; usually resolves over weeks to months; more common after laminectomy/laminoplasty

Cervical Spondylotic Myelopathy — Pathophysiology & Surgery

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