Ulnar Neuropathy vs. Myelopathy Hand

1. Origin

2. Motor Findings

3. Sensory Findings

4. Associated Features

5. Electrodiagnostics

6. Key Clinical Distinguishing Tests

• Finger escape sign → Myelopathy hand (positive), ulnar neuropathy (negative)
• Hoffmann sign / Babinski → Myelopathy only
• Ulnar claw (4th & 5th digits) → Ulnar neuropathy only
• Froment's sign → Ulnar neuropathy only
• NCS/EMG slowing across elbow → Ulnar neuropathy only
• Gait ataxia + bladder symptoms → Myelopathy only

Summary Mnemonic

"Ulnar = Peripheral, Pure, Peripheral signs" Claw + Froment's + Tinel's at elbow + 4th/5th digits only + NCS abnormal

"Myelopathy = Central, Diffuse, UMN" Finger escape + Hoffmann + Bilateral diffuse intrinsics + Gait + Bladder + Normal NCS + Abnormal cervical MRI

Mechanisms of Myelopathy Hand

1. Primary Pathophysiology: Spinal Cord Compression + Ischemia

Mechanical Compression

• Disc herniation, osteophytes, ligamentum flavum buckling, and ossification of the posterior longitudinal ligament (OPLL) reduce the anteroposterior diameter of the canal.
• Dynamic cord flattening occurs with neck flexion/extension, adding repetitive microtrauma.

Vascular Ischemia

• Flattening of the cord elongates the transversely directed terminal branches of the central arteries (arising from the anterior spinal artery).
• These attenuated vessels supply the lateral funiculi, where the corticospinal tracts run — making them selectively vulnerable.
• The anterior columns (supplied by ventral-directed vessels) are relatively spared.
• This explains why corticospinal dysfunction (hand dexterity loss, UMN signs) appears before anterior horn cell or posterior column failure.

Histopathology

• Cystic cavitation, gliosis
• Anterior horn cell dropout (→ LMN component: intrinsic wasting)
• Wallerian degeneration of corticospinal and posterior column fibers
• Severity correlates with degree: mild CSM → lateral funiculus changes only; severe CSM → medial gray, ventral dorsal column, extensive Wallerian degeneration

2. Corticospinal Tract Involvement → Fine Motor Loss + Finger Escape

• The corticospinal tract carries direct corticomotoneuronal projections to intrinsic hand muscles (especially for independent finger movement).
• Ulnar-innervated intrinsics (interossei, hypothenar muscles, medial lumbricals) are the most vulnerable because they receive proportionally more direct corticospinal input for precision tasks.
• With corticospinal tract damage, fine voluntary control of finger adduction and extension is lost first.

Finger Escape Sign (Ono's Sign)

• The patient cannot maintain extension and adduction of all fingers.
• The small and ring fingers spontaneously abduct and flex (ulnar drift into flexion/abduction).
• Mechanism: Loss of corticospinal drive to the palmar interossei (ulnar-innervated, responsible for finger adduction) allows the extensor digiti minimi and extensor digitorum communis (radially innervated, unopposed) to pull the small finger into abduction.
• This is the same principle as Wartenberg's sign in ulnar neuropathy — but here the cause is central, not peripheral.

3. Anterior Horn Cell Damage → Intrinsic Muscle Wasting (LMN Component)

• Intrinsic hand muscle atrophy — particularly interossei and thenar/hypothenar muscles
• Fasciculations may be present
• Hyporeflexia at the affected level (segmental)
• This is why myelopathy hand shows both UMN features (caudal to compression) and LMN features (at the compression level) — a key distinguishing point

4. Grip-and-Release Mechanism

• Requires highly coordinated, rapid alternating activation of flexors and extensors — a corticospinal-dependent function
• Corticospinal tract disruption slows or desynchronizes this reciprocal activation
• The ulnar digits (4th, 5th) are disproportionately affected — they require greater corticospinal precision for isolated flexion/extension

5. Posterior Column Involvement → Proprioception Loss

• Dorsal column compression causes loss of proprioception and vibration sense in the hands
• Contributes to perceived "clumsiness" — patients report difficulty typing, buttoning, writing even without marked weakness
• Romberg's test positive when lower limb proprioception also involved

6. Spinothalamic Tract Involvement → Sensory Changes

• Spinothalamic and corticospinal tracts are laterally located → affected first by lateral cord compression
• Leads to patchy pain/temperature sensory loss
• Unlike radiculopathy, sensory loss is not dermatomal but diffuse and bilateral

Summary Diagram of Mechanisms

Cervical cord compression (spondylosis/disc/OPLL)
            ↓
    Mechanical + Ischemic injury
            ↓
  ┌─────────────────────────────────────────────┐
  │  Lateral funiculus (corticospinal tract)    │  → Loss of fine finger control
  │  affected first (ischemia of lateral art.)  │  → Finger escape sign
  │                                             │  → Grip-release failure
  ├─────────────────────────────────────────────┤
  │  Anterior horn cells at level of lesion     │  → Intrinsic muscle wasting (LMN)
  │                                             │  → Segmental hyporeflexia
  ├─────────────────────────────────────────────┤
  │  Posterior columns                          │  → Proprioception loss
  │                                             │  → Clumsiness, Romberg +ve
  ├─────────────────────────────────────────────┤
  │  Spinothalamic tract                        │  → Diffuse sensory loss
  └─────────────────────────────────────────────┘
            ↓
    MYELOPATHY HAND:
    • Finger escape sign (interossei weakness)
    • Abnormal grip-and-release
    • Intrinsic wasting (bilateral)
    • No dermatomal pattern
    • UMN signs below the level