Is the presentation of symmetrical sensory deficits in both proximal and distal limbs, with loss of vibration and proprioception, and less prominent loss of pain and temperature, characteristic of Chronic Inflammatory Demyelinating Polyneuropathy (CIPD)?

Sensory Deficits in Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

The presentation of symmetrical sensory deficits in both proximal and distal limbs, with predominant loss of vibration and proprioception leading to sensory ataxia, and less prominent loss of pain and temperature sensation, is characteristic of classic CIDP. 1, 2

Clinical Sensory Features of CIDP

• CIDP typically presents with symmetrical sensory deficits affecting both proximal and distal limbs, unlike length-dependent neuropathies that primarily affect distal regions 2
• Large-fiber sensory abnormalities (vibration and proprioception) predominate in classic CIDP, often leading to sensory ataxia and impaired coordination 3
• Small-fiber sensory abnormalities (pain and temperature sensation) are generally less prominent in typical CIDP but can occur in atypical variants 3, 1
• Sensory deficits in CIDP often accompany motor symptoms, though pure sensory variants can occur 4

Pathophysiological Basis

• The sensory manifestations in CIDP result from inflammatory demyelination of peripheral nerves, particularly affecting large myelinated sensory fibers 3
• Demyelination predominantly affects the distal nerve terminals and nerve roots in typical CIDP, where the blood-nerve barrier is anatomically deficient 2
• Loss of proprioception and vibration sensation reflects the preferential involvement of large-diameter myelinated fibers that carry these sensory modalities 1
• The relative preservation of pain and temperature sensation in classic CIDP reflects the lesser involvement of small-diameter fibers that transmit these sensations 3

Distinguishing Features from Other Neuropathies

• Unlike Guillain-Barré syndrome (GBS), which has an acute onset reaching maximum disability within 2-4 weeks, CIDP has a progressive or relapsing course over at least 2 months 5
• In contrast to drug-induced neuropathies (like bortezomib or thalidomide-induced), which typically present with a length-dependent "stocking-and-glove" distribution, CIDP affects both proximal and distal regions 5
• CIDP can be distinguished from pure motor variants (PM-CIDP) where sensory conductions are normal and patients have no sensory signs or symptoms 6

CIDP Variants and Sensory Presentations

• Typical CIDP presents with symmetric involvement of proximal and distal portions of limbs with both sensory and motor symptoms 1
• The MADSAM variant (Multifocal Acquired Demyelinating Sensory and Motor Neuropathy) presents with asymmetric or multifocal sensorimotor deficits rather than the symmetric pattern seen in typical CIDP 7
• Pure sensory CIDP variants exist but are less common than the classic sensorimotor presentation 4
• Distal Acquired Demyelinating Symmetric (DADS) variant shows predominantly distal sensory involvement 1

Clinical Implications

• The presence of prominent proprioceptive and vibratory sensory loss leading to sensory ataxia should prompt consideration of CIDP in the differential diagnosis 3
• Sensory deficits in CIDP typically respond to immunomodulatory treatments such as intravenous immunoglobulin, plasma exchange, or corticosteroids 3, 4
• Objective improvement in sensory function should be used as one measure to evaluate treatment response in CIDP 4
• Regular monitoring of sensory deficits is essential to assess disease progression and treatment efficacy 3

Common Pitfalls in Diagnosis

• Failing to recognize that sensory symptoms in CIDP can affect both proximal and distal regions, unlike the classic length-dependent pattern seen in many other neuropathies 2
• Overlooking the significance of proprioceptive and vibratory sensory loss as cardinal features of CIDP 3
• Misinterpreting asymmetric sensory deficits as excluding CIDP, when they may represent the MADSAM variant 7, 1
• Not recognizing that sensory symptoms may evolve over time, with some patients initially presenting with predominantly motor symptoms before developing sensory deficits 6