Physiology · Year 1 · from Physiology
Case 1: Diabetic Peripheral Neuropathy - Sensory Loss and Pain
Clinical Image
Source: Wikimedia Commons - Neuropathic heel ulcer - CC BY-SA 3.0
Patient Presentation
A 62-year-old male with a 20-year history of poorly controlled type 2 diabetes mellitus presents for evaluation of numbness, tingling, and burning pain in his feet that has progressively worsened over 3 years. He describes the sensation as "walking on cotton" and has difficulty feeling the floor. The burning pain is worse at night and disturbs his sleep. He has noticed small wounds on his feet that he does not remember getting. His wife found a large blister on his heel from ill-fitting shoes that he never felt. He also reports difficulty maintaining balance in the dark.
Demographics
- Age: 62 years
- Sex: Male
- Past Medical History: Type 2 DM x 20 years, HbA1c 9.8%, hypertension, hyperlipidemia
Chief Complaint
Progressive numbness, tingling, burning pain in feet, and unnoticed wounds
Physical Examination
- General: Obese male in no acute distress
- Feet examination:
- Dry, cracked skin with absent hair on lower legs
- 2 cm ulcer on right heel, Wagner grade 2 (deep to tendon level, no infection)
- Calluses over metatarsal heads bilaterally
- Deformed toes (claw toe deformity from motor involvement)
- Neurological:
- Sensory: Loss of light touch, pinprick, and temperature sensation in stocking distribution to mid-calf; severe loss of vibration sense at toes, reduced at ankles
- 10-g monofilament test: Unable to perceive at 6/10 sites on each foot
- Proprioception: Impaired at great toes
- Motor: Mild weakness of toe extensors and intrinsic foot muscles
- Reflexes: Absent ankle jerks, 1+ knee jerks
- Gait: Wide-based, positive Romberg test (worsens with eyes closed)
Workup
- HbA1c: 9.8% (poor long-term control)
- Nerve conduction studies: Reduced sensory nerve action potential amplitudes in sural nerve (axonal pattern); mildly reduced conduction velocities
- EMG: Chronic denervation changes in intrinsic foot muscles
- Semmes-Weinstein monofilament: Unable to perceive 10-g filament (high risk for ulceration)
- Ankle-brachial index: 0.95 (rules out significant peripheral artery disease)
- Wound assessment: No signs of osteomyelitis clinically (MRI if concern)
Diagnosis
Diabetic Peripheral Neuropathy (distal symmetric polyneuropathy) with neuropathic pain and loss of protective sensation; Wagner grade 2 neuropathic foot ulcer
Treatment
- Glycemic control optimization: Refer to endocrinology, adjust medications, goal HbA1c <7%
- Neuropathic pain management:
- First-line: Duloxetine (SNRI) or pregabalin/gabapentin
- Alternatives: Tricyclic antidepressants (amitriptyline), topical capsaicin, lidocaine patches
- Foot ulcer management:
- Offloading: Total contact cast or removable cast walker
- Wound care: Debridement, moist wound healing
- Infection monitoring: Watch for signs of cellulitis, osteomyelitis
- Foot care education:
- Daily foot inspection (use mirror if needed)
- Proper footwear (protective, well-fitted shoes)
- Never walk barefoot
- Regular podiatry visits
- Fall prevention: Physical therapy for balance, home safety assessment
- Cardiovascular risk reduction: Blood pressure and lipid control
Physiological Principles Demonstrated
- Small vs. large fiber neuropathy: Diabetic neuropathy often affects small fibers (C fibers for pain/temperature, autonomic fibers) early, causing burning pain and autonomic dysfunction. Large fiber involvement (Aβ for vibration/touch, Aα for proprioception) causes numbness and ataxia.
- Neuropathic pain mechanism: Paradoxically, nerve damage can cause pain. Mechanisms include ectopic firing of damaged nociceptors, central sensitization, loss of inhibitory interneurons (gate control disruption), and ephaptic transmission (cross-talk between damaged fibers).
- Negative vs. positive sensory symptoms: Negative symptoms (numbness, loss of sensation) result from nerve fiber loss. Positive symptoms (tingling, burning, electric shocks) result from abnormal spontaneous activity in damaged fibers.
- Loss of protective sensation: The inability to perceive pain from injury removes the protective warning system. Patients with loss of 10-g monofilament perception have a 10-fold increased risk of foot ulceration.
- Stocking-glove distribution: The longest nerve fibers (to toes/fingers) are most vulnerable to metabolic insults, explaining why symptoms begin distally and progress proximally in a length-dependent pattern.
- Romberg sign: Proprioceptive loss from large fiber damage impairs position sense. With eyes closed (removing visual compensation), patients become unsteady, indicating reliance on vision to maintain balance.