What could be causing my tingling in the lower legs and feeling of ataxia, given my history of elevated inflammatory markers?

Evaluation of Tingling in Lower Legs with Ataxia and Elevated Inflammatory Markers

Given your symptoms of lower leg tingling, ataxia-like sensation, and elevated inflammatory markers, you most likely have a peripheral neuropathy affecting sensory and proprioceptive pathways, with inflammatory demyelinating polyradiculoneuropathy (such as CIDP) being a critical consideration that requires urgent evaluation.

Immediate Diagnostic Priorities

Your presentation warrants systematic evaluation focusing on treatable causes that can prevent permanent nerve damage:

Essential Laboratory Testing

• Vitamin B12 with metabolites (methylmalonic acid ± homocysteine) - B12 deficiency causes impaired proprioception and sensory ataxia due to dorsal column and peripheral nerve damage 1, 2
• Serum ferritin - values <50 ng/mL can contribute to neurological symptoms 3
• Serum protein electrophoresis with immunofixation - to detect monoclonal gammopathies that cause neuropathy 2
• Fasting glucose and HbA1c - diabetes accounts for >50% of peripheral neuropathy cases 2
• Copper levels - copper deficiency causes sensory ataxia 4

Critical Physical Examination Findings to Document

• Romberg test - positive result indicates sensory ataxia 1
• Deep tendon reflexes - reduced or absent reflexes suggest peripheral neuropathy 1, 5
• 10-gram monofilament testing plus one additional test (pinprick, temperature, ankle reflexes, or 128-Hz tuning fork vibration) for peripheral neuropathy 3
• Sensory distribution pattern - "glove and stocking" distribution is characteristic 1
• Bilateral pulse palpation - to exclude vascular causes 3

Differential Diagnosis Based on Your Presentation

High-Priority Inflammatory/Immune-Mediated Causes

Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) is particularly important given your elevated inflammatory markers:

• Presents with progressive sensory ataxia, numbness in feet, and gait disturbance 5, 6
• CSF protein is typically elevated (>45 mg/dL) 5
• Anti-contactin 1 IgG4 antibodies found in 2.4% of CIDP patients, strongly associated with sensory ataxia 6
• Critical distinction: 60% of anti-contactin 1 positive patients respond poorly to IVIG but 73% respond well to corticosteroids 6
• Steroid therapy can provide immediate improvement 5

Miller Fisher Syndrome (Guillain-Barré variant):

• Characterized by triad of ataxia, areflexia, and ophthalmoplegia 4, 1
• May require IVIG or plasmapheresis 1

Metabolic/Nutritional Causes

• Vitamin B12 deficiency - causes dorsal column dysfunction and peripheral nerve damage; supplementation is effective when identified 1, 2
• Vitamin E deficiency - associated with cerebellar atrophy and sensory ataxia 4, 1
• Copper deficiency - causes myelopathy with sensory ataxia 4

Demyelinating Diseases

• Multiple sclerosis - can cause ataxia through spinal cord involvement 4
• Neuromyelitis optica and acute disseminated encephalomyelitis - inflammatory demyelinating diseases affecting the cord 4
• Neurosarcoidosis - inflammatory cause with elevated markers 4

Recommended Imaging Strategy

First-Line Imaging

MRI of the spine (cervical, thoracic, lumbar) is the modality of choice:

• Evaluates spinal cord for edema, abnormal signal, compression, and inflammatory lesions 4
• Can detect transverse myelitis, demyelinating plaques, and cord infarction 4
• IV contrast helps identify inflammatory/demyelinating lesions 4

MRI of the brain if central causes suspected:

• Evaluates for demyelinating diseases, cerebellar lesions, and posterior fossa pathology 4
• Particularly important given your ataxia symptoms 4

Electrodiagnostic Studies

• Nerve conduction studies - can confirm peripheral neuropathy and distinguish demyelinating from axonal patterns 1, 5
• Slow motor conduction velocities with prolonged distal latencies suggest CIDP 5
• Absent sensory nerve action potentials indicate sensory nerve involvement 5

Treatment Approach Based on Etiology

If Inflammatory/Immune-Mediated (CIDP, Miller Fisher)

• Corticosteroids - first-line for CIDP, especially if anti-contactin 1 positive (73% response rate) 6
• IVIG - alternative for CIDP, though response may be poor in anti-contactin 1 positive cases (40% response) 6
• Plasmapheresis - option for severe or refractory cases 1

If Nutritional Deficiency

• Vitamin B12 supplementation - effective when deficiency identified 1, 2
• Vitamin E or copper supplementation - as indicated by testing 4, 1

Symptomatic Pain Management (if neuropathic pain develops)

First-line medications include 2:

• Gabapentin 1200 mg daily (38% achieve ≥50% pain reduction)
• Pregabalin 150-600 mg daily
• Duloxetine or other SNRIs
• Amitriptyline or nortriptyline

Important caveat: Pregabalin itself can cause ataxia (15% incidence at 600 mg/day), dizziness (32%), and somnolence (22%) 7, which could worsen your "drunk" sensation.

Critical Pitfalls to Avoid

• Do not delay evaluation - inflammatory causes like CIDP can cause permanent nerve damage if untreated 5, 6
• Do not assume all ataxia is central - spinal cord and peripheral nerve pathology commonly cause ataxia through proprioceptive dysfunction 4, 1
• Do not skip antibody testing - anti-contactin 1 IgG4 guides treatment choice (corticosteroids over IVIG) 6
• Do not overlook treatable causes - B12, copper deficiency, and inflammatory neuropathies are reversible if caught early 1, 2

Prognosis Considerations

• Complete reversal of nerve damage is uncommon even with treatment 2
• Early identification and treatment of inflammatory causes provides best outcomes 5, 6
• CIDP with anti-contactin 1 antibodies shows good corticosteroid response but may have aggressive onset 6