What are the possible causes of perioral paresthesia?

Perioral Paresthesia: Causes and Clinical Approach

Perioral paresthesia results from diverse etiologies including metabolic disturbances (hypocalcemia, copper deficiency), neurologic lesions (medullary infarction, facial nerve pathology), medication toxicity (streptomycin), nutritional deficiencies, and psychological disorders, requiring systematic evaluation based on associated symptoms and temporal pattern. 1, 2, 3, 4, 5

Primary Etiologic Categories

Metabolic and Electrolyte Disturbances

• Hypocalcemia is a classic cause of perioral paresthesia, often accompanied by carpopedal spasm and Chvostek's sign 3
• Copper deficiency can present with perioral paresthesia and burning mouth sensation, particularly in patients with malabsorption or excessive zinc intake (including zinc-containing denture adhesives), and may be associated with pancytopenia 2
• Check serum calcium, magnesium, phosphate, copper levels, and consider urinary zinc if copper deficiency suspected despite normal serum zinc 2

Neurologic Causes

Central Nervous System Lesions

• Lateral medullary infarction (Wallenberg syndrome) produces perioral paresthesia ipsilateral to the lesion, often with contralateral body paresthesia (crossed cheiro-oral syndrome), involving the descending trigeminal sensory tract 4
• This pattern serves as a warning sign for progressive neurologic disability, with three of four reported patients progressing to complete Wallenberg syndrome 4
• Evaluate for additional brainstem signs: dysphagia, dizziness, diplopia, ataxia, Horner syndrome 1, 4

Peripheral Nerve Pathology

• Facial nerve (CN VII) involvement can produce perioral symptoms when the nerve is affected within the temporal bone or at the stylomastoid foramen 1, 6, 7
• Bell's palsy may present with ipsilateral ear or facial pain, taste disturbance, hyperacusis, and dry eye in addition to motor weakness 6
• Distinguish peripheral from central facial weakness: peripheral lesions affect the entire ipsilateral face including forehead, while central lesions spare forehead muscles 6, 7

Trigeminal Nerve Pathology

• Trigeminal neuropathy affects perioral sensation through the maxillary (V2) and mandillary (V3) divisions 1
• MRI with contrast is the primary imaging modality for evaluating trigeminal nerve pathology 1

Medication-Induced Paresthesia

• Streptomycin commonly causes circumoral paresthesias immediately after injection, representing a direct neurotoxic effect 1
• This occurs in addition to streptomycin's more serious ototoxicity and nephrotoxicity risks 1
• Review all medications for neurotoxic potential, particularly aminoglycosides, chemotherapeutic agents, and anticonvulsants 3

Iatrogenic Causes

• Endodontic procedures can cause paresthesia through extravasation of filling material, periapical infection, or direct nerve trauma affecting the inferior alveolar, mental, or lingual nerves 8
• Diagnosis requires panoramic radiography, periapical films, and potentially CT imaging to identify material extravasation or nerve compression 8

Nutritional Deficiencies

• Vitamin B12, folate, and thiamine deficiencies can produce perioral paresthesia as part of a broader peripheral neuropathy pattern 3
• Check complete blood count, B12, folate, and consider methylmalonic acid if B12 deficiency suspected despite normal serum levels 2, 3

Psychological Causes

• Psychogenic oral paresthesia presents with spontaneous tingling, pricking, swelling, or burning sensations without objective findings 5
• Associated with anxiety disorders and depression; responds to antidepressant therapy (fluoxetine 40 mg daily demonstrated effective in case reports) 5
• This remains a diagnosis of exclusion after ruling out organic causes 5

Diagnostic Algorithm

Initial Assessment

1. Temporal pattern: Acute onset (<72 hours) suggests vascular or infectious etiology; gradual onset suggests metabolic, nutritional, or neoplastic causes 6, 7, 3
2. Distribution: Unilateral perioral paresthesia with ipsilateral facial weakness suggests facial nerve pathology; crossed pattern (perioral with contralateral limb) indicates medullary lesion 6, 4
3. Associated symptoms:
   • Facial weakness, taste disturbance, hyperacusis → facial nerve pathology 6
   • Dysphagia, dizziness, ataxia → brainstem lesion 4
   • Carpopedal spasm → hypocalcemia 3
   • Pancytopenia, burning mouth → copper deficiency 2

Laboratory Evaluation

• Serum calcium, magnesium, phosphate 3
• Complete blood count 2
• Vitamin B12, folate, methylmalonic acid 2, 3
• Serum copper and 24-hour urinary zinc if copper deficiency suspected 2
• Thyroid function tests 3
• Hemoglobin A1c for diabetic neuropathy screening 3

Imaging Studies

• MRI brain and brainstem with and without contrast for acute unilateral symptoms, crossed sensory patterns, or any additional cranial nerve involvement 1, 6, 4
• CT temporal bone with thin sections if facial nerve pathology suspected with trauma history 1
• Panoramic radiography and periapical films if dental procedure preceded symptoms 8

Critical Red Flags Requiring Urgent Evaluation

• Multiple cranial nerve involvement excludes isolated peripheral neuropathy and mandates immediate MRI to evaluate for brainstem pathology, skull base lesions, or meningeal disease 1, 6, 7
• Bilateral perioral paresthesia is extremely rare and requires investigation for Lyme disease, sarcoidosis, Guillain-Barré syndrome, or systemic metabolic disturbance 6, 7
• Progressive neurologic symptoms following initial perioral paresthesia may indicate evolving Wallenberg syndrome 4
• Forehead-sparing facial weakness with perioral symptoms suggests stroke rather than peripheral nerve pathology 6, 7

Common Pitfalls to Avoid

• Do not assume all perioral paresthesia is benign or psychogenic; 30% of facial sensory disturbances have identifiable organic causes requiring specific management 6
• Do not overlook medication history, particularly recent streptomycin or aminoglycoside use 1
• Do not miss copper deficiency in patients with malabsorption, parenteral nutrition, or excessive zinc exposure (denture adhesives); serum zinc may be normal despite toxic urinary zinc levels 2
• Do not accept bilateral presentation as idiopathic without extensive workup for systemic disease 6, 7
• Do not delay imaging when crossed sensory patterns or additional neurologic signs are present, as this indicates medullary pathology with potential for progression 4