What type of brain mass could cause joint pain in a patient over 50 with severe headaches responsive to prednisone (corticosteroid) treatment?

Giant Cell Arteritis (Temporal Arteritis)

In a patient over 50 with severe headaches responsive to prednisone and joint pain, giant cell arteritis is the most likely diagnosis—a systemic vasculitis that characteristically causes both cranial symptoms and musculoskeletal manifestations including polymyalgia rheumatica-like joint pain. 1

Why Giant Cell Arteritis Causes Both Brain and Joint Symptoms

Giant cell arteritis (GCA) is a medium and large-vessel vasculitis affecting the cranial arteries derived from the carotid artery, predominantly occurring in patients over 50 years of age. 1, 2 The disease causes:

• Severe headache (most common symptom) due to inflammation of temporal and other cranial arteries 1, 3
• Joint pain and stiffness occurring in the context of overlapping polymyalgia rheumatica, which affects 40-60% of GCA patients 3, 4
• Constitutional symptoms including low-grade fever, malaise, and weight loss 1

The dramatic response to corticosteroids is pathognomonic—symptoms resolve rapidly within 24-48 hours of initiating prednisone, which strongly reinforces the diagnosis. 1, 4

Clinical Presentation Pattern

Cranial Manifestations

• Localized severe headache, often temporal, is present in the majority of patients 1, 5
• Scalp tenderness and temporal artery tenderness on palpation 3, 5
• Visual symptoms including amaurosis fugax (20%) and permanent vision loss (10%) if untreated 1
• Jaw claudication from involvement of facial arteries 3

Musculoskeletal Manifestations

• Proximal muscle pain and stiffness affecting shoulders, neck, and hip girdle bilaterally 3, 4
• Morning stiffness lasting more than 45 minutes 3
• Joint pain without true arthritis—pain is typically in muscles and periarticular structures rather than synovitis 4

Laboratory Hallmarks

• Markedly elevated ESR (often >50 mm/hr, frequently >100 mm/hr) 1, 3, 4
• Elevated CRP 3, 5
• Moderate anemia of chronic disease may be present 4

Diagnostic Approach

Temporal artery biopsy remains the gold standard for diagnosis and should be performed after initiating corticosteroids—treatment must not be delayed while awaiting biopsy, as the pathologic findings remain positive for up to 2 weeks after starting steroids. 1, 5, 6

The diagnostic sensitivity of unilateral biopsy ranges from 67-97%, and bilateral biopsies increase yield by an additional 5-10%. 1

Alternative Imaging When Biopsy is Negative or Unavailable

• Color duplex ultrasonography showing halo sign (vessel wall edema) 3, 5
• MRI or PET scan demonstrating large-vessel inflammation 3, 5

Treatment Algorithm

Immediate Management (Do Not Delay)

For patients with visual symptoms or neurologic signs (neuro-ophthalmic emergency): 6

• Initiate IV methylprednisolone 250 mg every 6 hours for 3 days 6
• Follow with oral prednisone 80 mg daily (or 1 mg/kg) for 4-6 weeks 6

For patients without acute visual/neurologic symptoms: 4, 6

• Begin oral prednisone 40-60 mg daily 1, 4
• Symptom relief should occur within 24-48 hours, reinforcing the diagnosis 4

Tapering Strategy

• After ESR normalizes (typically 2-4 weeks), taper prednisone by 10 mg per month 6
• Monitor ESR, CRP, and clinical symptoms at each visit 5, 6
• Most patients require 2-3 years of therapy to avoid relapse 4, 6
• Approximately 50% of patients experience at least one relapse during tapering 3

Adjunctive Therapies

• Tocilizumab (IL-6 inhibitor) is FDA-approved for GCA and should be considered for initial therapy in addition to glucocorticoids, particularly in patients at high risk for corticosteroid complications 3
• Methotrexate may be considered as a steroid-sparing agent in patients with frequent relapses or significant corticosteroid-related morbidity 2, 3, 5

Mandatory Prophylaxis

• Calcium and vitamin D supplementation for bone protection 6
• PPI or H2-blocker for peptic ulcer prophylaxis 6
• PCP prophylaxis if high-dose corticosteroids continue beyond 12 weeks 1

Critical Pitfalls to Avoid

Never withhold corticosteroids while awaiting biopsy results—permanent vision loss can occur within hours to days if treatment is delayed. 5, 6 The window for preventing blindness is extremely narrow.

Do not rely solely on ESR—approximately 10% of biopsy-proven GCA cases have normal or low ESR at presentation. 5 Clinical suspicion in the appropriate age group with characteristic symptoms warrants empiric treatment.

Recognize atypical presentations including fever of unknown origin, persistent cough (respiratory involvement occurs in <10% of cases), or predominantly constitutional symptoms without headache. 1, 5 These can delay diagnosis by weeks to months.

Monitor closely during steroid taper—relapse rates are high (up to 50%), and symptoms may recur with even small dose reductions. 3, 5 Any return of symptoms or rising inflammatory markers requires dose escalation.

Why Other Brain Masses Don't Cause This Pattern

Metastatic disease, primary brain tumors, and infections causing brain masses do not respond dramatically to corticosteroids and do not cause the characteristic combination of severe headache with polymyalgia-like joint symptoms and markedly elevated inflammatory markers. 1

Neurocysticercosis can cause eosinophilic meningitis with headache but occurs in younger patients with travel to endemic areas and does not cause joint pain. 1

The triad of age >50 + severe headache + joint pain + dramatic steroid response is virtually pathognomonic for giant cell arteritis. 1, 3