Temporal arteritis or giant cell arteritis is a systemic disorder of unknown cause characterized by an inflammatory obliterative arteritis particularly, but not exclusively involving branches of the external carotid and ophthalmic arteries.  It is well known as a cause of anterior ischemic optic neuropathy and less well recognized as a cause of ophthalmoplegia.  The most common initial symptom is headache, often accompanied by diffuse aches and pains (polymyalgia rheumatica).²¹¹  Other common symptoms include jaw claudication, fever, anemia, and weight loss. In the study of Vilaseca et al.,²¹² the simultaneous presence of recent onset headache, jaw claudication and abnormalities of the temporal arteries on physical examination had a specificity of 94.8% compared to the histological diagnosis and 100% with respect to the final diagnosis.  

 Solomon and Cappa²¹³ point out that the headache of temporal arteritis may clearly involve more than the temporal area and include pain in the temporal, frontal, vertex and occipital regions. The headache is characterized by gradual onset, progressing to a diffuse, often severe, aching.  The headache may be intermittent, but usually becomes a prominent, if not daily, feature of patients with the disorder.  The headache usually is constant and perceived as superficial in the scalp. There may be exquisite tenderness of the scalp and blood vessels particularly in the temporal region.  The headache is usually worse at night and may be especially aggravated by exposure to cold.¹⁴ 

Sixty‑five percent of patients are women with the average age at onset of 70 (range 50‑85). It is a common disorder and must be actively sought in any headache patient presenting after the age of 50 particularly in those with systemic symptoms. Allen and Studenski²¹⁴ emphasize additional symptoms such as extremity and tongue claudication, ear pain, stroke, and angina as well as systemic panarteritis involving the peripheral nervous system and abdominal or pelvic viscera.

Other ocular complaints with temporal arteritis include tonic pupils from ischemia of the ciliary ganglia²¹⁵ and bilateral uveitic glaucoma which may be on an immunologic basis.¹³⁵  While most attention has been drawn to vascular complications in the distribution of the external carotid and ophthalmic arteries, rarely patients present with vertebral basilar symptomatology.²¹⁶  Among  the protean manifestations of temporal arteritis are those described in the following reports: bilateral carotid artery occlusion,²¹⁷ renal disease,²¹⁸ aortic arch arteritis,²¹⁹ temporal mandibular joint pain,²²⁰ painful facial swelling,²²¹ jaw claudication,²²² and sudden death from arteritis in the coronary arteries, dissection of the aorta and major cerebrovascular accident.²²³ 

An elevated sedimentation rate has been considered by some indispensable in diagnosing temporal arteritis.  Without an elevated sedimentation rate, even in patients with a classic history and clinical findings, the diagnosis might be abandoned without proceeding to a temporal artery biopsy. Nonetheless, it is now estimated that up to 9% of patients with temporal arteritis may have normal sedimentation rates.^224,225  Wong and Korn²²⁴ have identified 37 reported cases of biopsy‑proven temporal arteritis with a normal Westergren sedimentation rate (< 40 mm/hr in patients > than 50 years old).

Up to one third of temporal artery biopsies may be falsely negative, especially when one fails to examine a long segment of vessel by serial sections.  As recently stated, "because of the danger to vision, most authorities would start steroid treatment when they suspect the diagnosis clinically.  Any response other than prompt and striking improvement in clinical well‑being and symptoms, however, speaks against the diagnosis."²²⁶   Raskin¹⁴and Allen and Studenski,²¹⁴  and others believe steroid therapy should start immediately, before confirmation by laboratory and pathologic determinations.  They suggest in very ill patients, intravenous methylprednisolone may be better