In individuals with GCA, the most commonly presented conditions include headache, fever, bruits, tenderness and sensitivity of the scalp, claudication of the jaw, claudication of the jaw and necrosis, reduction in visual acuity, acute visual loss, diplopia, acute tinnitus and polymyalgia rehumatica in 50% of the cases [7].

With the inflammation, the supply of blood to the eye will be affected and this is the main cause of blurred vision and sudden blindness.

In most cases involving the eye, arteritic anterior ischemic optic neuropathy is caused due to the involvement of the ophthalmic artery. Since loss of vision in both eyes can happen abruptly, this case is regarded as a medical emergency.

Palpitations in the head denote temporal arteries regardless of presence of pulsation. In many cases, the temporal area remains tender. All around the body, decreased pulses may be found. During fundal examinations, evidence of ischemia may be noted [8].

Some of the laboratory tests that must be carried out include:

• Platelets count (may be elevated)
• C-reactive protein tests ( this may also be elevated)
• ESR ( Erythrocyte sedimentation rate will show readings of >6omm/hour
• Liver function tests (this will often show raised alkaline phosphatase)

Oral corticosteroids are highly and rapidly effective in temporal arteritis but are often associated with adverse effects.

Full recovery is the common result when there is adequate and prompt therapy. In recent years the reduced rate of neuro-ophthalmologic complications show a marked improvement in the recognition and treatment of the condition [9]. This explains why blindness can now be regarded as a rare complication.

If left untreated, the prognosis for individuals with this condition is very poor. Blindness and death is very common resulting from stroke, myocardial infarction and dissecting aortic aneurysm.

The specific cause of these autoimmune disorders is yet to be documented. Parvovirus B19 and mycoplasma infection have been denoted as possible causes but this is yet to be proven [4].

Between 1950 and 1975 in the USA, the distribution of GCA in Minnesota increased from 5.1 to 17.4 cases per 100,000 individuals each year in adults aged 50 years and above. The increase was attributed to improved rate of accurate diagnosis and clinical awareness [2]. By January 1, 1975 the prevalence was placed at 133 cases per 100,000 adults aged 50 and above.

Internationally, there have been few publications of epidemiological studies but the incidence rates do not vary greatly within the defined susceptible age bracket. The highest incidence can be traced to Scandinavia where 23-33 people per 100,000 are affected amongst people aged 50 and above.

The prevalence is heavily dependent on the number of individuals aged 50 years and above. The average age of onset is 75 years. Therefore, countries where there is lower life expectancy show a lower prevalence.

Although GCA can lead to MI, stroke or death it is yet to be associated with a statistically significant increase in any of these. GCA leads to death in generally 2% of cases. As is to be expected, the severity of the vasculitis and topographic extent is greater in fatal cases than what is obtainable in nonfatal cases.

It is however, difficult to quantify the number of patients who died indirectly or directly due to extensive use of corticosteroids [3].

There has not been any proven racial predisposition to GCA. However, the epidemiologic studies are limited due to the fact that they have mostly been performed on predominantly Caucasian population. This can signify that the condition is more common amongst this race.

The ration of occurrence in sexes is 3.7:1 against females. The average age for the onset of the condition is 75 years. The condition is the most common systemic vasculitis affecting elderly patients. It is rarely described in individuals younger than 40 years of age.

The condition is generally a disease affecting cellular immunity. The CD4+ T helper cells reacting to an antigen presented by macrophages mediates vasculitic damage. The internal elastic lamina is affected by the primary inflammatory response. The hallmark of GCA is the multinucleated giant cells and these may contain elastic fiber fragments. The antigen that triggers the condition is still not known but elastin is suspected by experts [5].

In many patients, the superficial temporal artery is involved. This offers a convenient biopsy site. However the topographic distribution of the condition extends towards the aortic arch and its branches. This reflects its predilection for the internal elastic lamina.

Since intracranial arteries do not have an internal elastic lamina, GCA does not cause widespread intracranial cerebral vasculitis. As well as the vertebral and carotid arteries, GCA involves cervicocephalic arteries. Below is a look at how the condition affects arteries [6].

• Internal, external and common internal carotid artery involvement occurs extracranially. On rare occasions, proximal intracranial segments get affected.

• The involvement of the pulmonary artery has been described in many cases.

• Ischemic mononeuropathies, crural infarction, renal infarction and intestinal infarction are common complications documented when the femoral, iliac, renal, mesenteric and the descending aorta arteries are affected. This is less often described.

• Vertebral arteries are frequently involved and the superficial temporal arteries are affected in fatal cases. Basal artery involvement is rare however.

• The posterior ciliary and ophthalmic arteries are intraorbital branches that are commonly affected.

• Although vertebral arteritis is extracranial, it may extend intracranially beyond the dural penetration.

• Coronary arteritis may lead to MI (myocardial infarction). This happens when the GCA involves the ascending aorta leading to aortic rupture.

• A characteristic angiographic pattern of vasculitis is produced when there is involvement of the subclavian, axillary and proximal brachial arteries.

There are no guidelines for prevention of temporal arteritis.

Temporal Arteritis, often known as Giant-cell arteritis, GCA or cranial arteritis is a disorder that affects the blood vessels [1]. It is an inflammatory disease which mostly involves the large and medium arteries located in the head.

The branch of the external carotid artery is the most affected. The disorder is a form of vasculitis. Blindness is the most serious complication of GCA but this complication can be easily corrected using corticosteroids.

The condition derives its name from the inflammatory cell involved as displayed in a biopsy. Temporal arteritis and giant-cell arteritis are often used interchangeably due to the temporal artery’s frequent involvement.

However, the condition can affect larger vessels like the aorta, leading to giant cell aortitis. The condition is equally known as cranial arteritis and Horton’s disease.

Patients need to be fully aware of the seriousness of reoccurring symptoms. This will help them seek for quick medical attention when they come back. Secondly, the importance of adhering strictly to the steroid dose schedule must be emphasized [10].

With the right administration of steroids, the disease can be treated in 3 years. When necessary, dietary restrictions and other interventions will help reduce the incidence of adverse effects arising from the intake of steroids a great deal.

Make sure you don’t stop taking the steroids abruptly. Missing out on a dose may not trigger off anything but as soon as the body gets used to taking the steroids, stopping suddenly will bring about serious bouts of withdrawal effects in just a couple of days.
Unless your doctor says so, taking anti-inflammatory painkillers while taking the painkillers must be avoided. Taking these two at once may lead to the development of stomach ulcers. Therefore, apart from low-dose aspirin, you have to avoid other anti-inflammatory painkillers.

While on steroids, don’t forget to carry your steroid card regularly. This card details your condition, dosage and other valuable information that will come in handy in the event of an emergency.

Your dosage of steroids will be increased if you become ill with other conditions or undergo surgery. This is to provide your body with the right dosage of steroid needed to properly combat physical stress.

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