Diagnosis of GCA is critical because delay can cause irreversible loss of vision in patients. Also, it can be challenging in those without the classic symptoms, such as headaches. The American College of Rheumatology criteria for the classification of GCA is not very specific in diagnosing clinical cases. Therefore, vascular imaging (ultra- sonography, computed tomography, magnetic resonance imaging, or positron emission tomography), temporal artery biopsy (TAB), or a combination of these tests help with a definitive diagnosis. (7)
GCA-related stroke is defined as if the stroke showed GCA or occurred between the onset of symptoms and four weeks after the beginning of treatment. A population-based study proved that GCA-related stroke mainly affects the vertebrobasilar territory and usually occurs in older men with a history of vascular risk factors. (8) Through cardiovascular risk factors, only having diabetes mellitus was significantly higher in people with stroke during follow-up. (6)As a point to consider in our case, stroke affects the internal carotid region, and diabetes was the main cardiovascular risk factor. In another study, patients with GCA who experience recent ophthalmic ischemic symptoms and present with low inflammatory variables were more susceptible to stroke. (9) Patients with stroke in vertebrobasilar regions had more commonly irreversible visual loss due to involvement of ophthalmic artery branches derived from the internal carotid than the other GCA patients. (10) In confirmation of the previous study, our patient had no significant change in visual acuity after treatment.
The GCA symptoms detected at the time of the CVA were: headaches, signs of polymyalgia rheumatica, and acute anterior neuropathy. Acute-phase reactants were increased by (83%) at the stroke event. At the time of the stroke, 22% of patients were on antiplatelet therapy. Of the 18 patients, only 5 had Magnetic resonance brain imaging that indicated ischemic lesions located in the carotid territories. Vascular stenosis or occlusion was observed in vertebral arteries in 11 individuals, with bilateral involvement in 6 patients; basilar artery in 2 cases, circle of Willis in 2 persons, and internal carotid in 1 patient. (6). According to the information mentioned in our case had a severe recent headache and sudden visual loss with moderately elevated CRP and ESR. Also, the brain's parenchymal territory involvement and the kind of vascular stenosis are rare and unusual.
Moghaddasi M et al. reported a 67-year-old man who was finally diagnosed with giant cell arteritis. The patient presented with a recently temporal headache, cranial nerves palsy, elevated ESR, and severe internal carotid artery stenosis. However, the biopsy of the temporal artery was normal. (11)A case report presented a 59-year-old man with multiple strokes who the conventional angiogram demonstrated stenosis of bilateral carotid and vertebral vessels. (12)Another case was presented with multiple acute infarctions in the territory of the vertebrobasilar arteries with the left vertebral artery stenosis in the MRI and an increase in inflammatory markers. (13). The cohort of all residents of Olmsted County, Minnesota, in whom GCA was diagnosed and followed up in the duration of 50 years, demonstrated that the incidence of large artery stenosis is 13%. (14). Several studies demonstrated that ischemic cerebrovascular attacks are mainly linked with the occlusion or stenosis of the extradural vessels instead of the intradural vasculitis. (15, 16) Siemonsen et al. assessed patients suspicious of GCA by using MRI protocol focused on evaluating the intradural arteries. Ten out of 25 cases presented with vessel wall enhancement (VWE) of the intradural ICA; eventually, all these cases were positive for GCA. Moreover, the involvement of the intradural vessels did not associate with the cerebral ischemic lesions. (17)
Few case reports published vertebral and carotid artery dissection and pseudo dissections with severe cerebral ischemic signs and symptoms without GCA. (18–22)A case report presented a 56-year-old man with arthralgia, weight loss, and progressing minor neurological symptoms over one month. Neurosoncological evaluation indicates occlusion in both internal carotid arteries (ICA) and intracranial segments of the left vertebral artery (VA) and the famous hypoechoic halo sign in both superficial temporal arteries. They confirmed GCA diagnosis by inflammatory markers and biopsy. During the treatment, brain MRI suggests watershed infarcts and intracranial dissections of both ICA and left VA. (18) In another report, Zheng X et al. presented a case that ICA dissection was the underlying reason for ION. They recommended that the threshold of suspicion of the ICA problems during ION and initiating treatment should be lowered. (23) As the same in our case CT-angiography indicated right internal carotid dissection.
A combination of corticosteroids and antiplatelets may help prevent stroke occurrence in patients with GCA. However, the combination of antithrombotic and corticosteroid therapy is less effective in GCA patients. Cause the stroke due to Giant cell arteritis is an unusual condition; there are no evidence-based recommendations or guidelines for the treatment. If GCA is suspected in patients with severe complications, high-dose glucocorticoids are the mainstay of treatment and should be started immediately. (9, 24)When we began the corticosteroid pulse, our patient dramatically responded to the treatment in the form of a reduction in the inflammatory markers.