Complex vasculitic overlap: temporal arteritis complicating suspected neuro-behçet disease with recurrent ischemic

Sanobar Shariff1,2, Samar Iltaf Mairajuddin2, Syed Habibullah Kamran2

  • 1Yerevan State Medical University, Yerevan, Armenia.

BMC Neurology
|July 6, 2026
PubMed

Insights

Diagnosing giant cell arteritis (GCA) can be challenging due to overlapping symptoms with other vasculitic disorders. This case demonstrates successful GCA management through integrated clinical, imaging, and treatment response evaluation.

Area of Science:

  • Rheumatology
  • Neurology
  • Vascular Medicine

Background:

  • Vasculitic disorders often present with overlapping clinical and radiologic features, complicating diagnosis and management.
  • Distinguishing Behçet disease-associated vasculitis from giant cell arteritis (GCA) is particularly challenging but crucial for effective treatment.

Purpose of the Study:

  • To present a case highlighting the diagnostic challenges in differentiating between vasculitic syndromes.
  • To emphasize the importance of integrating various diagnostic modalities for managing suspected GCA.

Main Methods:

  • A patient with a history of thrombosis and suspected Behçet disease presented with neurological deficits and temporal headache.
  • Neuroimaging revealed ischemic infarct and internal carotid artery occlusion; vascular imaging showed superficial temporal artery inflammation.
  • Diagnosis of GCA was considered based on clinical presentation, inflammatory markers, and imaging findings, after excluding other causes.

Main Results:

  • High-dose systemic corticosteroid therapy was initiated for suspected GCA.
  • The patient experienced significant clinical improvement, with headache resolution and neurological stabilization.

Conclusions:

  • This case underscores the diagnostic complexities of overlapping vasculitic syndromes.
  • Successful management of suspected GCA relies on a comprehensive approach integrating clinical, imaging, and treatment response data.
Abstract

Related Concept Videos

Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...