Cerebral white matter hyperintensities are not increased in patients with primary Sjögren's syndrome

E Harboe1, M K Beyer, O J Greve

  • 1Clinical Immunology Unit, Department of Internal Medicine, Stavanger University Hospital, Stavanger, Norway.

Abstract

Insights

Patients with primary Sjögren's syndrome (PSS) do not show increased white matter hyperintensities (WMHs) on MRI scans compared to healthy individuals. This controlled study found no significant differences in WMH load or distribution.

Area of Science:

  • Neuroimaging
  • Rheumatology
  • Neurology

Background:

  • Cerebral white matter hyperintensities (WMHs) are often associated with autoimmune diseases.
  • Previous reports suggest a higher frequency of WMHs in primary Sjögren's syndrome (PSS), but lack controlled evidence.

Purpose of the Study:

  • To investigate and compare the prevalence and distribution of WMHs in PSS patients versus healthy controls.
  • To apply the European-American criteria for PSS in this comparative analysis.

Main Methods:

  • A cross-sectional, controlled study design was employed.
  • Sixty-eight unselected PSS patients and 68 healthy subjects were included.
  • WMHs were systematically evaluated and rated using the Scheltens method.

Main Results:

  • No statistically significant differences were observed in the total WMH scores between PSS patients and healthy subjects.
  • Analysis of regional WMH scores also revealed no significant variations between the two groups.

Conclusions:

  • The study concludes that patients with primary Sjögren's syndrome do not exhibit an increased burden or altered distribution of white matter hyperintensities.
  • Findings suggest WMHs are not a distinguishing neuroimaging marker in PSS when compared to healthy populations.

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...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...