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Related Concept Videos

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...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
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...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...

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Granulocyte-dependent Autoantibody-induced Skin Blistering
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[Stroke revealing granulomatosis].

L Raissouni1, E Aitbenhaddou, N Ahbeddou

  • 1Service de neurologie B et de neurogénétique, hôpital des spécialités de Rabat, Rabat, Maroc.

Revue Neurologique
|June 22, 2010
PubMed
Summary

Wegener granulomatosis rarely affects the central nervous system. This case highlights stroke as a key indicator, involving vasculitis and granulomatous extension from the sinuses.

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Area of Science:

  • Neurology
  • Rheumatology
  • Ophthalmology

Background:

  • Central nervous system (CNS) involvement in Wegener granulomatosis (WG) is uncommon.
  • Stroke is the most frequent manifestation suggestive of WG affecting the CNS.

Observation:

  • A 35-year-old woman presented with progressive visual decline, nasal obstruction, headache, and left hemiparesis.
  • Clinical examination revealed right exophthalmos, optic nerve and abducens deficits, crusty rhinitis, and nasal stenosis.
  • Diagnosis of WG was confirmed by clinical, radiological findings, and anti-neutrophil cytoplasmic antibodies (ANCA).

Findings:

  • The patient experienced a stroke, a rare but significant CNS manifestation of WG.
  • Pathogenic mechanisms include vasculitis, contiguous spread from sinuses, and in situ granuloma formation.
  • Treatment involved antiplatelet agents, corticosteroids, and cyclophosphamide.

Implications:

  • This case underscores the importance of considering WG in patients presenting with stroke and neurological deficits.
  • Early diagnosis and multidisciplinary management are crucial for improving outcomes in WG-related CNS complications.
  • Understanding the pathogenic mechanisms aids in targeted therapeutic strategies for CNS involvement in WG.