Related Experiment Video
Updated: Aug 5, 2026
09:49
Isolation and Cannulation of Cerebral Parenchymal Arterioles
Published on: May 23, 2016
Pericapillary arteriovenous malformations angiographically manifested as cerebral venous malformations
S Yamada1, B H Liwnicz, J R Thompson
1Division of Neurosurgery, Loma Linda University School of Medicine, Loma Linda, CA, USA. Yamada1000@worldnet.att.net
Neurological Research
|July 28, 2001
Summary
Neurologically symptomatic patients with presumed cerebral venous malformations actually have pericapillary arteriovenous malformations. Histological analysis confirmed arterioles directly connected to venules in these cases.
Area of Science:
- Neurology
- Vascular Malformations
- Histopathology
Background:
- Cerebral venous malformations (CVMs) are typically diagnosed via angiography and considered benign.
- However, symptomatic presentations like stroke occur in patients with angiographically diagnosed CVMs.
- This suggests a potential misclassification of these vascular anomalies.
Purpose of the Study:
- To investigate the true nature of cerebral vascular malformations initially diagnosed as venous malformations.
- To confirm the presence of pericapillary arteriovenous malformations (pAVMs) in neurologically symptomatic patients.
- To correlate clinical, surgical, and histological findings.
Main Methods:
- Analysis of clinical history and surgical findings in 13 neurologically symptomatic patients.
- Patients met criteria including angiographic diagnosis of venous malformation and intraoperative identification of shunting arterioles.
- Histological examination of malformation tissue.
Main Results:
- All 13 patients exhibited neurologically symptomatic presentations.
- Angiography misdiagnosed these as venous malformations.
- Histology revealed a mix of venous channels and arterioles directly connected to venules, consistent with pAVMs.
Conclusions:
- The study identifies a distinct entity, pericapillary arteriovenous malformation (pAVM), in patients presenting with symptoms attributed to CVMs.
- Current angiographic techniques lack the resolution to differentiate pAVMs from CVMs.
- Technological advancements are needed for accurate diagnosis and differentiation.
Related Concept Videos
01:10The Arch of Aorta
The coronary arteries, originating from the ascending aorta, bifurcate from two sinuses located within the ascending aorta. Positioned just above the aortic semilunar valve, these sinuses house essential aortic baroreceptors and chemoreceptors, crucial for maintaining cardiac function. The left coronary artery and the right coronary artery branch off from the left posterior and anterior aortic sinuses, respectively.
Encircling the heart, the coronary arteries form a ring-like structure before...
Encircling the heart, the coronary arteries form a ring-like structure before...
01:20Venous Thrombosis II: Clinical Manifestations and Diagnostic Studies
The key difference between Superficial Vein Thrombosis (SVT) and Deep Vein Thrombosis (DVT) lies in their location and severity.Clinical ManifestationsSVT typically presents with localized pain, tenderness, and redness along the course of a superficial vein, often accompanied by a palpable, cord-like structure under the skin. This condition is usually less dangerous than DVT but can be uncomfortable and may lead to complications such as cellulitis or, rarely, a clot extension into the deep...
01:17Hemorrhagic 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...
01:14Increased Intracranial Pressure l: Introduction
Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...
01:19Cerebral 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...
01:22Cerebral 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...