Related Experiment Videos

[Cerebral venous hemodynamics in chronic disorders of cerebral circulation]

F I Todua, D G Gachechiladze, M V Beraia

    Angiologiia I Sosudistaia Khirurgiia = Angiology and Vascular Surgery
    |July 23, 2005
    PubMed

    Insights

    Patients with circulatory disorder-induced encephalopathy often have venous abnormalities. Atherosclerosis and venous sinus developmental issues contribute to venous congestion, worsening neurological symptoms and potentially leading to hydrocephalus and cerebral atrophy.

    Area of Science:

    • Neurology
    • Vascular Medicine
    • Radiology

    Background:

    • Circulatory disorder-induced encephalopathy (DE) presents with diverse neurological symptoms.
    • Arterial hypertension (AH) is a common comorbidity in DE patients.
    • Cerebral venous hemodynamics are crucial for brain health.

    Purpose of the Study:

    • To assess extra- and intracranial venous hemodynamics in patients with DE.
    • To investigate the relationship between DE severity, arterial disease, and venous abnormalities.
    • To identify contributing factors to venous congestion in DE.

    Main Methods:

    • 114 DE patients and 36 controls underwent neurological examination, brain MRI with venography, Color Doppler Imaging of extracranial vessels, and transcranial Doppler.
    • Patients were categorized into stages 1, 2, and 3 DE based on clinical manifestations.
    • Atherosclerotic plaques and venous sinus abnormalities were analyzed.

    Main Results:

    • DE patients exhibited jugular vein dilatation and reduced flow intensity compared to controls.
    • Significant carotid artery stenoses were found in 34% of patients.
    • Venous sinus developmental abnormalities (hypoplasia/aplasia) were present in 59% of cases, often associated with compensatory dilatation.
    • Elevated linear flow velocity in deep cerebral veins and reduced pulsatility index were noted in later DE stages.
    • Diffuse ischemic brain lesions were observed in 79% of patients.

    Conclusions:

    • Atherosclerosis and AH-induced brachiocephalic artery lesions impair the arteriovenous pump, causing venous congestion.
    • Compromised collateral venous outflow, especially with venous sinus abnormalities, exacerbates venous circulatory distress.
    • This can lead to increased CSF pulse pressure, benign intracranial hypertension, hydrocephalus, and cerebral atrophy.

    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 l: Introduction01:14

    Increased 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...
    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...
    Veins of Head and Neck01:19

    Veins of Head and Neck

    The blood drainage from the head and neck is primarily managed by three pairs of veins: the external jugular, internal jugular, and vertebral veins. The external jugular veins drain superficial scalp and face structures, passing over the sternocleidomastoid muscles to empty into the subclavian veins.
    On the other hand, the vertebral veins, unlike their arterial counterparts, are not primarily responsible for brain drainage. Instead, they drain the cervical vertebrae, spinal cord, and some small...
    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...
    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...