Related Experiment Video
Updated: Jun 1, 2026
26:48
Induction and Clinical Scoring of Chronic-Relapsing Experimental Autoimmune Encephalomyelitis
Published on: July 4, 2007
Posterior reversible encephalopathy syndrome: a review
1Harvard Medical School, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. sfeske@partners.org
Seminars in Neurology
|May 19, 2011
Summary
Posterior reversible encephalopathy syndrome (PRES) involves reversible brain swelling due to blood-brain barrier dysfunction. Understanding its varied presentations is key for accurate diagnosis and management of this neurological condition.
Area of Science:
- Neurology
- Pathophysiology
- Vascular Biology
Background:
- Posterior reversible encephalopathy syndrome (PRES) is a neurological condition characterized by reversible cerebral edema.
- It is associated with various underlying disorders and presents a diagnostic challenge due to atypical features.
- The core mechanism involves the breakdown of the blood-brain barrier, leading to fluid extravasation into the brain parenchyma.
Purpose of the Study:
- To review the history and pathophysiology of PRES.
- To discuss the clinical diagnosis of PRES, highlighting diagnostic challenges.
- To outline current management strategies for PRES.
Main Methods:
- Literature review focusing on the history, pathophysiology, clinical presentation, diagnosis, and management of PRES.
- Synthesis of information regarding blood-brain barrier dynamics in PRES.
- Analysis of typical and atypical clinical features.
Main Results:
- The pathophysiology of PRES is linked to blood-brain barrier failure, influenced by capillary hydrostatic pressure and vascular endothelium integrity.
- While typical presentations exist, atypical features are common, complicating diagnosis.
- Effective management relies on recognizing clinical variability for prompt diagnosis.
Conclusions:
- PRES is a critical cause of neurological morbidity linked to blood-brain barrier dysfunction.
- Awareness of the wide spectrum of clinical presentations is essential for timely diagnosis.
- This review provides a comprehensive overview for clinicians managing PRES.
Related Concept Videos
01:26Encephalitis 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...
01:29Hepatic Encephalopathy
DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
01:19Encephalitis 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...
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...
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...
01:15Ischemic 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...