A splenial lesion with transiently reduced diffusion in clinically mild encephalitis is not always reversible: A case

Related Experiment Video

Updated: Jun 27, 2026

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
10:50

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

Yuji Hashimoto1, Jun-ichi Takanashi, Keiko Kaiho

  • 1Department of Pediatrics and Radiology, Teikyo University Chiba Medical Center, Chiba, Japan. sdgcr596@ybb.ne.jp

Brain & Development
|December 3, 2008
PubMed

Insights

A reversible splenial lesion with reduced diffusion in mild encephalitis/encephalopathy may not always fully resolve. This finding, observed in a child, suggests potential long-term changes like gliosis.

Area of Science:

  • Neurology
  • Radiology
  • Pediatrics

Background:

  • A clinical-radiological syndrome, 'clinically mild encephalitis/encephalopathy with a reversible splenial lesion,' has been described.
  • This syndrome is characterized by specific Magnetic Resonance (MR) imaging findings in the brain's splenium.

Observation:

  • A 3-year-old boy presented with mild encephalitis and a splenial lesion showing transiently reduced diffusion on MR imaging.
  • The child experienced a complete clinical recovery within two weeks without specific intervention.

Findings:

  • While the splenial lesion size decreased, it remained detectable on T2-weighted imaging for over five months.
  • This case indicates that splenial lesions in this context may not be entirely reversible.

Implications:

  • The long-term persistence of splenial lesions suggests potential post-encephalitic changes, such as gliosis.
  • This challenges the notion of complete reversibility for all splenial lesions in clinically mild encephalitis/encephalopathy.

More Related Videos

Brain Infarct Segmentation and Registration on MRI or CT for Lesion-symptom Mapping10:25

Brain Infarct Segmentation and Registration on MRI or CT for Lesion-symptom Mapping

Published on: September 25, 2019

An In Vivo Assessment of Blood-Brain Barrier Disruption in a Rat Model of Ischemic Stroke12:19

An In Vivo Assessment of Blood-Brain Barrier Disruption in a Rat Model of Ischemic Stroke

Published on: March 11, 2018

Related Concept Videos

Encephalitis l: Introduction01:19

Encephalitis 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...
Encephalitis ll: Pathophysiology01:26

Encephalitis 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...
Hepatic Encephalopathy01:29

Hepatic 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...
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...
Brain Abscess l: Introduction01:26

Brain Abscess l: Introduction

A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial infections,...
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...