Related Experiment Video

Updated: Aug 19, 2026

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
12:28

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains

Published on: June 3, 2020

Cortical involvement in Marchiafava-Bignami disease

Ken Johkura1, Makoto Naito, Takayuki Naka

  • 1Department of Neurology, Hiratsuka Kyosai Hospital, Hiratsuka, Japan.

AJNR. American Journal of Neuroradiology
|March 12, 2005
PubMed

Insights

Marchiafava-Bignami disease (MBD), a rare condition linked to alcoholism, typically affects the corpus callosum. New findings suggest MBD may also involve widespread cerebral cortical lesions, expanding our understanding of this neurological disorder.

Area of Science:

  • Neurology
  • Radiology
  • Neuroscience

Background:

  • Marchiafava-Bignami disease (MBD) is a rare neurological disorder primarily affecting the corpus callosum.
  • It is most commonly associated with chronic alcoholism and characterized by demyelination.

Observation:

  • Two cases of MBD were analyzed using advanced neuroimaging techniques.
  • Fluid-attenuated inversion recovery (FLAIR) and diffusion-weighted imaging (DWI) were employed to visualize brain lesions.

Findings:

  • In addition to typical callosal lesions, symmetrical hyperintense lesions were observed in the cerebral cortex, particularly in lateral-frontal regions.
  • These cortical lesions suggest a potential association with conditions like Morel's laminar sclerosis.

Implications:

  • The findings expand the known spectrum of MBD, indicating potential diffuse cortical involvement.
  • This may necessitate revised diagnostic criteria and treatment strategies for Marchiafava-Bignami disease.
  • Further research is warranted to elucidate the precise relationship between MBD and cortical lesions.

More Related Videos

A Standardized Pipeline for Examining Human Cerebellar Grey Matter Morphometry using Structural Magnetic Resonance Imaging11:50

A Standardized Pipeline for Examining Human Cerebellar Grey Matter Morphometry using Structural Magnetic Resonance Imaging

Published on: February 4, 2022

Modeling Multiple Sclerosis in the Two Sexes: MOG35-55-Induced Experimental Autoimmune Encephalomyelitis05:44

Modeling Multiple Sclerosis in the Two Sexes: MOG35-55-Induced Experimental Autoimmune Encephalomyelitis

Published on: October 13, 2023

Related Concept Videos

Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Fibril-associated Collagen01:11

Fibril-associated Collagen

Fibril-associated collagens are a type of collagens present in the extracellular matrix with interrupted triple helices or FACIT (Fibril-associated collagens interrupted triple-helices). FACIT help connect and attach the collagen fibrils with each other as well as with other proteins of the extracellular matrix.
For example, the type II collagen fibrils in cartilage have covalently bound type IX fibril-associated collagens at regular intervals. Other types of fibril-associated collagens are...
Huntington Disease l: Introduction01:21

Huntington Disease l: Introduction

Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show reduced penetrance,...