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Related Experiment Video

Updated: Jun 27, 2026

The Mouse Hindbrain As a Model for Studying Embryonic Neurogenesis

The Mouse Hindbrain As a Model for Studying Embryonic Neurogenesis

Published on: January 29, 2018

Midbrain-hindbrain involvement in lissencephalies.

Patrice Jissendi-Tchofo¹, Simay Kara, A James Barkovich

¹Department of Radiology, University of California, San Francisco, CA, USA. jissendi@gmail.com

|November 21, 2008

Summary

This summary is machine-generated.

Midbrain and hindbrain involvement significantly differs across lissencephaly types. Cobblestone complex lissencephalies show the most severe midbrain and hindbrain abnormalities, correlating with cerebral malformations.

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Microdissection of Mouse Brain into Functionally and Anatomically Different Regions

Microdissection of Mouse Brain into Functionally and Anatomically Different Regions

Published on: February 15, 2021

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Last Updated: Jun 27, 2026

The Mouse Hindbrain As a Model for Studying Embryonic Neurogenesis

The Mouse Hindbrain As a Model for Studying Embryonic Neurogenesis

Published on: January 29, 2018

Microdissection of Mouse Brain into Functionally and Anatomically Different Regions

Microdissection of Mouse Brain into Functionally and Anatomically Different Regions

Published on: February 15, 2021

Area of Science:

Neuroscience
Radiology
Genetics

Background:

Lissencephalies are a group of brain malformations characterized by a smooth cerebral surface.
Classic lissencephaly (cLIS), variant lissencephaly (vLIS), and cobblestone complex lissencephalies (CBSC) represent distinct subtypes with varying genetic causes and clinical presentations.
Posterior fossa anomalies are recognized in CBSC but their involvement in other lissencephaly types requires further characterization.

Purpose of the Study:

To investigate the involvement of the midbrain and hindbrain (MHB) in cLIS, vLIS, and CBSC.
To determine if MHB abnormalities correlate with the severity of cerebral malformations in these lissencephaly groups.
To propose a refined classification of lissencephalies based on MHB involvement.

Main Methods:

Retrospective review of MRI scans from 111 patients with lissencephaly.
Classification of cases based on known mutations (LIS1, DCX, ARX, VLDLR, RELN, MEB, WWS) or mutation phenotypes.
Scoring of MHB abnormalities (0-3) and statistical analysis (Kruskal-Wallis, chi(2) McNemar tests) to assess differences and correlations.

Main Results:

Significant differences in MHB appearance were observed among cLIS, vLIS, and CBSC groups.
A severity gradient of MHB involvement was identified: cLIS (mild), vLIS (moderate), and CBSC (severe).
The extent of cerebral lissencephaly significantly correlated with the severity of MHB abnormalities (p = 0.0029).

Conclusions:

Posterior fossa anomalies are a key feature of CBSC and vary in severity across lissencephaly types.
The findings support a correlation between cerebral malformation and MHB abnormalities in lissencephalies.
A new classification of human lissencephalies incorporating MHB involvement is proposed.