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Updated: May 16, 2026

Electrophysiological Investigations of Retinogeniculate and Corticogeniculate Synapse Function

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Published on: August 7, 2019

[Gerstmann-Sträussler-Scheinker disease].

E A Katunina^1,2, I A Putyatin², M B Dolgushin¹

¹Federal Center of Brain Research and Neurotechnologies, Moscow, Russia.

Zhurnal Nevrologii I Psikhiatrii Imeni S.S. Korsakova

|May 14, 2026

Summary

This summary is machine-generated.

Gerstmann-Sträussler-Scheinker disease (GSSD), a rare prion disease, presents diagnostic challenges. Positron emission tomography identified metabolic brain changes before MRI, aiding early GSSD diagnosis.

Keywords:

Gerstmann—Sträussler—Scheinker disease PRNP gene neurodegenerative diseases positron emission tomography prion diseases

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Area of Science:

Neuroscience
Neurology
Medical Imaging

Background:

Prion diseases are rare, fatal neurodegenerative disorders.
Gerstmann-Sträussler-Scheinker disease (GSSD) is a genetic prionopathy.
Phenotypic heterogeneity complicates GSSD diagnosis.

Purpose of the Study:

To present a clinical case of GSSD.
To highlight the utility of 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) in early GSSD detection.
To discuss diagnostic challenges and differential diagnosis.

Main Methods:

Clinical case presentation.
Positron emission tomography (PET) with 18F-fluorodeoxyglucose.
Magnetic resonance imaging (MRI).

Main Results:

A patient with GSSD presented with cerebellar ataxia and cognitive/behavioral issues.
FDG-PET revealed metabolic abnormalities in the basal ganglia and cerebellum.
These metabolic changes preceded apparent MRI alterations and clinical symptoms.

Conclusions:

FDG-PET can detect early metabolic changes in GSSD.
Considering prion diseases is crucial for differential diagnosis of cerebellar and cognitive disorders.
Early diagnosis aids in managing GSSD and related prionopathies.