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Updated: Jun 12, 2026
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MRI-guided Focused Ultrasound Thalamotomy for Patients with Medically-refractory Essential Tremor
Published on: December 13, 2017
GABAergic dysfunction in essential tremor: an 11C-flumazenil PET study.
Henning Boecker1, Adolf Weindl, David J Brooks
1Nuklearmedizinische Klinik, Klinikum rechts der Isar, Technische Universität München, Munich, Germany. henning.boecker@ukb.uni-bonn.de
Summary
Essential tremor may stem from reduced gamma-aminobutyric acid (GABA) function. This study found increased benzodiazepine receptor availability in key brain areas of patients with essential tremor, supporting the GABA hypothesis.
Area of Science:
- Neuroscience
- Movement Disorders
- Neuroimaging
Background:
- Essential tremor (ET) is the most prevalent movement disorder, yet its pathophysiology remains unclear.
- Cerebellothalamic pathway overactivity is a key finding in ET.
- Impaired central inhibition, potentially linked to gamma-aminobutyric acid (GABA) dysfunction, is hypothesized to drive tremor generation.
Purpose of the Study:
- To investigate the role of GABAergic dysfunction in essential tremor.
- To quantify benzodiazepine receptor availability in the GABA(A) complex in ET patients.
Main Methods:
- Positron Emission Tomography (PET) with (11)C-flumazenil was used.
- Distribution volume, an index of benzodiazepine receptor availability, was calculated.
- Compared 8 ET patients with 11 healthy controls.
Main Results:
- Increased (11)C-flumazenil binding was observed in the cerebellum, ventrolateral thalamus, and lateral premotor cortex of ET patients.
- This indicates increased availability of benzodiazepine receptor sites in these regions.
- Findings suggest reduced GABAergic function in ET.
Conclusions:
- Essential tremor is linked to reduced GABAergic function and increased benzodiazepine receptor availability.
- These alterations occur in brain regions critical for tremor generation.
- The results support the GABA hypothesis of essential tremor pathophysiology.
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