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Updated: Aug 11, 2026

Utility of Dissociated Intrinsic Hand Muscle Atrophy in the Diagnosis of Amyotrophic Lateral Sclerosis
Published on: March 4, 2014
Subcortical reorganization in amyotrophic lateral sclerosis
C Konrad1, A Jansen, H Henningsen
1Department of Psychiatry and Psychotherapy, IZKF, University of Muenster, Albert-Schweitzer-Str. 11, 48149 Muenster, Germany. konradc@uni-muenster.de
Amyotrophic lateral sclerosis (ALS) causes increased brain activation in subcortical motor structures like the basal ganglia and cerebellum. This suggests the brain attempts to compensate for motor neuron loss, though this mechanism is ultimately ineffective.
Area of Science:
- Neuroscience
- Motor Control Research
- Neurodegenerative Diseases
Background:
- The cerebral cortex reorganizes following lesions, but the role of basal ganglia and cerebellum in motor reorganization is unclear.
- Slowly progressive neurodegenerative motor diseases may alter subcortical functional anatomy within the basal ganglia-thalamo-cerebellar circuitry.
Purpose of the Study:
- To investigate if amyotrophic lateral sclerosis (ALS) alters the subcortical functional anatomy of the basal ganglia-thalamo-cerebellar circuitry.
- To understand the role of subcortical structures in motor reorganization during neurodegeneration.
Main Methods:
- Functional magnetic resonance imaging (fMRI) was used to study ten ALS patients and ten healthy controls.
- Participants performed a controlled finger flexion task, squeezing a handgrip transducer at 10% of maximum voluntary contraction.
Main Results:
- ALS patients showed increased task-related BOLD (blood-oxygen-level-dependent) responses compared to controls.
- Significant activation increases were observed in the supplementary motor area, basal ganglia, brainstem, and cerebellum in ALS patients.
Conclusions:
- Degeneration of motor neurons in ALS leads to the recruitment of subcortical motor structures.
- These subcortical activation patterns resemble those seen in motor learning, suggesting a compensatory adaptation of cortico-subcortical motor loops to counteract motor neuron loss.
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