Objective: To explore the neurophysiological basis of impaired volitional thought initiation focusing on dorsal caudate dysfunction, aberrant pallidal-thalamic inhibition, and impaired corticostriatal integration.

Background: While freezing of gait (FOG) in Parkinson’s disease (PD) is well-known, a similar cognitive phenomenon –impaired volitional thought initiation (VTI)-may occur in basal ganglia disorders. Patients with auto-activation deficit (AAD) and severe apathy syndromes struggle to self-initiate thought and action despite intact externally cued responses, suggesting disrupted VTI akin to motor freezing.

Method: A narrative review of neuroimaging, neurophysiology, and lesion studies compared: 

1. PD FOG and VTI deficits in basal ganglia disorders,  

2. AAD and akinetic mutism. 

3. Apathy syndromes in psychiatric illness and neurodegeneration, linking VTI deficit to striatal and medial prefrontal underactivation.

Results: Impaired caudate activation leads to excessive GPi inhibition of VA/VL thalamic output, disrupting self-generated thought and action selection. FOG and VTI defects share overlapping basal ganglia-thalamocortical dysfunction, involving the dorsal caudate, GPi, VA/VL thalamus, and medial frontal cortex. AAD patients exhibit deficits in VTI despite intact externally triggered responses, implicating dorsal striatum dysfunction. Apathy syndromes show graded impairments in self-driven thought. Neuroimaging in PD patients experiencing cognitive slowing and decision hesitation reveals a pattern of striatal hypoactivity paired with persistent pallidal-thalamic inhibition, mirroring movement freezing.

Conclusion: The parallels between motor and cognitive freezing suggest basal ganglia dysfunction affects VTI. The dorsal caudate, traditionally linked to motor planning, appears to be involved in spontaneous cognition. Excessive GPi-mediated inhibition may reduce the threshold for VTI. 

While DBS targeting the STN or GPi has shown efficacy for motor freezing in PD, its effects on AAD and related states remain underexplored. Targeted neuromodulation of the caudate or medial prefrontal regions may help restore VTI. Deficits in VTI parallel motor freezing in underlying neurophysiological dysfunction. Understanding these mechanisms may improve diagnosis and treatment of these deficits and future research should investigate neuromodulation.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/aberrations-in-voluntary-thought-initiation-parallels-to-motor-freezing-in-basal-ganglia-dysfunction/