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muscle activation is the result of the gating of the DV signal by multiple inhibition-
excitation sequences of abnormal GO signal for the generation of multiple volitional
motor cortical commands sent down to the spinal cord for the completion of the
movement.
11.9 Conclusion
This chapter has focused on how the smooth organization of voluntary movement
observed in normal individuals is disrupted in Parkinson's disease. The neural net-
work model of voluntary movement preparation and execution presented in the pre-
vious chapter was extended by studying the effects of dopamine depletion in the
output of the basal ganglia and in key neuronal types in cortex and spinal cord. The
resulting extended DA-VITE-FLETE model offered an integrative perspective on
corticospinal control of Parkinsonian voluntary movement. The model accounted
for some of the known empirical signatures of Parkinsonian willful action:
•
Cellular disorganization in cortex
•
Increases in neuronal baseline activity
•
Reduction of firing intensity and firing rate of cells in primary motor cortex
•
Abnormal oscillatory GPi response
•
Disinhibition of reciprocally tuned cells
•
Repetitive bursts of muscle activation
•
Reduction in the size and rate of development of the first agonist burst of EMG
activity
•
Repetitive triphasic pattern of muscle activation
•
Non co-contraction of antagonist MN units in small amplitude movements
•
Co-contraction of antagonist MN units in large amplitude movements
The interested reader should refer to the modeling studies of Cutsuridis and
Perantonis [21] and Cutsuridis [18, 19, 20], where additional empirical signatures
of PD kinematics have been successfully simulated:
•
Increased duration of neuronal discharge in area 4 preceding and following onset
of movement
•
Prolongation of premotor and electromechanical delay times
•
Asymmetric increase in the time-to-peak and deceleration time
•
Decrease in the peak value of the velocity trace
•
Increase in movement duration
•
Movement variability
All these results provided sufficient evidence to support the main hypothesis of
the model, which stated that “elimination of DA modulation from the SNc disrupts,
via several pathways, the buildup of the pattern of movement-related responses in
the primary motor and parietal cortex, and results in a loss of directional specificity
of reciprocal and bidirectional cells in the motor cortex as well as in a reduction in
their activities and their rates of change. These changes result in delays in recruiting
