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. 2018 Apr 26;10:99. doi: 10.3389/fnagi.2018.00099

Table 1.

Maladies associated with the PPN in PD, the source and affected brain components, as well as its consequence/ indications.

Malady type Source Brain components affected Consequence/ Indications
LOCOMOTOR
Akinesia/bradykinesia/hypokinesia Overactive GABAergic BG output MCx, thalamus, BG, PPN, SC, MLR Decreases in velocity and amount of movement
Hypertonus Increases in BG inhibition Increases in PPN inhibition Decreases in cortical PPN excitation Direct-indirect pathway imbalance via increased SNr inhibition MCx, BG, PPN Increased muscle tone
Dystonia Diminution or instability of BG GABAergic outputs to the PPN BG (SNr, Gpi), PPN Central and spontaneous fluctuations in muscle tone, posture, or locomotion
Gait disturbances/ failure Excessive MLR inhibition via SNr-GABAergic output Cortical excitation of brainstem reticular formation Decreases in cortical stimulation of the brainstem reticular formation Inactivity of the PMC Dysfunction of BG-BS system Direct-indirect pathway imbalance MLR MCx, brainstem Primary MCx SNr, PPN, MLR, SC Uncontrolled gait Limited movement Freezing of gait, increases in stance phases in locomotor cycles and decreases in locomotor velocity
COGNITIVE
Impaired attention and memory learning PPN lesions PPN Inability to concentrate, unable to retain memory
Motivation and compulsion PPN lesions, impaired brain mechanisms and neural circuitry formation involved in reward processing NAcc, VTA, PPN Obsessive compulsive disorder
SLEEP
REMS Decreases in BG dopaminergic activity SNr, GPi, DRN, LDT, PPN REMS behavior disorder