Sensory input and basal ganglia

Abstract

Non-motor symptoms including sensory signs have recently been stressed in basal ganglia (BG) disorders. Why do sensory symptoms appear in BG disorders? Four closed loops have been shown between cortex and BG, but no sensory cortical-BG loops. I review two points: fiber connections between the somatosensory cortex and BG to explain sensory symptoms, and pain and basal ganglia.
Somatosensory system and BG
Many animal studies have shown somatosensory cortex- striatum- globus pallidus- motor thalamus connections, but no connections to the sensory thalamus. This indicates that sensory system may modulate four closed loops between the cortices and BG (motor loop, oculomotor loop, prefrontal loop and limbic loop) as an open loop system. Based on the above findings, two possible mechanisms may explain somatosensory symptoms in BG disorders. Motor modulation abnormalities may be considered as sensory symptoms in patients with BG disorders. Some sensory cognition abnormalities due to abnormal modulation of the prefrontal- BG loop may be considered as sensory symptoms.
Pain and dopamine
Two systems contribute to pain signs in patients with BG disorders.
Descending pain modulation system: several brainstem nuclei send descending pain modulation fibers to the spinal cord mediated by serotonin or noradrenalin. These nuclei are facilitated by D2 neurons from the striatum. Striatal dopamine must suppress the pain information input at the spinal cord.
Ascending pain relief system
D2 neurons from the ventral tegmental area to anterior cingulate cortex, accumbens and amygdala may reduce pain feeling at the association cortices.
In summary, dopamine system will reduce pain at the spinal cord and association cortices. Dopamine depletion, therefore, will enhance the pain sensation.