The role of pallidum in the neural integrator model of cervical dystonia

Abstract

Dystonia is the third most common movement disorder affecting three million people worldwide. Cervical dystonia is the most common form of dystonia. Despite common prevalence the pathophysiology of cervical dystonia is unclear. Traditional view is that basal ganglia is involved in pathophysiology of cervical dystonia, while contemporary theories suggested the role of cerebellum and proprioception in the pathophysiology of cervical dystonia. It was recently proposed that the cervical dystonia is due to malfunctioning of the head neural integrator-the neuron network that normally converts head velocity to position. Most importantly the neural integrator model was inclusive of traditional proposal emphasizing the role of basal ganglia while also accommodating the contemporary view suggesting the involvement of cerebellum and proprioception. It was hypothesized that the head neural integrator malfunction is the result of impairment in cerebellar, basal ganglia, or proprioceptive feedback that converge onto the integrator. The concept of converging input from the basal ganglia, cerebellum, and proprioception to the network participating in head neural integrator explains that abnormality originating anywhere in the network can lead to the identical motor deficits-drifts followed by rapid

Maladaptive striatal plasticity and abnormal reward‐learning in cervical dystonia

“…One potential point of convergence with this work is the top‐down influence of biased striatal plasticity on the pallidal output neurons as these have been proposed to modulate the brainstem neural integrator which controls head position. A future avenue that may prove useful for exploration, potentially via simulation, is whether asymmetries in GPi output can arise from upstream striatal plasticity abnormalities, as asymmetric GPi firing rates have been shown to correlate with the severity and direction of torticollis (Moll et al., ; Sedov et al., ).…”

Maladaptive striatal plasticity and abnormal reward-learning in cervical dystonia

“…One potential point of convergence with this work is the top-down influence of biased striatal plasticity on the pallidal output neurons as these have been proposed to modulate the brainstem neural integrator which controls head position. A future avenue that may prove useful for exploration, potentially via simulation, is whether asymmetries in GPi output can arise from upstream striatal plasticity abnormalities, as asymmetric GPi firing rates have been shown to correlate with the severity and direction of torticollis (Moll et al, 2014;Sedov et al, 2019).…”

Sensorimotor Control in Dystonia

“…Interestingly bradykinesia was also present during trunk turns, which may have caused the nystagmic gaze shifts [50]. These conclusions may be somewhat at odds with the compelling neural integrator hypothesis of cervical dystonia ([52]; for review, [53]), which suggests that abnormal head and eye movements are the result of rapid corrections to a drift in neural circuitry that holds steady a given orientation of the head or eyes. More work is required to further quantify ocular impairments in dystonia and broaden their study to other dystonia subtypes.…”

“…As mentioned earlier, emerging evidence may point to the dysfunction of neural integrators in the control of head position in CD [52,53]. Shaikh and colleagues [53] have proposed that deficits in head control may be the result of the inability of the CNS to maintain network signaling processes that hold the orientation of the head in a given state, thus requiring fast corrective actions manifesting as the aberrant head movements observed in CD.…”