The neural representation of postural control in humans

Abstract

Lesion of the “vestibular cortex” in the human posterior insula leads to a tilted perception of visual vertical but not to tilted body posture and loss of lateral balance. However, some stroke patients show the reverse pattern. Although their processing of visual and vestibular inputs for orientation perception of the visual world is undisturbed, they push away actively from the ipsilesional side (the side of lesion location), leading to a contraversive tilt of the body (tilt toward the side opposite to the lesion) and falling to that side. Recently, the origin of contraversive pushing was identified as an altered perception of the body's orientation in relation to gravity. These patients experience their body as oriented “upright” when actually tilted enormously to the ipsilesional side (18° on average). The findings argued for a separate pathway in humans for sensing body orientation in relation to gravity apart from the one projecting to the vestibular cortex. The present study aimed at identifying this brain area. The infarcted brain regions of 23 consecutively admitted patients with severe contraversive pushing were projected onto a template MRI scan, which had been normalized to Talairach space. The overlapping area of these infarctions centered on the posterolateral thalamus. Our finding necessitates reinterpretation of this area as being only a “relay structure” of the vestibular pathway on its way from the brainstem to the vestibular cortex. The ventral posterior and lateral posterior nuclei of the posterolateral thalamus (and probably its cortical projections) rather seem to be fundamentally involved in the neural representation of a second graviceptive system in humans decisive for our control of upright body posture.

Controle postural na síndrome de Pusher: influência dos canais semicirculares laterais

“…All patients were submitted to clinical neurological assessment and evaluation of neuropsychological symptoms of heminegligence and anosognosia. Patients were classified as presenting spatial heminegligence when they presented clear evidence of spontaneous deviation of the head and the eyes ipsilaterally to the lesion, ipsilateral orientation to the lesion when stimulated by the front or the side of the lesion and ignoring objects or people on the contrary side of the lesion 11 . Anosognosia was characterized through questions about the motor deficit of the patient and confirmed only when no knowledge of the motor weakness was expressed, even after the demonstration made by the examiner 17 .…”

“…Based on the observations made by Davies, SCP assesses: 1) symmetry of spontaneous posture, both seated and in orthostatic position; 2) extension of upper and/ lower limbs with the contact surface, both seated and in orthostatic position; and 3) resistance to passive correction of posture, both seated and in orthostatic position 11,19 . Pusher syndrome was confirmed if the patients presented all criteria, reaching a score of at least 1 in each criterion.…”

“…This syndrome was initially described by Davies, in 1985, who suggested the association of cerebral vascular accidents (CVA) on the right hemisphere and neuropsychological symptoms of heminegligence and anosognosia as part of this syndrome 9 . Later studies in patients with Pusher syndrome allowed the dissociation of posture control of neuropsychological symptoms and found frequent left side damage [10][11][12] .…”

“…Overlapping imaging studies by magnetic resonance (MRI) or computed tomography (CT scan) indicate the posterior ventral nucleus and the lateral-posterior nucleus of the posterior-lateral thalamus as critical structures to manifest the pushing behavior 11 . Other possible and already described areas are: internal capsule, supplementary motor area, upper parietal lobe, pallid globe, and parietal-insular vestibular cortex [13][14][15] .…”

Stroke Patients' Perception of an Inclined Sitting Support Surface: a Comparison between Visual and Proprioceptive Inputs

“…Lesions in the parietal lobe cause disorders of spatial recognition and self-body image, and patients with these disorders also have impairment of the sitting position 5) . However, hemiplegic patients, even those with no clear lesions in the parietal lobe, often employ various compensatory behaviors, which include the possibility of a new balance control based on excessive visual dependence 6) .…”