Brain mapping for long-term recovery of gait after supratentorial stroke

Abstract

The recovery of independent gait after stroke is a main goal of patients and understanding the relationship between brain lesions and the recovery of gait can help physicians set viable rehabilitation plans. Our study investigated the association between variables of gait parameters and brain lesions.Fifty poststroke patients with a mean age of 67.5 ± 1.3 years and an average duration after onset of 62.2 ± 7.9 months were included. Three-dimensional gait analysis and magnetic resonance imaging were conducted for all patients. Twelve quantified gait parameters of temporal-spatial, kinematic, and kinetic data were used. To correlate gait parameters with specific brain lesions, we used a voxel-based lesion symptom mapping analysis. Statistical significance was set to an uncorrected P value <.005 and cluster size >10 voxels.Based on the location of a brain lesion, the following results were obtained: The posterior limb of the internal capsule was significantly associated with gait speed and increased knee extension in the stance phase. The hippocampus and frontal lobe were significantly associated with cadence. The proximal corona radiata was significantly associated with stride length and affected the hip maximal extension angle in the stance phase. The paracentral lobule was significantly associated with the affected knee maximal flexion angle in the swing phase and with the affected ankle maximal dorsiflexion angle in the stance phase. The frontal lobe, thalamus, and the lentiform nucleus were associated with kinetic gait parameters.Cortical, proximal white matter, and learning-related and motor-related areas are mainly associated with one's walking ability after stroke.

Stroke Lesion Impact on Lower Limb Function

“…Contrary to various earlier VLSM studies that applied lesion flipping onto a single hemisphere template (e.g., Lo et al, 2010 ; Cheng et al, 2014 ; Reynolds et al, 2014 ; Meyer et al, 2016 ; Lee et al, 2017 ; Kim et al, 2018 ), here lesion impact was tested separately for LHD and RHD. This was done to prevent masking of important differences between the hemispheres in structure-function relationships ( Frenkel-Toledo et al, 2019 ; Handelzalts et al, 2019 ).…”

“…We asked whether HLL motor function and gait capacity in the chronic phase, when most neurological recovery is likely to be completed (Ward, 2005;Karnath and Rennig, 2017;Krakauer and Carmichael, 2017) are constrained by damage to the same or to different brain voxels. Contrary to various earlier VLSM studies that applied lesion flipping onto a single hemisphere template (e.g., Lo et al, 2010;Cheng et al, 2014;Reynolds et al, 2014;Meyer et al, 2016;Lee et al, 2017;Kim et al, 2018), here lesion impact was tested separately for LHD and RHD. This was done to prevent masking of important differences between the hemispheres in structurefunction relationships (Frenkel-Toledo et al, 2019;Handelzalts et al, 2019).…”

“…A few lesion studies avoided some of the above limitations by identifying the anatomical structures essential for HLL movement quality and/or walking capacity using voxel-based lesion symptom mapping (VLSM) analysis ( Reynolds et al, 2014 ; Jones et al, 2016 ; Moon et al, 2016 ; Lee et al, 2017 ; Kim et al, 2018 ; Handelzalts et al, 2019 ). In the subacute phase, reduced HLL movement quality (tested by the FMA-LE) was associated with damage to the basal ganglia, insula, internal capsule, and the corona radiata ( Moon et al, 2016 , 2017 ).…”

“…In the chronic phase, reduced Functional Ambulation Category was associated with damage to the corona radiata, internal capsule, basal ganglia, and primary motor cortex ( Lee et al, 2017 ), and reduced walking speed was associated with damage to the corona radiata and basal ganglia ( Reynolds et al, 2014 ). Kim et al (2018) found that damage to different brain structures leads to impairment in different gait parameters. For example, damage to the PLIC was associated with reduced walking speed and increased knee extension in the stance phase, and damage to the paracentral lobule was associated with reduced knee flexion in the swing phase and with the reduced ankle dorsiflexion in the stance phase.…”

Gait pattern analysis and clinical subgroup identification: a retrospective observational study

“…Stroke causes damage to the nerve cells and the central nervous system pathways; this results in diminished muscle strength with spasticity, which is the main contributor to gait impairment. 19 20 The hemiplegic group was characterized by an asymmetric decrease in motion on the affected side as compared to the unaffected side, mainly due to muscle weakness with extensor muscle spasticity. 2 19 21 …”