Prefrontal cortex controls human balance during over ground ataxic gait: A correlation study between cortical activity and gait pattern

Prefrontal cortex controls human balance during over ground ataxic gait: A correlation study between cortical activity and gait pattern

S30 SIAMOC 2013 abstracts / Gait & Posture 40 (2014) S1–S31 Prefrontal cortex controls human balance during over ground ataxic gait: A correlation s...

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S30

SIAMOC 2013 abstracts / Gait & Posture 40 (2014) S1–S31

Prefrontal cortex controls human balance during over ground ataxic gait: A correlation study between cortical activity and gait pattern P. Caliandro 1,∗ , M. Serrao 1 , G. Silvestri 1 , C. Iacovelli 3 , C. Simbolotti 3 , G. Russo 3 , L. Padua 1,3 , P. Bramanti 4 , P.M. Rossini 1,5 1 Department of Geriatrics-Neuroscience-Orthopaedics-Physiatrics, Institute of Neurology, Catholic University, Rome, Italy 3 Don Carlo Gnocchi Onlus Foundation, Rome, Italy 4 IRCCS Centro Neurolesi Bonino-Pulejo, Messina, Italy 5 IRCSS S. Raffaele Pisana Roma and Casa di Cura S. Raffaele Cassino, Rome, Italy

Introduction: In a previous study we demonstrated that prefrontal cortex (PFC) is bilaterally activated during over ground walking in ataxic patients and that it correlates with the severity of the clinical picture [1]. We hypothesized that these findings were associated with compensatory mechanisms involved in severe conditions when other nervous centres controlling balance are functionally not efficient. Our study aim is to verify if the PFC metabolic pattern is correlated with compensatory aspects of gait or with primary deficits of gait more specifically linked to the pathology. Methods: We enrolled 19 patients with Spino Cerebellar Ataxia (SCA). For clinical evaluation of ataxia we used the Scale for the Assessment and Rating of Ataxia (SARA). A 2-channel near-infrared system was used to investigate the changes in oxygenated concentrations on the PFC during gait ([O2Hb]t). To obtain [O2Hb] baseline-corrected activation value ([O2Hb]c), we calculated the difference between [O2Hb]t and [O2Hb] during upright posture ([O2Hb]b). The gait was analysed by an optoelectronic system with 8 infrared cameras. We used the Davis protocol that includes 22 markers. We calculated the spatiotemporal parameters and the segmental kinematic parameters. For each subject we calculated the coefficient of variation (CV) to quantify the variability of all parameters and the multiple correlation coefficient (CMC) to quantify the segmental kinematic parameters [2]. Results: The correlation coefficient between [O2Hb]c and the SARA gait score was respectively for the right and left PFC r:0.50 (p = 0.03) and r:0.52 (p = 0.02), between [O2Hb]c and the SARA stance score respectively r:0.64 (p = 0.003) and r:0.63 (p = 0.004). [O2Hb]c of both PFCs correlated with the step width, respectively r:0.46 (p = 0.04) for the right PFC and r:0.48 (p = 0.04) for the left PFC. We found no correlation between the cortical pattern and CV of spatio-temporal and segmental kinematic parameters nor between the cortical pattern and CMC of segmental kinematic parameters. Discussion: During over ground gait, SCA patients have a bilateral activation of PFC. This metabolic pattern of PFC is influenced by the clinical severity of ataxia being evident only in patients with severe balance deficits. PFC activation is linked to a compensatory mechanism and not to a primary deficit of the pathology. Indeed, in SCA patients PFC activation seems to have a role in the intentional control of gait through the dynamic modulation of the width of the support base.

[2] Serrao M, Pierelli F, Ranavolo A, Draicchio F, Conte C, Don R, et al. Gait pattern in inherited cerebellar ataxias. Cerebellum 2012;11(March (1)):194–211.

http://dx.doi.org/10.1016/j.gaitpost.2014.05.059 Equinovarus foot deformity correction by surgery and early rehabilitation: Retrospective analysis of effects on gait at one month Paolo Zerbinati 1,2,∗ , Erika Giannotti 1,3 , Maria Longhi 1 , Andrea Merlo 1 , Stefano Masiero 3 , Paolo Prati 1 , Davide Mazzoli 1 1 Gait & Motion Analysis Laboratory, Sol et Salus Hospital, Rimini, Italy 2 Neuroorthopedic Service, Hand Surgery Unit, MultiMedica Castellanza, Italy 3 Department of Orthopaedic Rehabilitation, University of Padova, Padova, Italy

Introduction: Equinovarus foot deformity (EVFD) is one of the most frequent and impairing consequences for stroke survivors. In this study, we present a quantitative assessment of the effects at one month of EVFD surgical correction followed by an early rehabilitation protocol. Methods: We retrospectively analysed gait analysis (GA) data on chronic stroke patients with hemiplegia who underwent surgical correction of unilateral EVFD, followed by a standardized rehabilitation treatment beginning one day after surgery and with pre-operative and post-operative GA data available. An articulated ankle-foot orthosis was used to allow for immediate gait training and to protect the surgical wounds. The presence of differences at one month from surgery in GA space/time parameters, in ankle dorsiflexion (DF) values and peaks at initial contact (DF@IC), during stance (DF@St) and swing (DF@Sw) was assessed by the Wilcoxon test. The presence of correlations between post- and pre-operative values was investigated by Spearman’s correlation coefficient. Results: Forty-seven patients were included in the study (L/R hemiplegia 20/27, age 56 ± 15 years, time from lesion 6 ± 5 years). Ankle DF increased one month after surgery at all investigated gait phases (p < 0.0001), becoming neutral at IC. Small but significant (p < 0.05) variations towards normality values were found for stride length, stride width, anterior step length of the affected side and for the duration of the double support phase of the contralateral side. Post-surgery ankle DF peak in stance was found to be correlated (R = 0.81, p < 0.0001) with its pre-surgery value.

References [1] Caliandro P, Masciullo M, Padua L, Simbolotti C, Di Sante G, Russo G, et al. Prefrontal cortex controls human balance during overground ataxic gait. Restor Neurol Neurosci 2012;30(5):397–405.

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