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Abnormal muscle activation patterns are associated with chronic gait deficits following traumatic brain injury.

ABSTRACT: BACKGROUND:Gait and balance disorders are common among individuals who have experienced a mild to moderate traumatic brain injury (TBI). However, little is known about how the neuromuscular control of gait is altered following a TBI. RESEARCH QUESTION:Investigate the relationship between lower limb muscle activation patterns and chronic gait deficits in individuals who previously experienced a mild to moderate TBI. METHODS:Lower extremity electromyographic (EMG) signals were collected bilaterally during treadmill and overground walking in 44 ambulatory individuals with a TBI >1?year prior and 20 unimpaired controls. Activation patterns of TBI muscles were cross-correlated with normative data from control subjects to assess temporal phasing of muscle recruitment. Clinical assessments of gait and balance were performed using dynamic posturography, the dynamic gait index, six-minute walk test, and preferred walking speed. RESULTS:TBI subjects exhibited abnormal activation patterns in the tibialis anterior, medial gastrocnemius, and rectus femoris muscles during both overground and treadmill walking. Activation patterns of the vastus lateralis and soleus muscles did not differ from normal. There was considerable heterogeneity in performance on clinical balance and gait assessments. Abnormal muscle activation patterns were significantly correlated with variations in the dynamic gait index among the TBI subjects. SIGNIFICANCE:Individuals who have experienced a prior TBI do exhibit characteristic changes in the temporal coordination of select lower extremity muscles, which may contribute to impairments during challenging walking tasks.

SUBMITTER: Acuna SA

PROVIDER: S-EPMC5998824 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature

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Abnormal muscle activation patterns are associated with chronic gait deficits following traumatic brain injury.

Acuña Samuel A SA Tyler Mitchell E ME Danilov Yuri P YP Thelen Darryl G DG

Gait & posture 20180412

<h4>Background</h4>Gait and balance disorders are common among individuals who have experienced a mild to moderate traumatic brain injury (TBI). However, little is known about how the neuromuscular control of gait is altered following a TBI.<h4>Research question</h4>Investigate the relationship between lower limb muscle activation patterns and chronic gait deficits in individuals who previously experienced a mild to moderate TBI.<h4>Methods</h4>Lower extremity electromyographic (EMG) signals wer ...[more]

PMID: 29684885

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Project description:ImportanceIschemia is an important pathophysiological mechanism after traumatic brain injury (TBI), but its incidence and spatiotemporal patterns are poorly characterized.ObjectiveTo comprehensively characterize the spatiotemporal changes in cerebral physiology after TBI.Design, setting, and participantsThis single-center cohort study uses 15oxygen positron emission tomography data obtained in a neurosciences critical care unit from February 1998 through July 2014 and analyzed from April 2018 through August 2019. Patients with TBI requiring intracranial pressure monitoring and control participants were recruited.ExposuresCerebral blood flow (CBF), cerebral blood volume (CBV), cerebral oxygen metabolism (CMRO2), and oxygen extraction fraction.Main outcomes and measuresRatios (CBF/CMRO2 and CBF/CBV) were calculated. Ischemic brain volume was compared with jugular venous saturation and brain tissue oximetry.ResultsA total of 68 patients with TBI and 27 control participants were recruited. Results from 1 patient with TBI and 7 health volunteers were excluded. Sixty-eight patients with TBI (13 female [19%]; median [interquartile range (IQR)] age, 29 [22-47] years) underwent 90 studies at early (day 1 [n?=?17]), intermediate (days 2-5 [n?=?54]), and late points (days 6-10 [n?=?19]) and were compared with 20 control participants (5 female [25%]; median [IQR] age, 43 [31-47] years). The global CBF and CMRO2 findings for patients with TBI were less than the ranges for control participants at all stages (median [IQR]: CBF, 26 [22-30] mL/100 mL/min vs 38 [29-49] mL/100 mL/min; P?<?.001; CMRO2, 62 [55-71] ?mol/100 mL/min vs 131 [101-167] ?mol/100 mL/min; P?<?.001). Early CBF reductions showed a trend of high oxygen extraction fraction (suggesting classical ischemia), but this was inconsistent at later phases. Ischemic brain volume was elevated even in the absence of intracranial hypertension and highest at less than 24 hours after TBI (median [IQR], 36 [10-82] mL), but many patients showed later increases (median [IQR] 6-10 days after TBI, 24 [4-42] mL; across all points: patients, 10 [5-39] mL vs control participants, 1 [0-3] mL; P?<?001). Ischemic brain volume was a poor indicator of jugular venous saturation and brain tissue oximetry. Patients' CBF/CMRO2 ratio was higher than controls (median [IQR], 0.42 [0.35-0.49] vs 0.3 [0.28-0.33]; P?<?.001) and their CBF/CBV ratio lower (median [IQR], 7.1 [6.4-7.9] vs 12.3 [11.0-14.0]; P?<?.001), suggesting abnormal flow-metabolism coupling and vascular reactivity. Patients' CBV was higher than controls (median [IQR], 3.7 [3.4-4.1] mL/100 mL vs 3.0 [2.7-3.6] mL/100 mL; P?<?.001); although values were lower in patients with intracranial hypertension, these were still greater than controls (median [IQR], 3.7 [3.2-4.0] vs 3.0 [2.7-3.6] mL/100 mL; P?=?.002), despite more profound reductions in partial pressure of carbon dioxide (median [IQR], 4.3 [4.1-4.6] kPa vs 4.7 [4.3-4.9] kPa; P?=?.001).Conclusions and relevanceIschemia is common early, detectable up to 10 days after TBI, possible without intracranial hypertension, and inconsistently detected by jugular or brain tissue oximetry. There is substantial between-patient and within-patient pathophysiological heterogeneity; ischemia and hyperemia commonly coexist, possibly reflecting abnormalities in flow-metabolism coupling. Increased CBV may contribute to intracranial hypertension but can coexist with abnormal CBF/CBV ratios. These results emphasize the need to consider cerebrovascular pathophysiological complexity when managing patients with TBI.

Project description:It is well established that chronic cognitive problems after traumatic brain injury relate to diffuse axonal injury and the consequent widespread disruption of brain connectivity. However, the pattern of diffuse axonal injury varies between patients and they have a correspondingly heterogeneous profile of cognitive deficits. This heterogeneity is poorly understood, presenting a non-trivial challenge for prognostication and treatment. Prominent amongst cognitive problems are deficits in working memory and reasoning. Previous functional MRI in controls has associated these aspects of cognition with distinct, but partially overlapping, networks of brain regions. Based on this, a logical prediction is that differences in the integrity of the white matter tracts that connect these networks should predict variability in the type and severity of cognitive deficits after traumatic brain injury. We use diffusion-weighted imaging, cognitive testing and network analyses to test this prediction. We define functionally distinct subnetworks of the structural connectome by intersecting previously published functional MRI maps of the brain regions that are activated during our working memory and reasoning tasks, with a library of the white matter tracts that connect them. We examine how graph theoretic measures within these subnetworks relate to the performance of the same tasks in a cohort of 92 moderate-severe traumatic brain injury patients. Finally, we use machine learning to determine whether cognitive performance in patients can be predicted using graph theoretic measures from each subnetwork. Principal component analysis of behavioural scores confirm that reasoning and working memory form distinct components of cognitive ability, both of which are vulnerable to traumatic brain injury. Critically, impairments in these abilities after traumatic brain injury correlate in a dissociable manner with the information-processing architecture of the subnetworks that they are associated with. This dissociation is confirmed when examining degree centrality measures of the subnetworks using a canonical correlation analysis. Notably, the dissociation is prevalent across a number of node-centric measures and is asymmetrical: disruption to the working memory subnetwork relates to both working memory and reasoning performance whereas disruption to the reasoning subnetwork relates to reasoning performance selectively. Machine learning analysis further supports this finding by demonstrating that network measures predict cognitive performance in patients in the same asymmetrical manner. These results accord with hierarchical models of working memory, where reasoning is dependent on the ability to first hold task-relevant information in working memory. We propose that this finer grained information may be useful for future applications that attempt to predict long-term outcomes or develop tailored therapies.

Dataset Information

Abnormal muscle activation patterns are associated with chronic gait deficits following traumatic brain injury.

Publications

Abnormal muscle activation patterns are associated with chronic gait deficits following traumatic brain injury.

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