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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:BackgroundDizziness and imbalance are common following traumatic brain injury (TBI). While these symptoms are often attributed to vestibular dysfunction, the relative contribution of peripheral vs. central mechanisms is unclear. This study investigated the prevalence of semicircular canal and otolith abnormalities in a cohort of patients with chronic TBI and symptoms of dizziness or imbalance. The relationship between vestibular, oculomotor and posturography results was further explored.MethodsClinical records of patients attending the New Zealand Dizziness and Balance Centre from January 2015 to December 2019 were reviewed for consideration in the study. Inclusion required: an age of 18-80 years, a diagnosed TBI, and vestibular assessment using three-dimensional video head impulses (vHIT), cervical and ocular vestibular-evoked myogenic potentials (c and o VEMPs, respectively) and caloric testing. Severe TBI, pre-existing vestibular diagnoses, and incomplete test results were excluded. Rates of abnormalities were determined for each test and compared with results of oculomotor function testing and postural control, measured using the sensory organization test (SOT).ResultsOf 158 reviewed records, 99 patients aged 49 ± 15 years (59 female) fulfilled criteria for inclusion in the study. The median time between the head injury and the clinical assessment was 12 (IQR 6-21) months. Abnormalities involving one or more components of the vestibular labyrinth and/or nerve divisions were identified in 33 of 99 patients (33.3%). The horizontal semicircular canal was most frequently affected (18.2%), followed by the saccule (14.1%), utricle (8.1%), posterior (7.1%) and anterior (2.0%) semicircular canals. Vestibular test abnormalities were associated with skull-base fractures, superior canal dehiscence, and focal ear trauma. Oculomotor dysfunction and postural instability were recorded in 41.1 and 75.5% of patients, respectively. Postural instability correlated with abnormal oculomotor function (p = 0.008) but not peripheral vestibular hypofunction (p = 0.336).ConclusionsDizziness and/or imbalance in chronic TBI was associated with impaired postural stability for tasks requiring high levels of use of vestibular and visual input for balance. Vestibular hypofunction identified through vHIT, VEMP and caloric testing was recorded but was less common, except when the injury involved a fractured skull-base. There was no specific pattern of end-organ or nerve involvement which characterized this group of patients.

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.

Dataset Information

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

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

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