Post-concussion syndrome (PCS) can affect up to 20%-30% of patients with mild closed head injury (mCHI), comprising incomplete recovery and debilitating persistence of post-concussional symptoms. Eye movements relate closely to the functional integrity of the injured brain and eye movement function is impaired post-acutely in mCHI. Here, we examined whether PCS patients continue to show disparities in eye movement function at 3-5 months following mCHI compared with patients with good recovery. We hypothesized that eye movements might provide sensitive and objective functional markers of ongoing cerebral impairment in PCS. We compared 36 PCS participants (adapted World Health Organization guidelines) and 36 individually matched controls (i.e. mCHI patients of similar injury severity but good recovery) on reflexive, anti- and self-paced saccades, memory-guided sequences and smooth pursuit. All completed neuropsychological testing and health status questionnaires. Mean time post-injury was 140 days in the PCS group and 163 days in the control group. The PCS group performed worse on anti-saccades, self-paced saccades, memory-guided sequences and smooth pursuit, suggesting problems in response inhibition, short-term spatial memory, motor-sequence programming, visuospatial processing and visual attention. This poorer oculomotor performance included several measures beyond conscious control, indicating that subcortical functionality in the PCS group was poorer than expected after mCHI. The PCS group had poorer neuropsychological function (memory, complex attention and executive function). Analysis of covariance showed oculomotor differences to be practically unaffected by group disparities in depression and estimated intellectual ability. Compared with neuropsychological tests, eye movements were more likely to be markedly impaired in PCS cases with high symptom load. Poorer eye movement function, and particularly poorer subcortical oculomotor function, correlated more with post-concussive symptom load and problems on activities of daily living whilst poorer neuropsychological function exhibited slightly better correlations with measures of mental health. Our findings that eye movement function in PCS does not follow the normal recovery path of eye movements after mCHI are indicative of ongoing cerebral impairment. Whilst oculomotor and neuropsychological tests partially overlapped in identifying impairment, eye movements showed additional dysfunction in motor/visuospatial areas, response inhibition, visual attention and subcortical function. Poorer subconscious oculomotor function in the PCS group supports the notion that PCS is not merely a psychological entity, but also has a biological substrate. Measurement of oculomotor function may be of value in PCS cases with a high symptom load but an otherwise unremarkable assessment profile. Routine oculomotor testing should be feasible in centres with existing access to this technology.
Patients with traumatic brain injury show clear impairments in behavioural flexibility and inhibition that often persist beyond the time of injury, affecting independent living and psychosocial functioning. Functional magnetic resonance imaging studies have shown that patients with traumatic brain injury typically show increased and more broadly dispersed frontal and parietal activity during performance of cognitive control tasks. We constructed binary and weighted functional networks and calculated their topological properties using a graph theoretical approach. Twenty-three adults with traumatic brain injury and 26 age-matched controls were instructed to switch between coordination modes while making spatially and temporally coupled circular motions with joysticks during event-related functional magnetic resonance imaging. Results demonstrated that switching performance was significantly lower in patients with traumatic brain injury compared with control subjects. Furthermore, although brain networks of both groups exhibited economical small-world topology, altered functional connectivity was demonstrated in patients with traumatic brain injury. In particular, compared with controls, patients with traumatic brain injury showed increased connectivity degree and strength, and higher values of local efficiency, suggesting adaptive mechanisms in this group. Finally, the degree of increased connectivity was significantly correlated with poorer switching task performance and more severe brain injury. We conclude that analysing the functional brain network connectivity provides new insights into understanding cognitive control changes following brain injury.
The findings indicate that multiple motor systems are measurably impaired up to 12 months following mild CHI and that instrumented motor assessment may provide sensitive and objective markers of cerebral dysfunction during recovery from mild head trauma independent of neuropsychological assessment and patient self-report.
Post-MTBI fatigue is a persistent post-concussion symptom, exacerbated by depression but not anxiety. It diminishes in the first 3 months and then becomes relatively stable, suggesting the optimum intervention placement is at 3 months or more post-MTBI.
Based on increasing evidence that even mild closed head injury (CHI) can cause considerable neural damage throughout the brain, we hypothesized that mild CHI will disrupt the complex cerebral networks concerned with oculomotor and upper-limb visuomotor control, resulting in impaired motor function. Within 10 days following mild CHI (Glasgow Coma Scale 13-15, alteration of consciousness <20 min), we compared 30 patients (15-37 years) and 30 matched controls on different types of saccades, oculomotor smooth pursuit (sine and random), upper-limb visuomotor performance and several neuropsychological tests known to be sensitive to head trauma. Simple reflexive saccades were not impaired, whereas, on the antisaccade task, the CHI group demonstrated prolonged saccadic latencies, a marginally higher number of directional errors and poorer spatial accuracy. The CHI group exhibited more directional errors and impaired motor accuracy on memory-guided sequences of saccades and produced fewer self-paced saccades within 30 s. Most measures of sinusoidal and random oculomotor smooth pursuit showed no deficits, with the exception of a prolonged lag on random smooth pursuit in the CHI group. While arm movement reaction time and arm steadiness were not impaired, the CHI group showed decreased arm movement speed and decreased upper-limb motor accuracy. Conversely, after controlling for IQ, the CHI group had few head trauma-related neuropsychological deficits. These results indicate that multiple motor systems can be impaired following mild CHI and that this can occur independently of neuropsychological impairment. Our study also indicates that quantitative tests of oculomotor and upper-limb visuomotor function may provide sensitive markers of cerebral dysfunction, suggesting the potential use of such tests to supplement patient assessment. To our knowledge, this study is the first to demonstrate the presence of oculomotor or visuomotor deficits following mild CHI.
Our previous research on traumatic brain injury (TBI) patients has shown a strong relationship between specific white matter (WM) diffusion properties and motor deficits. The potential impact of TBI-related changes in network organization of the associated WM structural network on motor performance, however, remains largely unknown. Here, we used diffusion tensor imaging (DTI) based fiber tractography to reconstruct the human brain WM networks of 12 TBI and 17 control participants, followed by a graph theoretical analysis. A force platform was used to measure changes in body posture under conditions of compromised proprioceptive and/or visual feedback. Findings revealed that compared with controls, TBI patients showed higher betweenness centrality and normalized path length, and lower values of local efficiency, implying altered network organization. These results were not merely a consequence of differences in number of connections. In particular, TBI patients displayed reduced structural connectivity in frontal, parieto-premotor, visual, subcortical, and temporal areas. In addition, the decreased connectivity degree was significantly associated with poorer balance performance. We conclude that analyzing the structural brain networks with a graph theoretical approach provides new insights into motor control deficits following brain injury.
Purpose: To investigate and localize cerebral abnormalities in professional boxers with no history of moderate or severe head trauma. Materials and Methods:Diffusion tensor imaging (DTI) was used to determine the apparent diffusion coefficient (ADC) and fractional anisotropy (FA) in the brains of 81 professional male boxers and 12 male control subjects. Voxel-based analysis (VBA) of both the diffusion and anisotropy values was performed using statistical parametric mapping (SPM). From this objective analysis, regions of microstructural abnormalities in the brains of the boxers were located.Results: Increases in the ADC, and decreases in FA were identified in deep white matter (WM), while decreases in ADC were identified in cortical gray matter (GM). Regions of positive correlation between ADC and age were also found in both the boxer and control groups, although the regions and strength of the correlation were not the same in each group. Conclusion:Using VBA, we localized previously unreported abnormalities in the brains of professional boxers. These abnormalities are assumed to reflect cumulative (chronic) brain injury resulting from nonsevere head trauma.Key Words: boxers; diffusion tensor imaging (DTI); apparent diffusion coefficient (ADC); fractional anisotropy (FA); traumatic brain injury (TBI); voxel-based analysis (VBA)
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.