**1. Introduction**

In recent years, an increasing number of studies have shown the impact of mild traumatic brain injury (mTBI) on cognitive functions. The fact that mTBIs are considered a major health issue involving long-term health risks raises questions as to how their impact can be best identified and measured in order to be treated and managed optimally.

A TBI is produced by a large transfer of energy generated by a direct impact of the head against a hard surface, or by forces (acceleration, deceleration, rotation) created during the impact [1]. In the case of mTBI, these forces are responsible for stretching of the axons and microbleeds, which lead to a complex neurometabolic cascade [2]. There is now growing and reproducible evidence that following mTBI microstructural damage and neurochemical imbalances occur in a number of brain regions (e.g., frontal, temporal, motor cortex) and in white matter integrity (e.g., corpus callosum) [3–8]. These alterations have been related to the known post-mTBI physical (e.g., headaches, drowsiness, fatigue, dizziness), cognitive (e.g., attention and memory problems, bradyphrenia), and a ffective (e.g., irritability, depression, anxiety) symptoms [1,9,10]. These symptoms are more intense in the first days and weeks following the injury and slowly decrease during the subacute recovery period, which has been described as the first three months post-trauma. However, in a non-negligible proportion of individuals these symptoms are at risk of becoming chronic [11].

Attentional problems such as di fficulties orienting and disengaging attention [12], sustaining it over time, and/or dividing attentional resources across multiple simultaneous demands [13,14] are amongs<sup>t</sup> the most common complaints reported by individuals after a mTBI. On a behavioural level, these deficits usually disappear over a period of seven to 10 days [10,12,15]. However, mTBI can have negative long-term neuropsychological impacts on subtle aspects of complex attention and working memory [16,17], even with normal behavioural performances, where some individuals report the persistence of attentional di fficulties that interfere with the demands of their daily life and social participation. The need for a more sensitive functional measure of the impact of mTBI on distinct steps involved in the deployment of attention thus remains.

Event-related brain potentials (ERPs) can represent a relatively simple, inexpensive, and precise answer to that question because they allow us to assess the integrity (reflected by the amplitude of a component) and e fficiency (reflected by its latency) of specific and complex cognitive processes [1,18]. With excellent temporal resolution, ERPs possess an advantage over reaction time measures because they provide measures of multiple stages of cognitive processing, instead of the summation of the duration of all the intervening mechanisms involved in the generation of a response [18].

Experimental paradigms have historically been designed to study precise cognitive processes along with their event-related components. For instance, oddball paradigms have been used to evoke the P3, a component reflecting a target stimulus upgrade in working memory [19]. Such paradigms have been shown to be sensitive following mTBI [20–24]. However, since mTBI can present with deficits at di fferent levels within the deployment of attention, one needs to be able to rapidly track the steps of the process that are distinctly a ffected.

The objective of this study was to track, with the help of a single task, the deployment of visuospatial attentional mechanisms and to identify underlying deficits at di fferent recovery time points after mTBI. The task we used allowed us to measure the integrity of the di fferent visual and cognitive processes involved in the deployment of visuospatial selective attention. We studied components reflecting earlier visual–attentional processing, such as the N1 (discrimination processes within the focus of visual attention and central attention) [25,26], P1 (facilitation e ffect for stimuli presented at an attended localisation) [27], and P2 (early attentional modulation) [28] components, which we expected would not be di fferent between the mTBI and control groups. We also investigated later attention-related and visuocognitive mechanisms such as the N2pc (deployment and orientation of visuospatial attention) [28], Ptc (target isolation once identified among distractors) [29], SPCN (encoding in visual short-term memory, working memory capacity) [30], P3a (disengaging of attention to re-orient toward novel stimuli) [31], and P3b (tracking of task-relevant stimuli during updating in working memory) [19] components, which were expected to be a ffected, at least for later components.

#### **2. Materials and Methods**
