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.

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After unilateral cerebral hemisphere stroke, resulting in contralateral arm symptoms but largely sparing higher cerebral function, ipsilateral arm function is generally considered to be unaffected. In this study, 8 subjects with acute unilateral cerebral infarction (confirmed by CT scan) and primarily motor deficits underwent 11 computerized and 6 clinical assessments between 11 days and 12 months poststroke, and were compared with 12 normal subjects. Computerized tests comprised 3 pursuit tracking tasks (preview-random, step and a combination of these), designed to measure different aspects of integrated sensory-motor (S-M) function, and 12 tasks aimed at breaking tracking into various sensory, perceptual and motor components (joint movement sense, visual resolution, object perception, static and dynamic visuospatial perception, range of movement, grip and arm strength, reaction time, speed, static and dynamic steadiness). The asymptomatic arm was impaired on all but one of the computerized tests throughout the 12-month period, although to a lesser degree than the symptomatic arm. Grip strength was marginally impaired initially. Incomplete neurological recovery was seen in the asymptomatic arm for all functions except strength, speed and steadiness, possibly indicating their resistance to improvement. Clinical assessment detected no asymptomatic arm impairment and only a mild transient deficit of higher mental function. Our data suggest that (1) all cerebral hemisphere areas involved in S-M functions can exert some degree of bilateral motor control; (2) ipsilateral influence is never greater than contralateral influence, and is usually considerably less; and (3) the proportion of ipsilateral to contralateral control is closely related to the degree of continuous sensory feedback required by the particular task. The mechanism and degree of ipsilateral dysfunction can be explained by a 3-tier cerebral model of S-M integration comprising a lower level of functions with high contralateral specificity (somatosensory and motor), a middle level of non-limb-specific partially lateralized functions (ideomotor praxis and visuospatial perception) and an upper level of global mental activities (intellect, alertness, etc.).

This suggestion is echoed by that of two other groups who proposed either general or specific working memory deficits in patients with Parkinson's disease. Cooper et al 7 found that early untreated patients showed deficits on "executive function" tasks, that were "dependent on an intact working memory system" and on certain memory tasks, which suggested that "the single origin of this [memory] impairment may be a reduction in the efficiency of working memory". On a more tenuous note, Della Sala et al interpreted a reduced primacy effect coupled with an intact recency effect in medicated patients as evidence for a specific working memory deficit in the context of Baddeley's model.8Working memory is considered important in a range of cognitive tasks and comprises the hypothetical set of information processing systems used to store, integrate and update information, especially when performing multiple cognitive operations. A system called the central executive represents the principal component of Baddeley'sI6 tripartite model, which was developed to accommodate data that were inconsistent with earlier models of short term memory and to encompass these data within a broader framework of working memory. The central executive, currently viewed as a limited capacity attentional system synonymous with Norman and Shallice's9 supervisory attentional system, is responsible for controlling non-routine current mental activities by coordinating and supervising subordinate short term memory processes and retrieval of information from long term memory.

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.

A PC-based system has been developed to automatically detect epileptiform activity in sixteen-channel bipolar EEG's. The system consists of three stages: data collection, feature extraction, and event detection. The feature extractor employs a mimetic approach to detect candidate epileptiform transients on individual channels, while an expert system is used to detect focal and nonfocal multichannel epileptiform events. Considerable use of spatial and temporal contextual information present in the EEG aids both in the detection of epileptiform events and in the rejection of artifacts and background activity as events. Classification of events as definite or probable overcomes, to some extent, the problem of maintaining high detection rates while eliminating false detections. So far, the system has only been evaluated on development data but, although this does not provide a true measure of performance, the results are nevertheless impressive. Data from 11 patients, totaling 180 minutes of sixteen-channel bipolar EEG's, have been analyzed. A total of 45-71% (average 58%) of epileptiform events reported by the human expert in any EEG were detected as definite with no false detections (i.e., 100% selectivity) and 60-100% (average 80%) as either definite or probable but at the expense of up to nine false detections per hour. Importantly, the highest detection rates were achieved on EEG's containing little epileptiform activity and no false detections were made on normal EEG's.