Improving activity recognition using a wearable barometric pressure sensor in mobility-impaired stroke patients.

© 2015 Massé et al.Background: Stroke survivors often suffer from mobility deficits. Current clinical evaluation methods, including questionnaires and motor function tests, cannot provide an objective measure of the patients mobility in daily life. Physical activity performance in daily-life can be assessed using unobtrusive monitoring, for example with a single sensor module fixed on the trunk. Existing approaches based on inertial sensors have limited performance, particularly in detecting transitions between different activities and postures, due to the inherent inter-patient variability of kinematic patterns. To overcome these limitations, one possibility is to use additional information from a barometric pressure (BP) sensor. Methods: Our study aims at integrating BP and inertial sensor data into an activity classifier in order to improve the activity (sitting, standing, walking, lying) recognition and the corresponding body elevation (during climbing stairs or when taking an elevator). Taking into account the trunk elevation changes during postural transitions (sit-to-stand, stand-to-sit), we devised an event-driven activity classifier based on fuzzy-logic. Data were acquired from 12 stroke patients with impaired mobility, using a trunk-worn inertial and BP sensor. Events, including walking and lying periods and potential postural transitions, were first extracted. These events were then fed into a double-stage hierarchical Fuzzy Inference System (H-FIS). The first stage processed the events to infer activities and the second stage improved activity recognition by applying behavioral constraints. Finally, the body elevation was estimated using a pattern-enhancing algorithm applied on BP. The patients were videotaped for reference. The performance of the algorithm was estimated using the Correct Classification Rate (CCR) and F-score. The BP-based classification approach was benchmarked against a previously-published fuzzy-logic classifier (FIS-IMU) and a conventional epoch-based classifier (EPOCH). Results: The algorithm performance for posture/activity detection, in terms of CCR was 90.4 %, with 3.3 % and 5.6 % improvements against FIS-IMU and EPOCH, respectively. The proposed classifier essentially benefits from a better recognition of standing activity (70.3 % versus 61.5 % [FIS-IMU] and 42.5 % [EPOCH]) with 98.2 % CCR for body elevation estimation. Conclusion: The monitoring and recognition of daily activities in mobility-impaired stoke patients can be significantly improved using a trunk-fixed sensor that integrates BP, inertial sensors, and an event-based activity classifier

Short-term effects of unilateral lesion of the primary motor cortex (M1) on ipsilesional hand dexterity in adult macaque monkeys

Although the arrangement of the corticospinal projection in primates is consistent with a more prominent role of the ipsilateral motor cortex on proximal muscles, rather than on distal muscles involved in manual dexterity, the role played by the primary motor cortex on the control of manual dexterity for the ipsilateral hand remains a matter a debate, either in the normal function or after a lesion. We, therefore, tested the impact of permanent unilateral motor cortex lesion on the manual dexterity of the ipsilateral hand in 11 macaque monkeys, within a time window of 60 days post-lesion. For comparison, unilateral reversible pharmacological inactivation of the motor cortex was produced in an additional monkey. Manual dexterity was assessed quantitatively based on three motor parameters derived from two reach and grasp manual tasks. In contrast to the expected dramatic, complete deficit of manual dexterity of the contralesional hand that persists for several weeks, the impact on the manual dexterity of the ipsilesional hand was generally moderate (but statistically significant) and, when present, lasted less than 20 days. Out of the 11 monkeys, only 3 showed a deficit of the ipsilesional hand for 2 of the 3 motor parameters, and 4 animals had a deficit for only one motor parameter. Four monkeys did not show any deficit. The reversible inactivation experiment yielded results consistent with the permanent lesion data. In conclusion, the primary motor cortex exerts a modest role on ipsilateral manual dexterity, most likely in the form of indirect hand postural control

Pharmacological Neuroprotection in Severe Traumatic Brain Injury

The basic pathophysiology of TBI consists of an initial, primary injury including rapid deformation of brain tissue with destruction of brain parenchyma and blood vessels and acute loss of neuronal and glial cells. A key concept in the management of TBI is that not all cell death occurs at the time of primary injury; instead, a cascade of molecular and neurochemical secondary events occur during the initial hours and days with a complex temporal profile. Ultimately, this secondary injury cascade markedly exacerbates the primary injury. Pharmacological attenuation of this secondary injury cascade with the aim of neuroprotection using, e.g. reactive oxygen species scavengers, glutamate receptor modulator, endocannabinoids, hypothermia or magnesium sulphate, has received much attention over several decades in numerous preclinical publications. To date, more than 20 phase III clinical trials have been conducted, and several trials are ongoing (Maas et al. 2010). Unfortunately, these trials all failed to demonstrate clinical efficacy, and there is no neuroprotective compound currently available for TBI patients. So is neuroprotection for TBI a dead concept not to be pursued clinically or experimentally? Arguably, no. There are likely numerous reasons for the failure of neuroprotective compounds used in clinical trials for TBI, including heterogeneous patient samples and general neurointensive care management. With few exceptions, the pharmacological and hypothermia TBI trials conducted to date have been rather small and have been frequently criticised in terms of study design, route of administration, time window and patient selection (e.g. Marklund and Hillered 2011; Maas et al. 2010). It should be emphasised that TBI is not one disease; instead, all the different subtypes of TBI may require markedly different treatments. Lack of early mechanistic or established surrogate endpoints and the insensitivity of the rather global outcome measures are specific problems in clinical TBI research. It is also obvious that numerous mistakes have been made in the past when attempting to translate preclinical information into the complex human situation. Such shortcomings of preclinical studies include the use of rodent TBI models reaching at most a moderate level of injury, and additionally, only rarely are pharmacological compounds administered beyond the first post-injury hours. Important lessons for future trials include improved patient classification, knowledge of brain penetration and action of the evaluated compound and more carefully defined and detailed outcome measures. Likely, future pharmacological management of TBI patients needs to combine neuroprotective drugs with compounds enhancing regeneration. Until such pharmacological treatment options are developed, neuroprotection for patients suffering from severe TBI is best provided by improved neurointensive care management with the avoidance, detection and treatment of avoidable factors such as seizures, fever, hypotension, hypoxemia, hyper- and hypoglycaemia, low CPP and high ICP. The present chapter reviews important aspects of pharmacological neuroprotection in severe traumatic brain injury. Hypothermia-induced neuroprotection is discussed in another chapter of this book

Profiling locomotor recovery: comprehensive quantification of impairments after CNS damage in rodents

Rodents are frequently used to model damage and diseases of the central nervous system (CNS) that lead to functional deficits. Impaired locomotor function is currently evaluated by using scoring systems or biomechanical measures. These methods often suffer from limitations such as subjectivity, nonlinearity and low sensitivity, or focus on a few very restricted aspects of movement. Thus, full quantitative profiles of motor deficits after CNS damage are lacking. Here we report the detailed characterization of locomotor impairments after applying common forms of CNS damage in rodents. We obtained many objective and quantitative readouts from rats with either spinal cord injuries or strokes and from transgenic mice (Epha4−/−) during skilled walking, overground walking, wading and swimming, resulting in model-specific locomotor profiles. Our testing and analysis method enables comprehensive assessment of locomotor function in rodents and has broad application in various fields of life science research