Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, August 26, 2015

Differential effects of parietal and cerebellar stroke in response to object location perturbation

This is a worthless piece of research unless someone takes it and translates it into a useful stroke protocol. That is exactly what a great stroke association would do, except we don't have one.
http://journal.frontiersin.org/article/10.3389/fnhum.2015.00293/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neurology-w35-2015

  • 1School of Psychology, College of Life and Environmental Sciences, University of Birmingham, Edgbaston, UK
  • 2School of Health Sciences, Faculty of Health and Medicine, The University of Newcastle, Callaghan, NSW, Australia
  • 3Hunter Medical Research Institute, The University of Newcastle, Callaghan, NSW, Australia
Background: The differential contributions of the cerebellum and parietal lobe to coordination between hand transport and hand shaping to an object have not been clearly identified.
Objective: To contrast impairments in reach-to-grasp coordination, in response to object location perturbation, in patients with right parietal and cerebellar lesions, in order to further elucidate the role of each area in reach-to-grasp coordination.
Method: A two-factor design with one between subject factor (right parietal stroke; cerebellar stroke; controls) and one within subject factor (presence or absence of object location perturbation) examined correction processes used to maintain coordination between transport-to-grasp in the presence of perturbation. Sixteen chronic stroke participants (eight with right parietal lesions and eight with cerebellar lesions) were matched in age (mean = 61 years; standard deviation = 12) and hand dominance with 16 healthy controls. Hand and arm movements were recorded during unperturbed baseline trials (10) and unpredictable trials (60) in which the target was displaced to the left (10) or right (10) or remained fixed (40).
Results: Cerebellar patients had a slowed response to perturbation with anticipatory hand opening, an increased number of aperture peaks and disruption to temporal coordination, and greater variability. Parietal participants also exhibited slowed movements, with increased number of aperture peaks, but in addition, increased the number of velocity peaks and had a longer wrist path trajectory due to difficulties planning the new transport goal and thus relying more on feedback control.
Conclusion: Patients with parietal or cerebellar lesions showed some similar and some contrasting deficits. The cerebellum was more dominant in controlling temporal coupling between transport and grasp components, and the parietal area was more concerned with using sensation to relate arm and hand state to target position.

Introduction

Successful control of reach-to-grasp requires coordination, “an ability to maintain a context-dependent and phase-dependent cyclical relationship between different body segments or joints in both spatial and temporal domains” (Krasovsky and Levin, 2010) of various body segments including the arm with the trunk, the shoulder with the elbow, and the hand with the arm. Studies in healthy adults have suggested hand and arm function are controlled as a single coordinated unit (Jeannerod, 1984; Wallace et al., 1990) demonstrated by significant correlations between reach and grasp components, including between the start time of the opening of the hand and the start time of hand movement toward the object (Jeannerod and Biguer, 1982; Jeannerod, 1984), between the time of maximum hand aperture and the time of peak deceleration (PD) of the hand (Jeannerod, 1984; Castiello et al., 1993), and between time of maximum aperture (TMA) and the time of peak velocity (TPV) of the hand (Wallace et al., 1990). Apart from a few situations (Gentilucci et al., 1991; Kudoh et al., 1997), for example, where correlations between the time of PD and the time of MA are not reliable when transport and grasp were manipulated by the distance and type of grasp (Gentilucci et al., 1991), temporal coupling of these events is a fairly consistent finding across reach-to-grasp tasks.
Stroke can adversely affect reach-to-grasp coordination (Pelton et al., 2012; vanVliet et al., 2013). Spatiotemporal relationships between transport and grasp in a heterogenous group of stroke patients with mild to moderate impairments, were investigated in a study where movements were performed at both fast and preferred speeds and to small and larger objects (vanVliet and Sheridan, 2007). There were significant correlations (p < 0.05) between times of start of hand movement and hand opening and between times of MA and PD in all conditions for both groups, although some of the correlations were numerically small (Pearson product-moment correlation coefficient r for the two groups ranged from 0.3 to 0.71). However, transport and grasp in patients were not as tightly coupled. In the condition which most challenged accuracy (i.e., the fast paced condition with small objects), the two events were less correlated in participants with stroke.
One informative paradigm used to investigate underlying control mechanisms for coordination of reach-to-grasp is to perturb the object location at movement onset in order to examine the resulting temporal adjustments made to the grasp component (Paulignan et al., 1990, 1991a,b), requiring modification of a pre-defined program (Goodale et al., 1986). Typically, the unexpected perturbation in the object produced adjustments to both the transport and grasp components, where the initial wrist acceleration was aborted and a new one started, and the initial grasp aperture was also aborted and reincreased in synchrony (Paulignan et al., 1990, 1991a,b) demonstrating that the two components are coordinated spatiotemporally.
The premise of a tight-coupling between the two components prompted the development of a model for the temporal coordination of transport and grasp (Hoff and Arbib, 1993). The model proposed that neural processes controlling transport and grasp are monitored on-line and adjusted for temporally so that the expected duration of each trajectory to reach the target is matched to the other component according to a consistent enclose time of the hand. The coordinated control of transport-to-grasp with object location perturbation also involves the integration of sensory signals from multiple modalities (principally visual information concerning the object and its relative position; and proprioceptive information about the position of the arm and the hand). It requires the feed-forward selection of perhaps one or two coupled motor commands for transport and grasp together with a forward representation of the desired movement. Smooth movement is dependent upon on-line updating of the initial pattern of muscle activation and detection of error between the actual positions of object relative to the hand. Large errors which are instigated by the introduction of a perturbation require either rapid modification of an ongoing internal forward model or rapid onset of a new internal forward model and cessation of the old forward model.
Two key brain areas responsible for processing of information pertaining to reach-to-grasp coordination are the parietal lobe and the cerebellum. Current theories attribute similar contributions by parietal and cerebellar regions. For example, both areas have been identified as potential areas that integrate the independent motor processes for reach and grasp into one common motor program (Desmurget et al., 1999; Zackowski et al., 2002). Given the specialization of cortical areas, it is unlikely that these areas perform identical roles. Thus, further research is needed to elucidate their exact role in control of reach-to-grasp. It has been pointed out that the two regions may work as a functional loop in estimating the current status of the motor system, since the parietal cortex receives input from the cerebellar dentate nucleus, and there are connections from parietal cortex to cerebellum via the pontine nuclei (Blakemore and Sirigu, 2003; Ramnani, 2012). Below, we review the current knowledge about roles of parietal cortex and cerebellum in control of reach-to-grasp.

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