• The economic cost of spinal cord injury and traumatic brain injury in Australia (1.31Mb)

• HyperMED/VNI HBO, Lokomat, Cerebrolysin Submission October 2009.pdf - SCI, STROKE, TBI - Project Submission for Funding

HyperMED Stroke Protocols are unique

We provide saturative blocks of Hyperbaric Oxygenation combined with Lokomat (Gait Training) and other supportive modalities including Median Nerve Stimulation, Whole Body Vibration, immune stimulating supplements etc to impact the disease process and salvage back functionality.

Hyperbaric Oxygenation provides the available fuel and acts as a catalyst to the underlying central issue (hypoxia).

Lokomat (Robotic Gait Assisted Walking) and other forms of intensive physical therapy are required to ‘drive’ neuroplasticity - the ability of the neurons in the nervous system to develop new connections and ‘learn’ new functions. The rate of neuroplasticity is directly impacted by the levels of continuing hypoxia which blocks recovery!  

This combined Hyperbaric Lokomat approach ‘awakens’ dormant neural pathways and provides accurate neurological repetition enhancing and re-training connections and pathways in the brain and spinal cord.

Patients have the ability to ‘salvage back’ what has been damaged improving brain and spinal cord function - to regain walking ability or learn to walk!

• Transfer of scientific concepts to clinical practice: recent robot-assisted training studies.

Restoration of motor function is a priority of post-stroke rehabilitation, the aim being to facilitate the patient's reintegration into society. Innovative technologies for neurological rehabilitation must be easy to use and offer patients real benefits, and the treatments they provide must be efficacious and efficient. All these aspects must be carefully evaluated in their development. To achieve restoration of motor function after stroke, task-specific repetitive robot-assisted training of the upper and the lower extremity is currently the most promising approach. The results of clinical trials of robotic devices for upper limb (MIT-Manus, MIME, NeReBot, BiManuTrack, ARMin, ARMOR) and lower limb (LokoHelp, GangTrainer GT1, Haptic Walker, G-EO-Systems, Lokomat) training are here presented with the aim of highlighting the possible gains in motor function due to robotic therapy. Patients who receive robot-assisted training in combination with physiotherapy after stroke are more likely to achieve better motor function than patients trained without these devices, or only with these devices.

• HyperMED Clinical Research/STROKE-2009-563247v2-Hornby.pdf 'Locomotor training improves daily stepping activity and gait efficiency in individuals post stroke who have reached a 'plateau' in recovery Prof George Hornby'

• Exercise-mediated (Lokomat) locomotor recovery and lower-limb neuroplasticity after stroke

  
  Approximately 700,000 strokes occur annually in the United States; 50 percent of the 550,000 survivors experience residual hemiparesis affecting one side of the body and approximately 165,000 of those individuals have mobility deficits requiring assistance with walking [1-3]In this population, hemiparetic gait is a major problem that limits mobility, increases risk of falls, and imposes higher energy demands for basic daily activities [4-5]. Gait deviations due to hemiparesis are well documented, in terms of both clinical manifestation and biomechanical analyses [6-7]. Classic models of stroke recovery indicate that improvements in both upper- and lower-limb motor function plateau between 3 and 6 months poststroke [8]. Recent studies have challenged this assumption by suggesting that specific training interventions that target use of the hemiparetic limbs can improve motor control and neural plasticity. The research community now widely accepts that the central nervous system comprises inherently plastic neural networks that are continuously amenable to reorganization in the service of functional behaviors [9]. As a consequence, new therapeutic approaches seek to exploit experience-based CNS plasticity to mediate functional improvements. A common thread among most of these interventions is an adherence to the principles of motor learning, as defined by incorporating high volumes of task-oriented practice along with the added dimensions of goal setting and performance feedback [10].
  
  Studies of therapies that improve function and induce neuroplasticity in hemiparetic upper limbs in human survivors of stroke have supported an emerging focus on developing new learning-based strategies for improving gait and balance function in individuals with lower-limb hemiparesis after stroke [11-17]. Here we review evidence that one particular mode of exercise, treadmill (TM) training as applied in a number of approaches, can be employed to improve gait function in survivors of stroke with residual hemiparesis. We will suggest that basic motor learning strategies can alter underlying neural mechanisms to improve hemiparetic function of the lower limb and may also be effective in recovery of walking ability after stroke. Following a brief overview of the rationale and early results from studies using TM training with stroke, we provide examples that illustrate the role of the CNS in lower-limb motor control and gait. Our focus then shifts to an overview of how the neurophysiology of lower-limb motor control is sensitive to short-term adaptations and rapid plasticity. Finally, we review the early evidence of central neuroplasticity underlying lower-limb function and gait using long-term TM training protocols.
  
  RATIONALE FOR TREADMILL LOCOMOTOR LEARNING AFTER STROKE
  
  Findings from spinalized animal models demonstrate that walking without supraspinal inputs can occur when the animal is placed on a moving TM [18]. Thus, several investigations have studied TM training as a means to improve locomotor function in subjects with incomplete spinal cord injury and stroke. Visintin et al. first adapted the findings from spinalized animals to human experiments, reasoning that activation of subcortical neural structures by TM walking could provide a physiological stimulus for recovery of gait function [19-20]. These studies support the rationale that TM-generated stepping patterns in neurologically injured humans can help deliver repetitive sensory inputs to the spinal cord, which in turn could mediate locomotor learning and neural plasticity through a process of sensory motor integration [21]. Additional feasibility for this idea was shown in a study of the immediate effects of the TM stimulus on hemiparetic gait patterns in naive subjects with chronic stroke [22]. While controlling for walking speed, paretic paretic /pa·ret·ic/ (pah-ret´ik) pertaining to or affected with paresis.  limb stance-swing parameters and loading impulse immediately became more symmetrical on the TM compared with usual overground
  
  TREADMILL-BASED EXERCISE TRAINING IMPROVES GAIT FUNCTION
  
  The initial studies with human SCI and subacute stroke subjects used TM training in conjunction with partial body-weight suspension (PBWS PBWS Performance Based Work Statement (contracting mechanism) ). In a randomized study of more severely impaired subjects with subacute stroke, Barbeau and Visintin found TM with PBWS to be more effective than TM without PBWS for improving selected mobility outcomes in those subjects with more severe motor deficits (i.e., <0.2 m/s walking velocity and Berg Balance scores <15) [24]. By week 6 of training, 79 percent of subjects were able to train at 0 percent PBWS. In a noncontrolled 3-week study, 25 PBWS TM training sessions improved mobility scores and gait temporal-distance parameters in nine nonambulatory stroke subjects [25]. PBWS was not required after day 6 of training in seven of these nine cases. Similar results were reported in a follow-up study using the same approach in an A-B-A design [26]. These studies indicate an important role for PBWS as a bridge to full-weight-bearing TM exercise, particularly in subjects more severely affected.

What Happens With Stroke?

• Most victims of stroke have years of progressive vascular insufficiency leading to a catastrophic event. Those that survive have a long road ahead. Stroke recovery is slow and many do not survive past 3-5 years due to 'secondary cascade complications'

• The event of stroke causes widespread hypoxic damage which can be measured on MRI - often referred to as 'encephalomalacia' which leads to progressive 'softening and liquefaction' of the brain. Google search this term for additional information. The MRI has a typical 'watershed' that delineates the area affected by stroke. However many stroke survivors with further MRI years later demonstrate expansion of the original watershed. This is due to Hypoxic Induced Apoptosis. Hypoxia fosters progressive neurodegeneration compounded by 'learned non-use'  

• Breakthrough Stroke Therapy - Malay Mail - The two machines, the Lokomat and the Armeo, were developed by Swiss-based Hocoma - renowned leaders in robotic rehabilitation therapy for neurological ...

• How robotics are assisting Stroke victims

• HyperMED Australia : Beyond Therapy - Treatment Program

• HyperMED Australia : Lokomat NeuroRecovery

• HyperMED/HyperMED Lokomat 2009.pdf

• HyperMED/Lokomat - Australian Experience HyperMED NeuroRecovery.pdf